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Role of endothelial cell apoptosis in regulation of skeletal muscle angiogenesis during high and low salt intake.

Role of endothelial cell apoptosis in regulation of skeletal muscle angiogenesis during high and low salt intake. Research Abstract Details 

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  • Role of endothelial cell apoptosis in regulation of skeletal muscle angiogenesis during high and low salt intake. Abstract Text:

    micheline m de resendeMicheline M de Resende,sandra l amaralSandra L Amaral,diane h munzenmaierDiane H Munzenmaier,andrew s greeneAndrew S Greene,

    Angiogenesis, under normal conditions, is a tightly regulated balance between pro- and antiangiogenic factors. The goal of this study was to investigate the mechanisms involved in the control of the skeletal muscle angiogenic response induced by electrical stimulation during the suppression of plasma renin activity (PRA) with a high-salt diet. Rats fed 0.4% or 4% salt diets were exposed to electrical stimulation for 7 days. The tibialis anterior (TA) muscles from stimulated and unstimulated hindlimbs were removed and prepared for gene expression analysis, CD31-terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL) double-staining assay, and Bcl-2 and Bax protein expression by Western blot. Rats fed a low-salt diet showed a dramatic angiogenesis response in the stimulated limb compared with the unstimulated limb. This angiogenesis response was significantly attenuated when rats were placed on a high-salt diet. Microarray analysis showed that in the stimulated limb of rats fed a low-salt diet many genes related to angiogenesis were upregulated. In contrast, in rats fed a high-salt diet most of the genes upregulated in the stimulated limb function in apoptosis and cell cycle arrest. Endothelial cell apoptosis, as analyzed by CD31-TUNEL staining, increased by fourfold in the stimulated limb compared with the unstimulated limb. There was also a 48% decrease in the Bcl-2-to-Bax ratio in stimulated compared with unstimulated limbs of rats fed a high-salt diet, confirming severe apoptosis. This study suggests that the increase in endothelial cell apoptosis in TA muscle might contribute to the attenuation of angiogenesis response observed in rats fed a high-salt diet.

    Role of endothelial cell apoptosis in regulation of skeletal muscle angiogenesis during high and low salt intake. Publishing Authors By Initials

    mm de resendeMM de Resende,sl amaralSL Amaral,dh munzenmaierDH Munzenmaier,as greeneAS Greene,

    For similar peptides: intracellular signaling peptides and proteins: apoptosis regulatory proteins: proto-oncogene proteins c-bcl-2: bcl-2-associated x protein research abstracts see: peptides: intracellular signaling peptides and proteins: apoptosis regulatory proteins: proto-oncogene proteins c-bcl-2: bcl-2-associated x protein research

    PUBMED ID PMID:

    MEDLINE DATE:

    Role of endothelial cell apoptosis in regulation of skeletal muscle angiogenesis during high and low salt intake. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Physiological genomics

    VOLUME: 25

    Page Numbers: 325-35

    Journal Abbreviation: Physiol. Genomics

    ISSN: 1531-2267

    DAY: 7

    MONTH: 02

    YEAR: 2006

    Role of endothelial cell apoptosis in regulation of skeletal muscle angiogenesis during high and low salt intake. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 9815683

    Role of endothelial cell apoptosis in regulation of skeletal muscle angiogenesis during high and low salt intake. Keywords Mesh Terms:

    KEYWORDS: bcl-2-Associated X Protein

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Role of endothelial cell apoptosis in regulation of skeletal muscle angiogenesis during high and low salt intake. Information

    Substance Name: Renin

    Registry Number: EC 3.4.23.15

    Grant and Affiliation Information for Role of endothelial cell apoptosis in regulation of skeletal muscle angiogenesis during high and low salt intake.

    AFFILIATION: Biotechnology and Bioengineering Center, Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NHLBI

    GRANT: N01-HV-28182

    ACRONYM: HV

    MEDLINETA: Physiol Genomics

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