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1

Growth factors and their receptors derived from human amniotic cells in vitro

100%

Grzywocz Z., Pius-Sadowska E., Klos P., Gryzik M., Wasilewska D., Aleksandrowicz B., Dworczynska M., Sabalinska M., Hoser G., Machalinski B., Kawiak J.

Folia Histochemica et Cytobiologica

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2014

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tom 52

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nr 3

2

The cytotoxic effect of diphtheria toxin on the actin cytoskeleton

100%

Varol B., Bektas M., Nurten R., Bermek E.

Cellular and Molecular Biology Letters

|

2012

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tom 17

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nr 1

Diphtheria toxin (DT) and its N-terminal fragment A (FA) catalyse the transfer of the ADP-ribose moiety of nicotinamide adenine dinucleotide (NAD) into a covalent linkage with eukaryotic elongation factor 2 (eEF2). DT-induced cytotoxicity is versatile, and it includes DNA cleavage and the depolymerisation of actin filaments. The inhibition of the ADP-ribosyltransferase (ADPrT) activity of FA did not affect the deoxyribonuclease activity of FA or its interaction with actin. The toxin entry rate into cells (HUVEC) was determined by measuring the ADP-ribosyltransferase activity. DT uptake was nearly 80% after 30 min. The efficiency was determined as Km = 2.2 nM; Vmax = 0.25 pmol.min−1. The nuclease activity was tested with hyperchromicity experiments, and it was concluded that G-actin has an inhibitory effect on DT nuclease activity. In thepresence of DT and mutant of diphtheria toxin (CRM197), F-actin depolymerisation was determined with gel filtration, WB and fluorescence techniques. In the presence of DT and CRM197, 60–65% F-actin depolymerisation was observed. An in vitro FA-actin interaction and F-actin depolymerisation were reported in our previous paper. The present study thus confirms the depolymerisation of actin cytoskeleton in vivo.

3

Effect of unfractionated heparin, enoxaparin and sulodexide on the relations between secretion and expression of OPG, RANKL and vWF in HUVEC

84%

Lekesiz K., Naumnik B., Borysewicz-Sanczyk H., Koc-Zorawska E., Mysliwiec M.

Folia Histochemica et Cytobiologica

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2013

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tom 51

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nr 2

4

Atorvastatin-induced endothelial nitric oxide synthase (eNOS) expression in endothelial cells is mediated by endoglin

84%

Zemankova L., Varejckova M., Dolezelova E., Fikrova P., Jezkova K., Rathouska J., Cerveny L., Botella L. M., Bernabeu C., Nemeckova I., Nachtigal P.

Journal of Physiology and Pharmacology

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2015

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tom 66

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nr 3

5

Monocytes and vascular endothelial cells apoptosis. Role of p-HSP27

84%

Gawad A., Ptak-Belowska A., Brzozowski T., Pawlik W. W.

Journal of Physiology and Pharmacology

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2009

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tom 60

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nr 4

55-61

The aim of this study was to find out whether stimulated monocytes could trigger apoptosis of vascular endothelial cells. Human umbilical vein endothelial cells (HUVEC) (EC) were co-cultured for 24 h and 48 h with monocytes isolated from peripheral blood (peripheral blood monocytes) or MonoMac6 cell line activated previously with proinflammatory cytokines. Real-time PCR was conducted to investigate p53 up-regulated modulator of apoptosis (PUMA), heat shock protein HSP70 and HSP27 genes expression. Changes in the level of PUMA, HSP70, HSP27 and phospho-heat shock protein 27 (p-HSP27) proteins were analyzed by means of immunoprecipitation. Apoptosis was determined by TUNEL and poli-(ADP ribose) polymerase ( PARP ) cleavage assay. In HUVEC cells stimulated with monocytes hardly any increase of PUMA mRNA was observed, but the PUMA protein level was significantly up regulated especially after 24 h. Heat shock proteins (HSP70 and HSP27) mRNA expression was elevated after 24 h and 48h and confirmatory up regulation of these proteins was observed in HUVEC cells stimulated with peripheral blood monocytes but not with MonoMac6 cells. Interestingly, in nuclear compartment of HUVECs exposed to the monocytic line and native monocytes, a significant increase of p-HSP27 level has appeared. TUNEL and PARP cleavage assay did not show any apoptotic HUVEC cells after stimulation with monocytes. The main observations of this study indicate that monocytes do not trigger apoptosis of vascular endothelial cells. Proapoptotic activation mediated by PUMA that was observed seemed to be counterbalanced by significant increase of antiapoptotic HSP70, HSP27 and especially phospho-HSP27 proteins level.

6

The influence of unfractionated and low-molecular weight heparins on the properties of human umbilical vein endothelial cells [HUVEC]

84%

Gasowska K., Naumnik B., Klejna K., Mysliwiec M.

Folia Histochemica et Cytobiologica

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2009

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tom 47

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nr 1

17-23

7

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Transcription factors as targets of the anti-inflammatory treatment. A cell culture study with extracts from some Mediterranean diet plants

84%

Stalinska K., Guzdek A., Rokicki M., Koj A.

Journal of Physiology and Pharmacology. Supplement

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2005

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tom 56

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nr 1

157-169

During the inflammatory response at least 2 transcription factors, NF-kB and AP-1, are involved in the altered profile of gene expression. We used human hepatoma (HepG2) and human umbilical vein endothelial cells (HUVEC) as a model system: NF-kB and AP-1 were activated by the proinflammatory cytokine IL-1 in the absence or presence of 21 selected plant extracts and the effect was evaluated by the electrophoretic mobility shift assay (EMSA). In both types of cells activation of NFkB by IL-1 was significantly inhibited by extracts from Scandix australis and Artemisia alba, whereas extracts from Amaranthus sp., Eryngium campestre, Thymus pulegioides and Reichardia picroides elicited cell-type dependent response. The IL-1-induced AP-1 activation was diminished by extracts from Scandix australis, Amaranthus sp. and Artemisia alba more potently in HUVEC, while extracts from Urospermum picroides and Scandix pecten-veneris in HepG2 cells. Inhibitory activities of plant extracts towards cytokine activated NF-kB and AP-1 depend to some extent on the order of addition of IL-1 and plant extract to the cell culture, but the mechanism of action of extract components is not clear: although plant polyphenols may participate they are unlikely to be the only mediators, and MAP kinases were found generally not involved in down-regulation of transcription factors activity by plant extracts.

8

The anti-apoptotic activity of albumin for endothelium is inhibited by advanced glycation and products restricting intramolecular movement

84%

Zoellner H., Siddiqui S., Kelly E., Medbury H.

Cellular and Molecular Biology Letters

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2009

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tom 14

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nr 4

575-586

Human serum albumin (HSA) inhibits endothelial apoptosis in a highly specific manner. CNBr fragmentation greatly increases the effectiveness of this activity, suggesting that this type of protection is mediated by a partially cryptic albumin domain which is transiently exposed by intramolecular movement. Advanced glycation end-product (AGE) formation in HSA greatly reduces its intra-molecular movement. This study aimed to determine if this inhibits the anti-apoptotic activity of HSA, and if such inactivation could be reversed by CNBr fragmentation. HSA-AGE was prepared by incubating HSA with glucose, and assessed using the fructosamine assay, mass spectrometry, SDS-PAGE and fluorometry. Low levels of AGE in the HSA had little effect upon its anti-apoptotic activity, but when the levels of AGE were high and the intra-molecular movement was reduced, endothelial cell survival was also found to be reduced to levels equivalent to those in cultures without HSA or serum (p > 0.001). Survival was restored by the inclusion of native HSA, despite the presence of HSA with high levels of AGE. Also, CNBr fragmentation of otherwise inactive HSA-AGE restored the anti-apoptotic activity for endothelium. Apoptosis was confirmed by DNA gel electrophoresis, transmission electron microscopy and fluorescence-activated cell sorting analysis, and there was no evidence for direct toxicity in the HSA-AGE preparations. The results are consistent with the proposed role of intra-molecular movement in exposing the anti-apoptotic domain in HSA for endothelium. The levels of AGE formation required to inhibit the anti-apoptotic activity of HSA exceeded those reported for diabetes. Nonetheless, the data from this study seems to be the first example of reduced protein function due to AGE-restricted intra-molecular movement.

9

Stimulation of large-conductance Ca2plus-activated Kplus channels by the Naplus-Ca2plus exchanger inhibitor dichlorobenzamil in cultured human umbilical vein endothelial cells and mouse aortic smooth muscle cells

84%

Liang G. H., Park S., Kim J. A., Choi S., Suh S. H.

Journal of Physiology and Pharmacology

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2009

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tom 60

|

nr 1

43-50

We investigated the effects of the selective inhibitor of Na+/Ca2+ exchanger (NCX), 2',4'- and 3',4'-dichlorobenzamil (DCB), on large-conductance Ca2+-activated K+ (BKCa) channels in cultured human umbilical vein endothelial cells (HUVECs) and fresh isolated mouse aortic smooth muscle cells (MASMCs) using the patch clamp techniques. Both kinds of DCB reversibly activated BKCa currents in whole-cell clamped HUVECs or MASMCs. The EC50 of 2',4'-DCB for BKCa current activation in HUVECs was 2.64 ± 0.10 µM. In inside-out and outside-out patches, 2',4'-DCB remarkably increased BKCa channels activity. 2',4'-DCB increased open frequency, but had no significant effect on mean open time. In inside-out patches, 2',4'-DCB shifted the relationship curve between [Ca2+]i and open probability (NPo) to the left; the [Ca2+]i required to evoke half-maximal activation changed from 1087.45 ± 142.91 nM to 500.24 ± 66.83 nM by 10 µM 2',4'-DCB. In addition, 2',4'-DCB shifted the relationship curve between membrane potential and NPo to the left; the membrane potential to evoke half-maximal activation changed from 81.1 ± 2.4 to 64.7 ± 3.1 mV by 10 µM 2',4'-DCB. 3',4'-DCB also increased BKCa channels activity. There was no significant difference in the effect of DCB on BKCa channels between both excised patches. These results suggested that 2',4'- and 3',4'-DCB activate BKCa channels activity in HUVECs and MASMCs by increasing the sensitivity of BKCa channels to cytosolic free Ca2+ and membrane potential. Our report would provide a consideration if they are used as NCX blocker in vascular endothelial cells or smooth muscle cells.

10

Rumex acetosa L. induces vasorelaxation in rat aorta via activation of PI3-kinase/Akt- and Ca2plus-eNOS-no signaling in endothelial cells

84%

Sun Y. Y., Su X. H., Jin J. Y., Zhou Z. Q., Sun S. S., Wen J. F., Kang D. G., Lee H. S., Cho K. W., Jin S. N.

Journal of Physiology and Pharmacology

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2015

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tom 66

|

nr 6

11

Differences in anti-endothelial and anti-retinal antibody titers: implications for the pathophysiology of acute and chronic central serous chorioretinopathy

84%

Karska-Basta I., Pociej-Marciak W., Chrzaszcz M., Wilanska J., Jager M. J., Markiewicz A., Romanowska-Dixon B., Sanak M., Kubicka-Trzaska A.

Journal of Physiology and Pharmacology

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2020

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tom 71

|

nr 2

12

GATA-1 binding to the alphaV promoter negatively regulates expression of the integrin alphaV subunit in human leukemic K562 cells

84%

Czyz M., Stasiak M., Boncela J., Cierniewski C. S.

Acta Biochimica Polonica

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2002

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tom 49

|

nr 1

Recently we observed that the transcription factors Sp1 and Sp3 bind to the CTCCTCCTC sequence located between positions -194 and -172 of the αv promoter region and are directly involved in the regulation of transcriptional activity of the αv gene in human umbilical vascular endothelial cells (HUVECs) (Czyz & Cierniewski, 1999, Eur. J. Biochem. 265, 638). In this report we provide evidence that the GATA-1 factor regulates αv expression during differentiation of pluripotent K562 cells induced either by phorbol 12-myristate 13-acetate (PMA) or butyric acid (BA) through interaction with the GATA element in the «v gene promoter. DNase I footprinting analysis revealed that region -413 to -408, covering the GATA binding site, was protected by nuclear extract from K562 cells. There was no protection of this region by HUVEC nuclear extract. Electrophoretic mobility shift assay (EMSA) analysis of nuclear extract of K562 cells treated with BA revealed an increase in GATA binding activity, which was associated with reduced αv mRNA and αv protein on the cell surface. Stimulation of K562 cells with PMA resulted in opposite effects: lower expression of GATA-1 was associated with increased levels of αv. We conclude that the GATA-1 transcription factor specifically binds to the GATA element in the αv gene promoter and negatively regulates αv gene expression.

13

Beta-carotene and arachidonic acid induced DNA methylation and the regulation of pro-chemotactic activity of endothelial cells and its progenitors

84%

Kiec-Wilk B., Polus A., Mikolajczyk M., Mathers J. C.

Journal of Physiology and Pharmacology

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2007

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tom 58

|

nr 4

DNA methylation is one of the important mechanisms regulating gene expression. Since beta-carotene (BC) was shown to have pro-chemotactic activity and stimulates expression of pro-angiogenic genes, this study was undertaken to define the possible changes in DNA methylation in endothelial cell and its progenitors in the presence of BC. The culture medium for human umbilical vein endothelial cells (HUVEC) and endothelial progenitor cells (EPC) was supplemented with BC (1 - 10 µM) with the presence of arachidonic acid (AA) (3 µM). Global DNA methylation tended to be lower in both endothelial cell lines, after incubation with BC and AA. HUVEC incubated with AA demonstrated the lowest DNA methylation. The decrease of DNA methylation in EPC, induced by BC, was concentration - dependent. The microarray study revealed, that the angiogenesis and homing – related genes were mostly influenced by BC and AA in investigated cells. Our results indicate that BC and AA-induced DNA hypomethylation in EPC and HUVEC, might be a mechanism which may alter gene expression in endothelial cells what in certain conditions may be connected with the suggested pro-malignant effect of this compounds.

14

Human endothelial lectin-like oxLDL receptor-1 (LOX-1) expression is not associated with impairment of endothelium-dependent vasoreactivity in conduit vessels

67%

Wetterau E., Stecher S.-S., Wolff B., Khouri S., Staudt A., Felix S. B., Landsberger M.

Journal of Physiology and Pharmacology

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2013

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tom 64

|

nr 4

15

Superoxide is a potential culprit of caspase-3 dependent endothelial cell death induced by lysophosphatidylcholine

67%

Park S., Kim J. A., Choi S., Suh S. A.

Journal of Physiology and Pharmacology

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2010

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tom 61

|

nr 4

375-381

Oxidative stress in the vascular wall has intimately been implicated in the apoptosis of human umbilical vein endothelial cells (HUVECs) by lysophosphatidylcholine (LPC). However, the major type of reactive oxygen species (ROS) in this apoptotic signaling pathway remains to be clarified. In this study, we report that superoxide mediate LPC-induced caspase-3 dependent apoptosis in cultured HUVECs. The stimulation of HUVECs with LPC evoked apoptosis and ROS generation, and inhibited nitric oxide (NO) production in a dose-dependent manner. The classical caspase-3 dependent apoptosis was determined after 16 hours treatment by Western blotting using an antibody against cleaved caspase-3. The caspase-3 activation induced by LPC was prominently inhibited by antioxidants or NO donors and enhanced by NO inhibitors. Especially, LPC-induced caspase-3 activation was inhibited by superoxide dismutase (SOD) and enhanced by ammonium tetrathiomolybdate, SOD inhibitor. Additionally, xanthine/xanthine oxidase mixture increased the caspase-3 activation but catalase failed to reduce this superoxide-induced caspase-3 activation. These findings indicate that the superoxide generation caused by LPC activates the caspase-3 which results in HUVECs death. This study reveals some evidences linking superoxide with caspase-3 activation and provides a new dimension to superoxide-mediated caspase-3 activation in developing the endothelial dysfunction and atherosclerosis.

16

Cellfood improves respiratory metabolism of endothelial cells and inhibits hypoxia-induced reactive oxygen species (ROS) generation

67%

Ferrero E., Fulgenzi A., Belloni D., Foglieni C., Ferrero M. E.

Journal of Physiology and Pharmacology

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2011

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tom 62

|

nr 3

Endothelial mitochondria, the major site of ATP generation, modulate the intracellular dynamics of reactive oxygen species (ROS), which, in turn, control endothelial function. Adequate oxygen (O2) supply is required by endothelial cells (EC). Both hypoxia and hyperoxia may favor the overproduction of ROS leading to oxidative stress, mitochondrial damage and endothelial dysfunction. We investigated the capability and mechanisms of CellfoodTM (CF), an antioxidant compound, to modulate O2 availability and mitochondrial respiratory metabolism and to regulate ROS generated by hypoxia in EC in vitro. Human umbilical vein endothelial cells (HUVEC) and ECV-304 were evaluated for the O2 consumption using a Clark's electrode. The O2 consumption rate rose, during the first minutes after CF addition and was associated with increase in mitochondrial oxidative capacity and good cell viability. Similar behaviours were observed when EC were exposed to CF for up to 8 days. The O2 consumption increased and was accompanied by both intracellular rise of ATP and maintainment of LDH concentration. Hypoxia-induced ROS generation was significantly inhibited by CF, through the up-regulated expression of MnSOD, an anti-oxidant responsible for mitochondrial function preservation. The EC hypoxic response is mediated by the hypoxia master regulator HIF-1alpha whose activation was attenuated by CF, in concomitance with MnSOD up-regulation. Our results suggest a role for CF in improoving respiratory metabolism and in activating anti-oxidant mechanisms in EC, thus preserving endothelial function.

17

Resveratrol reduces endothelial oxidative stress by modulating the gene expression of superoxide dismutase 1 (SOD1), glutathione peroxidase 1 (GPx1) and NADPH oxidase subunit (Nox4)

67%

Spanier G., Xu H., Xia N., Tobias S., Deng S., Wojnowski L., Forstermann U., Li H.

Journal of Physiology and Pharmacology. Supplement

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2009

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tom 60

|

nr 4

18

Mantidis ootheca induces vascular relaxation through PI3K/Akt-mediated nitric oxide-cyclic GMP-protein kinase G signaling in endothelial cells

67%

Kim H. Y., Lee Y. J., Han B. H., Yoon J. J., Ahn Y. M., Hong M. H., Tan R., Kang D. G., Lee H. S.

Journal of Physiology and Pharmacology

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2017

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tom 68

|

nr 2

19

Expression of MUC1 mucin in human umbilical vein endothelial cells (HUVEC)

59%

Porowska H., Paszkiewicz-Gadek A., Wosek J., Wnuczko K., Rusak M., Szczepanski M.

Folia Histochemica et Cytobiologica

|

2010

|

tom 48

|

nr 3

Ograniczanie wyników

Growth factors and their receptors derived from human amniotic cells in vitro

The cytotoxic effect of diphtheria toxin on the actin cytoskeleton

Effect of unfractionated heparin, enoxaparin and sulodexide on the relations between secretion and expression of OPG, RANKL and vWF in HUVEC

Atorvastatin-induced endothelial nitric oxide synthase (eNOS) expression in endothelial cells is mediated by endoglin

Monocytes and vascular endothelial cells apoptosis. Role of p-HSP27

The influence of unfractionated and low-molecular weight heparins on the properties of human umbilical vein endothelial cells [HUVEC]

Transcription factors as targets of the anti-inflammatory treatment. A cell culture study with extracts from some Mediterranean diet plants

The anti-apoptotic activity of albumin for endothelium is inhibited by advanced glycation and products restricting intramolecular movement

Stimulation of large-conductance Ca2plus-activated Kplus channels by the Naplus-Ca2plus exchanger inhibitor dichlorobenzamil in cultured human umbilical vein endothelial cells and mouse aortic smooth muscle cells

Rumex acetosa L. induces vasorelaxation in rat aorta via activation of PI3-kinase/Akt- and Ca2plus-eNOS-no signaling in endothelial cells

Differences in anti-endothelial and anti-retinal antibody titers: implications for the pathophysiology of acute and chronic central serous chorioretinopathy

GATA-1 binding to the alphaV promoter negatively regulates expression of the integrin alphaV subunit in human leukemic K562 cells

Beta-carotene and arachidonic acid induced DNA methylation and the regulation of pro-chemotactic activity of endothelial cells and its progenitors

Human endothelial lectin-like oxLDL receptor-1 (LOX-1) expression is not associated with impairment of endothelium-dependent vasoreactivity in conduit vessels

Superoxide is a potential culprit of caspase-3 dependent endothelial cell death induced by lysophosphatidylcholine

Cellfood improves respiratory metabolism of endothelial cells and inhibits hypoxia-induced reactive oxygen species (ROS) generation

Resveratrol reduces endothelial oxidative stress by modulating the gene expression of superoxide dismutase 1 (SOD1), glutathione peroxidase 1 (GPx1) and NADPH oxidase subunit (Nox4)

Mantidis ootheca induces vascular relaxation through PI3K/Akt-mediated nitric oxide-cyclic GMP-protein kinase G signaling in endothelial cells

Expression of MUC1 mucin in human umbilical vein endothelial cells (HUVEC)