Wyniki wyszukiwania

1

Trans fatty acids induce apoptosis in human endothelial cells

100%

Zapolska-Downar D., Kosmider A., Naruszewicz M.

Journal of Physiology and Pharmacology

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2005

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tom 56

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nr 4

The present study was designed to investigate the hypothesis that trans fatty acids can induce apoptosis of human umbilical vein endothelial cells (HUVEC). To test this hypothesis apoptosis was measured in HUVEC treated with 0.1, 1.0 or 5.0 mM trans elaidic acid (t-18:1) or linoelaidic acid (t,t-18:2) for 24 hours. For the detection of apoptosis, TdT-mediated dUTP nick end labelling assay (TUNEL), cell binding of annexin V and propidium iodide uptake were measured. Active Caspase-3 and cleaved PARP (poly-ADP-ribose polymerase) were also measured in the cell lysate. Moreover, cellular ability to produce ROS (reactive oxygen species) was measured by DCF fluorescence Both acids studied induce both early (annexin-positive cells) and late stages of apoptosis (cells stained by propidium iodide) in a dose-dependent manner. Also the appearance of TUNEL-positive cells was induced by both trans fatty acids tested, in a dose dependent manner. Both trans acids induce apoptosis through their effect on Caspase-3 activity and on intracellular ROS production. It is worth emphasising that linoelaidic acid proved to be a more potent inducer of apoptosis and ROS production in endothelial cells than elaidic acid. The present studies suggest that trans fatty acids may play a role in damaging and death of vascular endothelial cells in atherosclerosis.

2

Effect of heavy metal cations on the activity of cathepsin D (in vitro study)

84%

Karwowska A., Lapinski R., Gacko M., Grzegorczyk E., Zurawska J., Karczewski J. K.

Folia Histochemica et Cytobiologica

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2012

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tom 50

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nr 3

3

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.

4

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

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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.

5

The influence of lovastatin on thrombomodulin gene expression in vascular endothelial cells - in vitro study

84%

Goralczyk K., Soszynska K., Haus O., Bielis R., Rosc D.

Folia Histochemica et Cytobiologica

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2009

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tom 47

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nr 1

43-45

6

Endothelial-mediated regulation of cerebral microcirculation

67%

McCarron R. M., Chen Y., Tomori T., Strasser A., Mechoulam R., Shohami E., Spatz M.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

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nr 11

133-144

Vascular endothelial cells are important not only for maintaining homeostasis, but also in pathogenesis of vascular disorders. Cerebral capillary and microvascular endothelial cells play an active role in maintaining cerebral blood flow, microvascular tone and blood brain barrier functions. Factors produced and released by endothelial cells, other brain cells and circulating blood cells participate in these regulatory functions. In particular, endothelin-1 (ET-1) and nitric oxide (NO) are known to contribute to the functional vascular changes under pathological conditions (e.g., hypertension, arteriosclerosis, and stroke). This report describes the involvement of endothelial cell mediators in the post-ischemic hypoperfusion induced by brain ischemia and in vitro endothelial responses (Ca2+ mobilization and cytoskeletal rearrangements) to ET-1 and its interactions with NO or 2-AG. The capacity of NO and endocannabinoids to counteract ET-1-induced cerebral capillary and microvascular endothelial responses indicates that they may actively participate in EC function and implicates them in physiological and pathophysiological conditions.

7

Influence of nuclear factor-kappaB inhibition on endothelin-1 induced lung edema and oxidative stress in rats

67%

Piechota A., Goraca A.

Journal of Physiology and Pharmacology

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2011

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tom 62

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nr 2

The aim of the present study is to determine the effects of the BAY 11-7082, a nuclear factor-kappaB (NF-B) inhibitor, on endothelin-1 (ET-1) induced lung edema, the level of reactive oxygen species (ROS) and tumor necrosis factor alpha (TNF-) in the lungs. Experiments were carried out on adult male Wistar-Kyoto rats. The animals were divided into 4 groups: Group I: saline-treated control; Group II: saline followed by ET-1 (12.5 µg/kg b.w., i.v.); Group III: BAY 11-7082 (10 mg/kg b.w., i.v.) administered one hour before saline; Group IV: BAY 11-7082 (10 mg/kg b.w., i.v.) administered 1 hour before ET-1 (12.5 µg/kg b.w., i.v.). Injection of ET-1 alone showed a significant (P<0.001) increase in thiobarbituric acid reactive substances (TBARS) and hydrogen peroxide (H2O2) level as well as a decrease (P<0.01) in GSH level and GSH/GSSG ratio (P<0.02). BAY 11-7082 significantly decreased TBARS (P<0.01) and H2O2 (P<0.05) level as well as improved the redox status (P<0.02) in the lungs. BAY 11-7082 also prevented ET-1 induced lung edema (P<0.05). The concentration of TNF- (P<0.02) and p65 subunit of NF-B signaling compound (P<0.001) was increased in the presence of ET-1, while BAY 11-7082 decreased both TNF- level (P<0.05) and p65 subunit concentration (P<0.01). Our results indicate that BAY 11-7082 plays a protective role in ET-1 induced oxidative lung injury. It successfully prevents lung edema as well as ROS and TNF- overproduction. Our results also highlight the important role of the NF-B pathway in ET-1 induced lung injury and ROS overproduction.

8

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

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nr 2

9

Assessment of S100 protein expression in the epididymis of juvenile and adult European bison

67%

Czykier E., Zabel M., Surdyk-Zasada J., Lebelt A., Klim B.

Folia Histochemica et Cytobiologica

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2010

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tom 48

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nr 3

10

Advances in the structural biology, design and clinical development of VEGF-R kinase inhibitors for the treatment of angiogenesis

67%

Manley P. W., Bold G., Fendrich G., Furet P., Mestan J., Meyer T., Meyhack B., Stark W., Strauss A., Wood J.

Cellular and Molecular Biology Letters

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2003

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tom 08

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nr 2A

Ograniczanie wyników

Trans fatty acids induce apoptosis in human endothelial cells

Effect of heavy metal cations on the activity of cathepsin D (in vitro study)

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

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

The influence of lovastatin on thrombomodulin gene expression in vascular endothelial cells - in vitro study

Endothelial-mediated regulation of cerebral microcirculation

Influence of nuclear factor-kappaB inhibition on endothelin-1 induced lung edema and oxidative stress in rats

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

Assessment of S100 protein expression in the epididymis of juvenile and adult European bison

Advances in the structural biology, design and clinical development of VEGF-R kinase inhibitors for the treatment of angiogenesis