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4 Journal of Physiology and Pharmacology

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Serum response factor: discovery, biochemistry, biological roles and implications for tissue injury healing

100%

Chai J. , Tarnawski A. S.

nr 2

Serum response factor (SRF) is a transcription factor, which binds to a serum response element (SRE) associated with a variety of genes including immediate early genes such as c-fos, fosB, junB, egr-1 and –2, neuronal genes such as nurr1 and nur77 and muscle genes such as actins and myosins. By regulating expression of these genes, SRF controls cell growth and differentiation, neuronal transmission as well as muscle development and function. SRF can be activated by a variety of agents, including serum, lysophosphatidic acid (LPA), lipopolysaccharide (LPS), 12-O-tetradecanoylphorbol- 13-acetate (TPA), cytokines, tumor necrosis factor-. (TNF.... ), agents that increase intracellular Ca 2+, T-cell virus1 activator protein, hepatitis B virus activator proteins pX, activated oncogenes and protooncogenes as well as extracellular stimuli such as antioxidant and UV light. SRF itself is regulated by both cellular signal transduction pathways and interaction with other transcription factors e.g. Sp1, ATF6 and myogenic regulatory factors. Its biological function is best eluci-dated for myocardium. Specific cardiac SRF transgenesis demonstrated that overex-pression of SRF caused hypertrophic cardiomyopathy in mouse and the mouse died of heart failure within 6 months after birth. Other transgenic data suggested that suf-ficient SRF was needed for embryogenesis and early development. Since SRF is important regulator of numerous genes involved in cell growth and differentiation, including muscle and neural components, SRF may also play a crucial role in tissue injury and ulcer healing, e.g. healing of gastrointestinal ulcers.

Formation of new blood vessels during gastric ulcer healing. Role of bone marrow derived endothelial progenitor cells

71%

Ahluwalia A. , Brzozowski T. , Jones M. K. , Ichikawa Y. , Tarnawski A. S.

nr 4

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

71%

Nakai Y. , Shinoura S. , Ahluwalia A. , Tarnawski A. S. , Chang K. J.

tom 63

nr 6

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

71%

Ahluwalia A. , Narula J. , Jones M. K. , Deng X. , Tarnawski A. S.

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.