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1
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Survivin is a key factor in the differential susceptibility of gastric endothelial and epithelial cells to alcohol-induced injury

100%
Jones M. K., Padilla O. R., Zhu E.
Journal of Physiology and Pharmacology
|
2010
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tom 61
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nr 3
253-264
We previously demonstrated that the anti-apoptosis protein, survivin, plays a protective role against alcohol-induced gastric injury. Since the endothelium is a primary target of alcohol-induced gastric damage, we investigated whether survivin expression is a key factor in the greater susceptibility of gastric endothelial vs. epithelial cells to alcohol-induced injury. Here, we demonstrate that rat gastric epithelial cells (RGM1 cells, an epithelial cell line derived from normal rat gastric mucosa) expressed 7.5-fold greater survivin protein levels vs. rat gastric endothelial cells. Survivin expression correlated with resistance of gastric epithelial vs. endothelial cells to both alcohol-induced cell damage and alcohol-induced apoptosis. Suppression of survivin protein expression levels using siRNA rendered the gastric epithelial cells as susceptible to both alcohol-induced cell damage and apoptosis as the gastric endothelial cells. Conversely, forced overexpression of survivin by transient transfection rendered gastric endothelial cells as resistant to both alcohol-induced cell damage and apoptosis as mock-transfected gastric epithelial cells. Moreover, overexpression of a threonine-34 to glutamate phosphorylation mimic mutant survivin construct rendered gastric endothelial cells significantly more resistant to alcohol-induced damage and apoptosis vs. mock-transfected gastric epithelial cells. These findings indicate that disparate survivin expression levels can explain the discrepancy between gastric epithelial and endothelial cell susceptibility to alcohol-induced injury; and, that a negative charge at amino acid residue 34 on survivin, such as that which naturally occurs by phosphorylation of threonine-34, enhances its property in conferring gastric mucosal protection.
2
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Expression of nerve growth factor in rat stomach. Implications for interactions between endothelial, neural and epithelial cells

100%
Tarnawski A. S., Ahluwalia A., Jones M. K., Brzozowski T.
Journal of Physiology and Pharmacology
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2016
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tom 67
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nr 6
3
Content available remote

In vitro model of vasculo-angiogenesis: demonstration that bone marrow derived endothelial progenitor cells form new hybrid capillary blood vessels jointly with gastric endothelial cells

100%
Ahluwalia A., Jones M. K., Brzozowska I., Tarnawski A. S.
Journal of Physiology and Pharmacology
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2017
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tom 68
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nr 6
4
Content available remote

Aging impairs transcriptional regulation of vascular endothelial growth factor in human microvascular endothelial cells: implications for angiogenesis and cell survival

100%
Ahluwalia, Jones M. K., Szabo S., Tarnawski A. S.
Journal of Physiology and Pharmacology
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2014
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tom 65
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nr 2
5
Content available remote

Impaired angiogenesis in aging myocardial microvascular endothelial cells is associated with reduced importin alpha and decreased nuclear transport of HIF1alpha: mechanistic implications

88%
Ahluwalia A., Narula J., Jones M. K., Deng X., Tarnawski A. S.
Journal of Physiology and Pharmacology
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2010
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tom 61
|
nr 2
Aging is associated with increased incidence of myocardial infarctions and impaired angiogenesis - new capillary blood vessel formation from preexisting vessels. The molecular mechanism(s) of aging-related impairment of angiogenesis are unknown. In the present study we focused on the mechanism of activation of the gene for vascular endothelial growth factor (VEGF - the most potent stimulator of angiogenesis) in young and aging myocardial microvascular endothelial cells (MMEC). Activation of VEGF gene in the cell nucleus is mediated in part by the transcription factor hypoxia-inducible factor 1 (HIF1). In order to activate VEGF gene, HIF1 must first be transported to the nucleus, but the mechanisms of this transport are unknown. We hypothesized that reduced VEGF gene activation and impaired angiogenesis in myocardium during aging can result from downregulation of the nuclear transport receptor - importin that leads to decreased transport of HIF1 to the nucleus. We examined in MMEC isolated from young (3 months of age) and aging (24 months old) Fisher F-344 rats: 1) in vitro angiogenesis; and 2) the expression of VEGF, importin and HIF1. Aging MMEC exhibited a 3.7-fold reduction in angiogenesis and a corresponding reduction in VEGF (by 3-fold) and importin (by 1.9-fold) levels compared to young MMEC. Aging MMEC also exhibited cytoplasmic accumulation (by 1.8-fold) of HIF1 protein, reduced HIF1 transport to the nucleus and decreased binding of HIF1 protein to the VEGF gene promoter. This study is the first demonstration of the downregulation of importin in aging MMEC and reduced nuclear transport of HIF1, which likely lead to decreased VEGF gene activation and impaired angiogenesis.
6
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Formation of new blood vessels during gastric ulcer healing. Role of bone marrow derived endothelial progenitor cells

88%
Ahluwalia A., Brzozowski T., Jones M. K., Ichikawa Y., Tarnawski A. S.
Journal of Physiology and Pharmacology
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2017
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tom 68
|
nr 4
7
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ATP-induced Ca2plus-signalling enhances rat gastric microvascular endothelial cell migration

88%
Ehring G. R., Szabo I. L., Jones M. K., Sarfeh I. J., Tarnawski A. S.
Journal of Physiology and Pharmacology
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2000
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tom 51
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nr 4,2
8
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Isolation and characterization of rat gastric microvascular endothelial cells as a model for studying gastric angiogenesis in vitro

76%
Jones M. K., Wang H., Tomikawa M., Szabo I. L., Kawanaka H., Sarfeh I. J., Tarnawski A. S.
Journal of Physiology and Pharmacology
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2000
|
tom 51
|
nr 4,2
9
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Expression of adrenomedullin in portal hypertensive gastric mucosa of rats

76%
Tomikawa M., Wang H., Jones M. K., Sugimachi K., Sarfeh I. J., Tarnawski A. S.
Journal of Physiology and Pharmacology
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1998
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tom 49
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nr 2
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