Displaying publications 21 - 40 of 134 in total

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  1. Fulltext In vitro treatment of lipopolysaccharide increases invasion of Pasteurella multocida serotype B:2 into bovine aortic endothelial cells
    Yap SK, Zakaria Z, Othman SS, Omar AR
    J Vet Sci, 2018 Mar 31;19(2):207-215.
    PMID: 28693312 DOI: 10.4142/jvs.2018.19.2.207
    Pasteurella multocida serotype B:2 causes hemorrhagic septicemia in cattle and buffalo. The invasion mechanism of the bacterium when invading the bloodstream is unclear. This study aimed to characterize the effects of immunomodulatory molecules, namely dexamethasone and lipopolysaccharide, on the invasion efficiency of P. multocida serotype B:2 toward bovine aortic endothelial cells (BAECs) and the involvement of actin microfilaments in the invasion mechanism. The results imply that treatment of BAECs with lipopolysaccharide at 100 ng/mL for 24 h significantly increases the intracellular bacteria number per cell (p ＜ 0.01) compared with those in untreated and dexamethasone-treated cells. The lipopolysaccharide-treated cells showed a significant decrease in F-actin expression and an increase in G-actin expression (p ＜ 0.001), indicating actin depolymerization of BAECs. However, no significant differences were detected in the invasion efficiency and actin filament reorganization between the dexamethasone-treated and untreated cells. Transmission electron microscopy showed that P. multocida B:2 resided in a vacuolar compartment of dexamethasone-treated and untreated cells, whereas the bacteria resided in cellular membrane of lipopolysaccharide-treated cells. The results suggest that lipopolysaccharide destabilizes the actin filaments of BAECs, which could facilitate the invasion of P. multocida B:2 into BAECs.
    Matched MeSH terms: Endothelium, Vascular/drug effects; Endothelium, Vascular/microbiology*
  2. Vasorelaxation effect of Glycyrrhizae uralensis through the endothelium-dependent Pathway
    Tan CS, Ch'ng YS, Loh YC, Zaini Asmawi M, Ahmad M, Yam MF
    J Ethnopharmacol, 2017 Mar 06;199:149-160.
    PMID: 28161542 DOI: 10.1016/j.jep.2017.02.001
    ETHNOPHARMACOLOGICAL RELEVANCE: Glycyrrhiza uralensis (G. uralensis) is one of the herbs used in traditional Chinese medicine (TCM) and serves as an envoy medicinal. Since G. uralensis plays a major role in the anti-hypertensive TCM formulae, we believe that G. uralensis might possess vasorelaxation activity.

    AIM OF THE STUDY: This study is designed to investigate the vasorelaxation effect of G. uralensis from various extracts and to study its pharmacology effect.

    MATERIALS AND METHODS: The vasorelaxation effect of G. uralensis extracts were evaluated on thoracic aortic rings isolated from Sprague Dawley rats.

    RESULTS: Among these three extracts of G. uralensis, 50% ethanolic extract (EFG) showed the strongest vasorelaxation activity. EFG caused the relaxation of the aortic rings pre-contracted with phenylephrine either in the presence or absence of endothelium and pre-contracted with potassium chloride in endothelium-intact aortic ring. Nω-nitro-L-arginine methyl ester, methylene blue, or 1H-[1,2,4]Oxadiazolo[4,3-a]quinoxalin-1-one inhibit the vasorelaxation effect of EFG in the presence of endothelium. On the other hand, in the presence of the potassium channel blockers (tetraethylammonium and barium chloride), the vasorelaxation effect of EFG was not affected, but glibenclamide and 4-aminopyridine did inhibit the vasorelaxation effect of EFG. With indomethacin, atropine and propranolol, the vasorelaxation effect by EFG was significantly reduced. EFG was also found to be effective in reducing Ca(2+) release from sarcoplasmic reticulum and the blocking of calcium channels.

    CONCLUSIONS: The results obtained suggest that EFG is involved in the NO/sGC/cGMP pathway.

    Matched MeSH terms: Endothelium, Vascular/drug effects*; Endothelium, Vascular/physiology
  3. Mechanisms of Blood Brain Barrier Disruption by Different Types of Bacteria, and Bacterial-Host Interactions Facilitate the Bacterial Pathogen Invading the Brain
    Al-Obaidi MMJ, Desa MNM
    Cell Mol Neurobiol, 2018 Oct;38(7):1349-1368.
    PMID: 30117097 DOI: 10.1007/s10571-018-0609-2
    This review aims to elucidate the different mechanisms of blood brain barrier (BBB) disruption that may occur due to invasion by different types of bacteria, as well as to show the bacteria-host interactions that assist the bacterial pathogen in invading the brain. For example, platelet-activating factor receptor (PAFR) is responsible for brain invasion during the adhesion of pneumococci to brain endothelial cells, which might lead to brain invasion. Additionally, the major adhesin of the pneumococcal pilus-1, RrgA is able to bind the BBB endothelial receptors: polymeric immunoglobulin receptor (pIgR) and platelet endothelial cell adhesion molecule (PECAM-1), thus leading to invasion of the brain. Moreover, Streptococcus pneumoniae choline binding protein A (CbpA) targets the common carboxy-terminal domain of the laminin receptor (LR) establishing initial contact with brain endothelium that might result in BBB invasion. Furthermore, BBB disruption may occur by S. pneumoniae penetration through increasing in pro-inflammatory markers and endothelial permeability. In contrast, adhesion, invasion, and translocation through or between endothelial cells can be done by S. pneumoniae without any disruption to the vascular endothelium, upon BBB penetration. Internalins (InlA and InlB) of Listeria monocytogenes interact with its cellular receptors E-cadherin and mesenchymal-epithelial transition (MET) to facilitate invading the brain. L. monocytogenes species activate NF-κB in endothelial cells, encouraging the expression of P- and E-selectin, intercellular adhesion molecule 1 (ICAM-1), and Vascular cell adhesion protein 1 (VCAM-1), as well as IL-6 and IL-8 and monocyte chemoattractant protein-1 (MCP-1), all these markers assist in BBB disruption. Bacillus anthracis species interrupt both adherens junctions (AJs) and tight junctions (TJs), leading to BBB disruption. Brain microvascular endothelial cells (BMECs) permeability and BBB disruption are induced via interendothelial junction proteins reduction as well as up-regulation of IL-1α, IL-1β, IL-6, TNF-α, MCP-1, macrophage inflammatory proteins-1 alpha (MIP1α) markers in Staphylococcus aureus species. Streptococcus agalactiae or Group B Streptococcus toxins (GBS) enhance IL-8 and ICAM-1 as well as nitric oxide (NO) production from endothelial cells via the expression of inducible nitric oxide synthase (iNOS) enhancement, resulting in BBB disruption. While Gram-negative bacteria, Haemophilus influenza OmpP2 is able to target the common carboxy-terminal domain of LR to start initial interaction with brain endothelium, then invade the brain. H. influenza type b (HiB), can induce BBB permeability through TJ disruption. LR and PAFR binding sites have been recognized as common routes of CNS entrance by Neisseria meningitidis. N. meningitidis species also initiate binding to BMECs and induces AJs deformation, as well as inducing specific cleavage of the TJ component occludin through the release of host MMP-8. Escherichia coli bind to BMECs through LR, resulting in IL-6 and IL-8 release and iNOS production, as well as resulting in disassembly of TJs between endothelial cells, facilitating BBB disruption. Therefore, obtaining knowledge of BBB disruption by different types of bacterial species will provide a picture of how the bacteria enter the central nervous system (CNS) which might support the discovery of therapeutic strategies for each bacteria to control and manage infection.
    Matched MeSH terms: Endothelium, Vascular/metabolism; Endothelium, Vascular/microbiology
  4. Endothelium-dependent vascular relaxation is abnormal in the coronary microcirculation of atherosclerotic primates
    Sellke FW, Armstrong ML, Harrison DG
    Circulation, 1990 May;81(5):1586-93.
    PMID: 2110036
    Atherosclerosis impairs endothelium-dependent relaxation of large conduit arteries. Because coronary resistance vessels are spared from the development of overt atherosclerosis, endothelium-dependent responses were examined in these vascular segments. Malaysian cynomolgus monkeys (n = 6) were made atherosclerotic by being fed a 0.7% cholesterol diet for 18 months. Control monkeys (n = 6) were fed a standard diet. Coronary microvessels (122-220 microns) were studied in a pressurized (20 mm Hg), no-flow state using a video-imaging apparatus. Relaxations of microvessels, preconstricted with the thromboxane analogue U46619, were determined in response to acetylcholine, bradykinin, the calcium ionophore A23187, adenosine, and sodium nitroprusside. Microvascular relaxations to bradykinin and A23187 were reduced in atherosclerotic monkeys compared with controls, whereas acetylcholine produced additional contraction in atherosclerotic monkeys. Responses of preconstricted microvessels to adenosine and sodium nitroprusside were identical in atherosclerotic and control animals. Indomethacin did not alter responses in control or atherosclerotic animals. Histologic examination revealed neither intimal thickening nor plaque formation in microvessels of this size class despite marked changes in conduit arteries. Electron microscopy showed minor alterations of endothelial cell morphology in microvessels of atherosclerotic animals. In conclusion, long-term hypercholesterolemia markedly impairs endothelium-dependent vascular relaxation in the coronary microcirculation where overt atherosclerosis does not develop. These changes in endothelial cell function may significantly alter regulation of myocardial perfusion by neurohumoral stimuli.
    Matched MeSH terms: Endothelium, Vascular/pathology; Endothelium, Vascular/physiopathology*
  5. Fulltext Escherichia coli K1 utilizes host macropinocytic pathways for invasion of brain microvascular endothelial cells
    Loh LN, McCarthy EMC, Narang P, Khan NA, Ward TH
    Traffic, 2017 11;18(11):733-746.
    PMID: 28799243 DOI: 10.1111/tra.12508
    Eukaryotic cells utilize multiple endocytic pathways for specific uptake of ligands or molecules, and these pathways are commonly hijacked by pathogens to enable host cell invasion. Escherichia coli K1, a pathogenic bacterium that causes neonatal meningitis, invades the endothelium of the blood-brain barrier, but the entry route remains unclear. Here, we demonstrate that the bacteria trigger an actin-mediated uptake route, stimulating fluid phase uptake, membrane ruffling and macropinocytosis. The route of uptake requires intact lipid rafts as shown by cholesterol depletion. Using a variety of perturbants we demonstrate that small Rho GTPases and their downstream effectors have a significant effect on bacterial invasion. Furthermore, clathrin-mediated endocytosis appears to play an indirect role in E. coli K1 uptake. The data suggest that the bacteria effect a complex interplay between the Rho GTPases to increase their chances of uptake by macropinocytosis into human brain microvascular endothelial cells.
    Matched MeSH terms: Endothelium, Vascular/metabolism; Endothelium, Vascular/microbiology
  6. Fulltext Parasite biomass-related inflammation, endothelial activation, microvascular dysfunction and disease severity in vivax malaria
    Barber BE, William T, Grigg MJ, Parameswaran U, Piera KA, Price RN, et al.
    PLoS Pathog, 2015 Jan;11(1):e1004558.
    PMID: 25569250 DOI: 10.1371/journal.ppat.1004558
    Plasmodium vivax can cause severe malaria, however its pathogenesis is poorly understood. In contrast to P. falciparum, circulating vivax parasitemia is low, with minimal apparent sequestration in endothelium-lined microvasculature, and pathogenesis thought unrelated to parasite biomass. However, the relationships between vivax disease-severity and total parasite biomass, endothelial autocrine activation and microvascular dysfunction are unknown. We measured circulating parasitemia and markers of total parasite biomass (plasma parasite lactate dehydrogenase [pLDH] and PvLDH) in adults with severe (n = 9) and non-severe (n = 53) vivax malaria, and examined relationships with disease-severity, endothelial activation, and microvascular function. Healthy controls and adults with non-severe and severe falciparum malaria were enrolled for comparison. Median peripheral parasitemia, PvLDH and pLDH were 2.4-fold, 3.7-fold and 6.9-fold higher in severe compared to non-severe vivax malaria (p = 0.02, p = 0.02 and p = 0.015, respectively), suggesting that, as in falciparum malaria, peripheral P. vivax parasitemia underestimates total parasite biomass, particularly in severe disease. P. vivax schizonts were under-represented in peripheral blood. Severe vivax malaria was associated with increased angiopoietin-2 and impaired microvascular reactivity. Peripheral vivax parasitemia correlated with endothelial activation (angiopoietin-2, von-Willebrand-Factor [VWF], E-selectin), whereas markers of total vivax biomass correlated only with systemic inflammation (IL-6, IL-10). Activity of the VWF-cleaving-protease, ADAMTS13, was deficient in proportion to endothelial activation, IL-6, thrombocytopenia and vivax disease-severity, and associated with impaired microvascular reactivity in severe disease. Impaired microvascular reactivity correlated with lactate in severe vivax malaria. Findings suggest that tissue accumulation of P. vivax may occur, with the hidden biomass greatest in severe disease and capable of mediating systemic inflammatory pathology. The lack of association between total parasite biomass and endothelial activation is consistent with accumulation in parts of the circulation devoid of endothelium. Endothelial activation, associated with circulating parasites, and systemic inflammation may contribute to pathology in vivax malaria, with microvascular dysfunction likely contributing to impaired tissue perfusion.
    Matched MeSH terms: Endothelium, Vascular/immunology; Endothelium, Vascular/physiopathology*
  7. Exploring the mechanism of endothelial involvement in acidosis-induced vasodilatation of aortic tissues from normal and diabetic rats
    Yeo JL, Tan BT, Achike FI
    Eur J Pharmacol, 2010 Sep 10;642(1-3):99-106.
    PMID: 20553918 DOI: 10.1016/j.ejphar.2010.05.040
    Acidosis modulates physiologic and pathophysiologic processes but the mechanism of acidotic vasodilatation remains unclear. We therefore explored this in aortic rings from normal and streptozotocin-induced diabetic Sprague-Dawley rats. Phenylephrine (PE)-induced contraction in endothelium-intact and -denuded rings were recorded under normal and acidotic pH with or without drug probes. Acidosis exerted a relaxant effect in endothelium-intact and -denuded euglycaemic and diabetic tissues. l-NAME or methylene blue partially inhibited acidotic relaxation in these endothelium-intact but not the -denuded tissues, with greater inhibition in the diabetic tissues, indicating that acidosis induces relaxation by endothelium-dependent and -independent mechanisms, the former being EDNO-cGMP mediated. Indomethacin had no effect on the tissues, indicating that cyclooxygenase products are neither involved in acidosis-induced vasodilatation nor in the modulation of phenylephrine-contraction. In euglycaemic tissues under normal pH, no K(+) channel blocker altered phenylephrine-contraction, but all (except glibenclamide) enhanced diabetic tissue contraction, indicating that normally, these channels (K(ir), K(V), BK(Ca), K(ATP)) do not modulate phenylephrine-contraction, but they (except K(ATP)) are expressed in diabetes where they attenuate phenylephine-induced contraction and modulate acidosis. Only the K(ir) channel modulates acidotic relaxation in euglycaemic tissues. Only tetraethylammonium and iberiotoxin enhanced phenylephrine-induced contraction in endothelium-denuded diabetic tissues indicating that BK(Ca) attenuates phenylephrine-contraction and that acidotic relaxation in this condition is modulated by a tetraethylammonium-sensitive mechanism. In conclusion, acidosis causes vasodilatation in normal and diabetic tissues via endothelium-dependent and -independent mechanisms differentially modulated by a combination of a NO-cGMP process and K(+) channels, some of which are dormant in the normal state but activated in diabetes mellitus.
    Matched MeSH terms: Endothelium, Vascular/drug effects; Endothelium, Vascular/pathology*; Endothelium, Vascular/physiopathology*
  8. Fulltext ‘Boating’ out migrated dexamethasone implant; surgical management of removal of anterior chamber migrated dexamethasone intravitreal implant: a case report
    Teo, B.H., Safinaz, M.K., Mae-Lynn, C.B., Amin, A., Edward, R., Mushawiahti, M.
    Medicine & Health, 2018;13(2):175-179.
    MyJurnal
    It is rare for anterior chamber migration of an Ozurdex® implant from vitreous cavity, but it is seen more frequently in aphakic eyes or in pseudophakic cases with zonular dehiscense. We describe a case of a middle-aged gentleman who had persistent diabetic macular oedema not responding to anti-VEGF (vascular endothelium growth factor), who was treated with intravitreal Ozurdex® in his post vitrectomized eye and developed anterior migration of the implant to the anterior chamber. Anterior dislocation of an intravitreal implant of dexamethasone can be managed by repositioning it to the vitreous cavity or removing it through a corneal limbal incision. Ozurdex® is a friable implant, especially after a few weeks of implantation. Therefore, removal of the implant by grasping or aspiration may lead to its fracture or dispersion of the implant material. This is a report of a simple,fast and effective technique to remove a migrated Ozurdex® from the anterior chamber using a modified silicone tip.
    Matched MeSH terms: Endothelium, Vascular
  9. Fulltext Correlation of host inflammatory cytokines and immune-related metabolites, but not viral NS1 protein, with disease severity of dengue virus infection
    Soe HJ, Manikam R, Raju CS, Khan MA, Sekaran SD
    PLoS One, 2020;15(8):e0237141.
    PMID: 32764789 DOI: 10.1371/journal.pone.0237141
    Severe dengue can be lethal caused by manifestations such as severe bleeding, fluid accumulation and organ impairment. This study aimed to investigate the role of dengue non-structural 1 (NS1) protein and host factors contributing to severe dengue. Electrical cell-substrate impedance sensing system was used to investigate the changes in barrier function of microvascular endothelial cells treated NS1 protein and serum samples from patients with different disease severity. Cytokines and metabolites profiles were assessed using a multiplex cytokine assay and liquid chromatography mass spectrometry respectively. The findings showed that NS1 was able to induce the loss of barrier function in microvascular endothelium in a dose dependent manner, however, the level of NS1 in serum samples did not correlate with the extent of vascular leakage induced. Further assessment of host factors revealed that cytokines such as CCL2, CCL5, CCL20 and CXCL1, as well as adhesion molecule ICAM-1, that are involved in leukocytes infiltration were expressed higher in dengue patients in comparison to healthy individuals. In addition, metabolomics study revealed the presence of deregulated metabolites involved in the phospholipid metabolism pathway in patients with severe manifestations. In conclusion, disease severity in dengue virus infection did not correlate directly with NS1 level, but instead with host factors that are involved in the regulation of junctional integrity and phospholipid metabolism. However, as the studied population was relatively small in this study, these exploratory findings should be confirmed by expanding the sample size using an independent cohort to further establish the significance of this study.
    Matched MeSH terms: Endothelium, Vascular/cytology; Endothelium, Vascular/immunology; Endothelium, Vascular/pathology
  10. Fulltext Boldine Ameliorates Vascular Oxidative Stress and Endothelial Dysfunction: Therapeutic Implication for Hypertension and Diabetes
    Lau YS, Ling WC, Murugan D, Mustafa MR
    J Cardiovasc Pharmacol, 2015 Jun;65(6):522-31.
    PMID: 25469805 DOI: 10.1097/FJC.0000000000000185
    Epidemiological and clinical studies have demonstrated that a growing list of natural products, as components of the daily diet or phytomedical preparations, are a rich source of antioxidants. Boldine [(S)-2,9-dihydroxy-1,10-dimethoxy-aporphine], an aporphine alkaloid, is a potent antioxidant found in the leaves and bark of the Chilean boldo tree. Boldine has been extensively reported as a potent "natural" antioxidant and possesses several health-promoting properties like anti-inflammatory, antitumor promoting, antidiabetic, and cytoprotective. Boldine exhibited significant endothelial protective effect in animal models of hypertension and diabetes mellitus. In isolated thoracic aorta of spontaneously hypertensive rats, streptozotocin-induced diabetic rats, and db/db mice, repeated treatment of boldine significantly improved the attenuated acetylcholine-induced endothelium-dependent relaxations. The endothelial protective role of boldine correlated with increased nitric oxide levels and reduction of vascular reactive oxygen species via inhibition of the nicotinamide adenine dinucleotide phosphate oxidase subunits, p47 and nicotinamide adenine dinucleotide phosphate oxidase 2, and angiotensin II-induced bone morphogenetic protein-4 oxidative stress cascade with downregulation of angiotensin II type 1 receptor and bone morphogenetic protein-4 expression. Taken together, it seems that boldine may exert protective effects on the endothelium via several mechanisms, including protecting nitric oxide from degradation by reactive oxygen species as in oxidative stress-related diseases. The present review supports a complimentary therapeutic role of the phytochemical, boldine, against endothelial dysfunctions associated with hypertension and diabetes mellitus by interfering with the oxidative stress-mediated signaling pathway.
    Matched MeSH terms: Endothelium, Vascular/drug effects*; Endothelium, Vascular/metabolism; Endothelium, Vascular/physiopathology
  11. Establishment of rat brain endothelial cells susceptible to rat cytomegalovirus ALL-03 infection
    Camalxaman SN, Zeenathul NA, Quah YW, Loh HS, Zuridah H, Hani H, et al.
    In Vitro Cell Dev Biol Anim, 2013 Mar;49(3):238-44.
    PMID: 23435855 DOI: 10.1007/s11626-012-9553-5
    Endothelial cells have been implicated as key cells in promoting the pathogenesis and spread of cytomegalovirus (CMV) infection. This study describes the isolation and culture of rat brain endothelial cells (RBEC) and further evaluates the infectious potential of a Malaysian rat CMV (RCMV ALL-03) in these cultured cells. Brain tissues were mechanically fragmented, exposed to enzymatic digestion, purified by gradient density centrifugation, and cultured in vitro. Morphological characteristics and expression of von Willebrand factor (factor VIII-related antigen) verified the cells were of endothelial origin. RBEC were found to be permissive to the virus by cytopathic effects with detectable plaques formed within 7 d of infection. This was confirmed by electron microscopy examination which proved the existence of the viral particles in the infected cells. The susceptibility of the virus to these target cells under the experimental conditions described in this report provides a platform for developing a cell-culture-based experimental model for studies of RCMV pathogenesis and allows stimulation of further studies on host cell responses imposed by congenital viral infections.
    Matched MeSH terms: Endothelium, Vascular/metabolism; Endothelium, Vascular/pathology; Endothelium, Vascular/virology
  12. Fulltext Chronic treatment with paeonol improves endothelial function in mice through inhibition of endoplasmic reticulum stress-mediated oxidative stress
    Choy KW, Lau YS, Murugan D, Mustafa MR
    PLoS One, 2017;12(5):e0178365.
    PMID: 28562691 DOI: 10.1371/journal.pone.0178365
    Endoplasmic reticulum (ER) stress leads to endothelial dysfunction which is commonly associated in the pathogenesis of several cardiovascular diseases. We explored the vascular protective effects of chronic treatment with paeonol (2'-hydroxy-4'-methoxyacetophenone), the major compound from the root bark of Paeonia suffruticosa on ER stress-induced endothelial dysfunction in mice. Male C57BL/6J mice were injected intraperitoneally with ER stress inducer, tunicamycin (1 mg/kg/week) for 2 weeks to induce ER stress. The animals were co-administered with or without paeonol (20 mg/kg/oral gavage), reactive oxygen species (ROS) scavenger, tempol (20 mg/kg/day) or ER stress inhibitor, tauroursodeoxycholic acid (TUDCA, 150 mg/kg/day) respectively. Blood pressure and body weight were monitored weekly and at the end of treatment, the aorta was isolated for isometric force measurement. Protein associated with ER stress (GRP78, ATF6 and p-eIF2α) and oxidative stress (NOX2 and nitrotyrosine) were evaluated using Western blotting. Nitric oxide (NO) bioavailability were determined using total nitrate/nitrite assay and western blotting (phosphorylation of eNOS protein). ROS production was assessed by en face dihydroethidium staining and lucigenin-enhanced chemiluminescence assay, respectively. Our results revealed that mice treated with tunicamycin showed an increased blood pressure, reduction in body weight and impairment of endothelium-dependent relaxations (EDRs) of aorta, which were ameliorated by co-treatment with either paeonol, TUDCA and tempol. Furthermore, paeonol reduced the ROS level in the mouse aorta and improved NO bioavailability in tunicamycin treated mice. These beneficial effects of paeonol observed were comparable to those produced by TUDCA and tempol, suggesting that the actions of paeonol may involve inhibition of ER stress-mediated oxidative stress pathway. Taken together, the present results suggest that chronic treatment with paeonol preserved endothelial function and normalized blood pressure in mice induced by tunicamycin in vivo through the inhibition of ER stress-associated ROS.
    Matched MeSH terms: Endothelium, Vascular/drug effects*; Endothelium, Vascular/metabolism; Endothelium, Vascular/physiology
  13. Fulltext In vivo slit scanning confocal microscopic observation in a patient with moderate and severe keratoconus: a case report
    Mutalib HA, Ghosh S, Sharanjeet-Kaur, Ghoshal R
    Clin Optom (Auckl), 2016;8:79-83.
    PMID: 30214352 DOI: 10.2147/OPTO.S106421
    A 22-year-old Indian female was referred to Sg Buloh hospital with the diagnosis of bilateral keratoconus. On examination, slit lamp biomicroscopy and corneal topography revealed stage 3 keratoconus in the right eye and stage 2 keratoconus in the left eye. Corneal cell morphology in both eyes was evaluated using confocal microscope. In qualitative observation, almost all corneal layers in right eye except endothelium were partially or completely obscured by haze. Additionally, morphological alterations, such as elongation of keratocyte nuclei and cluster of cells, and dark bands in the anterior stroma were observed in right eye. In the left eye, the amount of haze was less, allowing better visibility of the corneal layers compared with the right eye. The dark bands were evident in the posterior stroma. Quantitative analysis showed that anterior and posterior stromal keratocyte density and endothelium cell density were relatively low in the right eye (834.0, 700.5, and 2,133 cells/mm2, respectively) compared with the left eye (934.1, 750.6, and 2,361 cells/mm2, respectively). In this case, the right eye, exhibiting stage 3 keratoconus, showed more morphological alteration, particularly in the anterior stroma compared with the left eye with stage 2 keratoconus. Increased severity of the disease can explain these differences in corneal cell morphology.
    Matched MeSH terms: Endothelium
  14. Fulltext Changes in corneal endothelial cells morphology due to different cataract surgery procedures: a retrospective study from November 2014 to November 2016
    Bariah, M.A ., Leong, S.Y.
    International Medical Journal Malaysia, 2018;17(2):117-124.
    MyJurnal
    Introduction: The corneal endothelium is made up of an extremely thin layer of non -regenerating cells essential in keeping the cornea clear. The purpose of this study was to quantify the corneal endothelial cells morphology, visual acuity (VA) and refractive error in patients having femtosecond laser-assisted cataract surgery (FLACS) and conventional phacoemulsification surgery (CPS). Methods: Clinical data from 56 eyes were included in this study. 28 eyes had FLACS surgery and another 28 eyes had CPS. Distance VA, refractive error, corneal thickness and endothelial cells morphology were evaluated pre-operatively and at 1 month follow up. Refractive error was determined subjectively and VA was taken using Snellen chart. Specular microscope was used to measure endothelial cells morphology and central corneal thickness. Mann Whitney test and Spearman correlation analysis were used to analyse the results. Results: There were no statistically significant difference in the mean endothelial cell density (p=0.24), mean central corneal thickness (p=0.68), mean coefficient of variance (p=0.19), mean hexagonality (p=0.44), VA (p=0.72) and postoperative refractive outcome (p=0.66) between both groups. The duration of surgery was noted to have no statistically significant difference between both groups (p=0.08), while the cumulative dissipated energy and torsional time showed a significant difference between groups (p=0.01 and p
    Matched MeSH terms: Endothelium, Corneal
  15. Vitamin D deficiency attenuates endothelial function by reducing antioxidant activity and vascular eNOS expression in the rat microcirculation
    Wee CL, Mokhtar SS, Banga Singh KK, Rasool AHG
    Microvasc Res, 2021 Nov;138:104227.
    PMID: 34324883 DOI: 10.1016/j.mvr.2021.104227
    This study examined the effects of vitamin D deficiency on vascular function and tissue oxidative status in the microcirculation; and whether or not these effects can be ameliorated with calcitriol, the active vitamin D metabolite. Three groups (n = 10 each) of male Sprague Dawley rats were fed for 10 weeks with control diet (CR), vitamin D-deficient diet without (DR), or with oral calcitriol supplementation (0.15 μg/kg) for the last four weeks (DSR). After 10 weeks, rats were sacrificed; mesenteric arterial rings were studied using wire myograph. Oxidative stress biomarkers malondialdehyde (MDA) levels and superoxide dismutase (SOD) activity were measured in the mesenteric arterial tissue. Vascular protein expression of endothelial nitric oxide synthase (eNOS) was determined by Western blotting. Acetylcholine-induced endothelium-dependent relaxation of DR was lower than CR. eNOS expression and SOD activity were lower in mesenteric arterial tissue of DR compared to CR. Calcitriol supplementation to DSR did not ameliorate the above parameters; in fact, augmented endothelium-dependent contraction was observed. Serum calcium was higher in DSR compared to CR and DR. In conclusion, vitamin D deficiency impaired microvascular vasodilation, associated with eNOS downregulation and reduced antioxidant activity. Calcitriol supplementation to vitamin D-deficient rats at the dosage used augmented endothelium-dependent contraction, possibly due to hypercalcaemia.
    Matched MeSH terms: Endothelium, Vascular/drug effects; Endothelium, Vascular/enzymology*; Endothelium, Vascular/physiopathology
  16. Descemetorhexis for Fuchs' dystrophy
    Moloney G, Chan UT, Hamilton A, Zahidin AM, Grigg JR, Devasahayam RN
    Can J Ophthalmol, 2015 Feb;50(1):68-72.
    PMID: 25677286 DOI: 10.1016/j.jcjo.2014.10.014
    To describe 2 cases of spontaneous corneal clearing after Descemetorhexis: 1 after iatrogenic trauma (Case 1) and 1 as an intentional surgical intervention for Fuchs endothelial dystrophy (Case 2).
    Matched MeSH terms: Endothelium, Corneal/pathology
  17. New method for the isolation of endothelial cells from large vessels
    Ataollahi F, Pingguan-Murphy B, Moradi A, Wan Abas WA, Chua KH, Abu Osman NA
    Cytotherapy, 2014 Aug;16(8):1145-52.
    PMID: 24831838 DOI: 10.1016/j.jcyt.2014.01.010
    Numerous protocols for the isolation of bovine aortic endothelial cells have been described in the previous literature. However, these protocols prevent researchers from obtaining the pure population of endothelial cells. Thus, this study aimed to develop a new and economical method for the isolation of pure endothelial cells by introducing a new strategy to the enzymatic digestion method proposed by previous researchers.
    Matched MeSH terms: Endothelium, Vascular/cytology*
  18. Endothelial cell responses in terms of adhesion, proliferation, and morphology to stiffness of polydimethylsiloxane elastomer substrates
    Ataollahi F, Pramanik S, Moradi A, Dalilottojari A, Pingguan-Murphy B, Wan Abas WA, et al.
    J Biomed Mater Res A, 2015 Jul;103(7):2203-13.
    PMID: 24733741 DOI: 10.1002/jbm.a.35186
    Extracellular environments can regulate cell behavior because cells can actively sense their mechanical environments. This study evaluated the adhesion, proliferation and morphology of endothelial cells on polydimethylsiloxane (PDMS)/alumina (Al2 O3 ) composites and pure PDMS. The substrates were prepared from pure PDMS and its composites with 2.5, 5, 7.5, and 10 wt % Al2 O3 at a curing temperature of 50°C for 4 h. The substrates were then characterized by mechanical, structural, and morphological analyses. The cell adhesion, proliferation, and morphology of cultured bovine aortic endothelial (BAEC) cells on substrate materials were evaluated by using resazurin assay and 1,1'-dioctadecyl-1,3,3,3',3'-tetramethylindocarbocyanine perchlorate-acetylated LDL (Dil-Ac-LDL) cell staining, respectively. The composites (PDMS/2.5, 5, 7.5, and 10 wt % Al2 O3 ) exhibited higher stiffness than the pure PDMS substrate. The results also revealed that stiffer substrates promoted endothelial cell adhesion and proliferation and also induced spread morphology in the endothelial cells compared with lesser stiff substrates. Statistical analysis showed that the effect of time on cell proliferation depended on stiffness. Therefore, this study concludes that the addition of different Al2 O3 percentages to PDMS elevated substrate stiffness which in turn increased endothelial cell adhesion and proliferation significantly and induced spindle shape morphology in endothelial cells.
    Matched MeSH terms: Endothelium, Vascular/cytology*
  19. Reproducibility of laser Doppler fluximetry and the process of iontophoresis in assessing microvascular endothelial function using low current strength
    Al-Tahami BA, Yvonne-Tee GB, Halim AS, Ismail AA, Rasool AH
    Methods Find Exp Clin Pharmacol, 2010 Apr;32(3):181-5.
    PMID: 20448860 DOI: 10.1358/mf.2010.32.3.1423887
    Iontophoresis of acetylcholine (ACh) and sodium nitroprusside (SNP) combined with laser Doppler fluximetry (LDF) is a tool used to determine microvascular endothelial function. Our aim was to study the reproducibility of different parameters of this technique using iontophoresis with low current strength on the forearm skin of healthy subjects. Baseline skin perfusion was done before application of five current pulses with 1 min of current-free interval. Current strength of 0.007 mA, current density of 0.01 mA/cm(2) and charge density of 6 mC/cm(2) were used, along with 1% ACh and 1% SNP. The absolute maximum change in perfusion (max), percent change in perfusion (% change), peak change in perfusion (peak) and area under the curve during iontophoresis (AUC) at the anodal and cathodal leads were recorded. Measurements were performed in three sessions for 2 days. The coefficient of variation (CV) was calculated for each parameter. Among the parameters studied, maximum change in perfusion and peak flux were the most reproducible parameters.
    Matched MeSH terms: Endothelium, Vascular/metabolism*
  20. Scanning electron microscopy of cornea re-epithelization after transplanted with bilayered corneal construct
    Masrudin SS, Ghafar NA, Saidi M, Aminuddin BS, Rahmat A, Ruszymah BH, et al.
    Med J Malaysia, 2008 Jul;63 Suppl A:109-10.
    PMID: 19025009
    The present work was to determine the development and re-epithelization of bilayered corneal construct (BCC) in vitro and in vivo using scanning electron microscopy (SEM). The in vitro BCC was transplanted to the rabbit's eye and after 90 days the BCC was harvested and analyzed. The corneas were processed for morphology studies. The result indicates that the BICC that was transplanted for 90 days showed good development and re-epithelization of epithelial layer similar to the normal cornea.
    Matched MeSH terms: Endothelium, Corneal/physiology*
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