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1
Content available remote Activation of the metabolic sensor - AMP activated protein kinase reverses impairment of angiogenesis in aging myocardial microvascular endothelial cells. Implications for the aging heart
100%
Ahluwalia A. , Tarnawski A. S.
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tom 62
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nr 5
2
Content available remote Expression of nerve growth factor in rat stomach. Implications for interactions between endothelial, neural and epithelial cells
80%
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
80%
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 Impaired angiogenesis in aging myocardial microvascular endothelial cells is associated with reduced importin alpha and decreased nuclear transport of HIF1alpha: mechanistic implications
70%
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
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nr 2
EN
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.
5
Content available remote In vivo visualization of epidermal growth factor receptor and survivin expression in porcine pancreas using endoscopic ultrasound guided fine needle imaging with confocal laser-induced endomicroscopy
70%
Nakai Y. , Shinoura S. , Ahluwalia A. , Tarnawski A. S. , Chang K. J.
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2012
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tom 63
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nr 6
6
Content available remote Reduced ghrelin in endothelial cells plays important mechanistic role in aging-related impairment of angiogenesis
70%
Ahluwalia A. , li A. , Cheng G. , Deng X. , Tarnawski A. S.
Journal of Physiology and Pharmacology
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2009
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tom 60
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nr 2
29-34
EN
Ghrelin, a hormone produced mainly by gastric mucosal cells stimulates growth hormone (GH) release. Ghrelin is also expressed in the endothelial cells of blood vessels suggesting its physiological role and a function in these cells. We recently demonstrated that ghrelin induces angiogenesis - new capillary blood vessel formation- in neonatal human microvascular endothelial cells (HMVECs). Angiogenesis is impaired in aging individuals both in vitro and in vivo, but the precise mechanism(s) of this phenomenon is unknown. We examined whether HMVECs derived from aging individuals (66 years and 90 years old), 66-HMVECs and 90-HMVECs have reduced ghrelin levels vs. neonatal (Neo) HMVECs and whether treatment with exogenous ghrelin can restore impaired in vitro angiogenesis on matrigel in aged HMVECs. Ghrelin levels were reduced in the aged HMVECs by 3.2-fold (p<0.05) compared to Neo-HMVECs. Angiogenesis was significantly decreased in the aged 66- and 90-HMVECs by 39.7% (p = 0.003) and 62.4% (p = 0.003), respectively compared to Neo-HMVECs. Treatment with exogenous ghrelin significantly reversed impaired angiogenesis in aged HMVECs with the EC50 0.05 nM. Ghrelin induced angiogenesis in Neo-HMVECs mainly through ERK2 activation. This study is the first demonstration that reduced ghrelin is one of the factors responsible for aging-related impairment of angiogenesis.
7
Content available remote Formation of new blood vessels during gastric ulcer healing. Role of bone marrow derived endothelial progenitor cells
70%
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
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nr 4
8
Content available remote Molecular imaging of epidermal growth factor-receptor and survivin in vivo in porcine esophageal and gastric mucosae using probe-based confocal laser-induced endomicroscopy: proof of concept
70%
Nakai Y. , Shinoura S. , Ahluwalia A. , Tarnawski A. S. , Chang K. J.
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2012
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tom 63
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nr 3
9
Content available remote Nerve growth factor injected into the gastric ulcer base incorporates into endothelial, neuronal, glial and epithelial cells: implications for angiogenesis, mucosal regeneration and ulcer healing
70%
Tanigawa T. , Ahluwalia A. , Watanabe T. , Arakawa T. , Tarnawski A. S.
Journal of Physiology and Pharmacology
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2015
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tom 66
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nr 4
10
Content available remote Expression of nerve growth factor, its TRKA receptor, and several neuropeptides in porcine esophagus. Implications for interactions between neural, vascular and epithelial components of the esophagus
61%
Samarasena J. B. , Ahluwalia A. , Tarnawski A. S. , Shinoura S. , Choi K. D. , Lee J. G. , Chang K. J.
Journal of Physiology and Pharmacology
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2015
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tom 66
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nr 3
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