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MAPK signaling is associated with acute exercise‐induced changes in mRNA levels of telomere‐related genes
Author(s) -
Lima Laila,
Ludlow Andrew,
Spangenburg Espen,
Roth Stephen
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1107.18
Subject(s) - telomere , messenger rna , gene expression , gene , p38 mitogen activated protein kinases , biology , endocrinology , telomere binding protein , medicine , mapk/erk pathway , phosphorylation , andrology , microbiology and biotechnology , transcription factor , dna binding protein , genetics
We examined the effects of an acute exercise bout on mRNA levels of telomere related genes in cardiac muscle. A secondary aim was to investigate stress response pathways (p38 and Erk1/2 MAPKs) previously associated with shelterin proteins. Twenty female C57/BL6J mice were assigned to 3 groups: baseline animals (BL; N=4) not exposed to exercise; and two groups of animals exposed to 30 min of treadmill running (66% peak speed; 23±4m/min; 7° incline) and sacrificed immediately (EXIMD; N=8) and 1h following (EX1h; N=8) the running bout. Protein content and mRNA levels for various targets were analyzed via immunoblotting and semiquantitative RT‐PCR. Compared to BL, EXIMD animals showed increases in mRNA levels of telomere‐repeat binding factor 1 ( Trf1 ; +61%; p = .01) and 2 ( Trf2 ; +47%; p = .04), DNA damage response gene Ku80 (+76%; p = .01) and cell cycle gene Chk2 (+69%; p = .03). In EX1h animals, up‐regulation of mRNA levels of protection of telomeres 1a ( Pot1a ; +35%; p = .04) and Ku80 (+69%; p = .02) were observed compared to BL. Trf1 mRNA levels differed from EXIMD (+61% vs +11%; p = .01). Preliminary experiments indicated increases in phosphorylated p38‐MAPK and decreases in phosphorylated Erk1/2 in EXIMD animals compared to BL. These findings indicate a novel regulatory pathway for cardiac telomere binding proteins in response to acute exercise. Supported by UMD Graduate Research Initiative Fund and NIH training grant AG000268