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Reductions in RIP140 are not required for exercise- and AICAR-mediated increases in skeletal muscle mitochondrial content.
J Appl Physiol (1985). 2011 Sep; 111(3):688-95.JA

Abstract

Receptor interacting protein 1 (RIP140) has recently been demonstrated to be a key player in the regulation of skeletal muscle mitochondrial content. We have shown that β-guanadinopropionic acid (β-GPA) feeding reduces RIP140 protein content and mRNA levels concomitant with increases in mitochondrial content (Williams DB, Sutherland LN, Bomhof MR, Basaraba SA, Thrush AB, Dyck DJ, Field CJ, Wright DC. Am J Physiol Endocrinol Metab 296: E1400-E1408, 2009). Since β-GPA feeding reduces high-energy phosphate levels and activates AMPK, alterations reminiscent of exercise, we hypothesized that exercise training would reduce RIP140 protein content. We further postulated that an acute bout of exercise, or interventions known to induce the expression of mitochondrial enzymes or genes involved in mitochondrial biogenesis, would result in decreases in nuclear RIP140 content. Two weeks of daily swim training increased markers of mitochondrial content in rat skeletal muscle independent of reductions in RIP140 protein. Similarly, high-intensity exercise training in humans failed to reduce RIP140 content despite increasing skeletal muscle mitochondrial enzymes. We found that 6 wk of daily 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR) injections had no effect on RIP140 protein content in rat skeletal muscle while RIP140 content from LKB1 knockout mice was unaltered despite reductions in mitochondria. An acute bout of exercise, AICAR treatment, and epinephrine injections increased the mRNA levels of PGC-1α, COXIV, and lipin1 independent of decreases in nuclear RIP140 protein. Surprisingly these interventions increased RIP140 mRNA expression. In conclusion our results demonstrate that decreases in RIP140 protein content are not required for exercise and AMPK-dependent increases in skeletal muscle mitochondrial content, nor do acute perturbations alter the cellular localization of RIP140 in parallel with the induction of genes involved in mitochondrial biogenesis.

Authors+Show Affiliations

Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21700896

Citation

Frier, Bruce C., et al. "Reductions in RIP140 Are Not Required for Exercise- and AICAR-mediated Increases in Skeletal Muscle Mitochondrial Content." Journal of Applied Physiology (Bethesda, Md. : 1985), vol. 111, no. 3, 2011, pp. 688-95.
Frier BC, Hancock CR, Little JP, et al. Reductions in RIP140 are not required for exercise- and AICAR-mediated increases in skeletal muscle mitochondrial content. J Appl Physiol. 2011;111(3):688-95.
Frier, B. C., Hancock, C. R., Little, J. P., Fillmore, N., Bliss, T. A., Thomson, D. M., Wan, Z., & Wright, D. C. (2011). Reductions in RIP140 are not required for exercise- and AICAR-mediated increases in skeletal muscle mitochondrial content. Journal of Applied Physiology (Bethesda, Md. : 1985), 111(3), 688-95. https://doi.org/10.1152/japplphysiol.00279.2011
Frier BC, et al. Reductions in RIP140 Are Not Required for Exercise- and AICAR-mediated Increases in Skeletal Muscle Mitochondrial Content. J Appl Physiol. 2011;111(3):688-95. PubMed PMID: 21700896.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Reductions in RIP140 are not required for exercise- and AICAR-mediated increases in skeletal muscle mitochondrial content. AU - Frier,Bruce C, AU - Hancock,Chad R, AU - Little,Jonathan P, AU - Fillmore,Natasha, AU - Bliss,Tyler A, AU - Thomson,David M, AU - Wan,Zhongxiao, AU - Wright,David C, Y1 - 2011/06/23/ PY - 2011/6/25/entrez PY - 2011/6/28/pubmed PY - 2012/1/12/medline SP - 688 EP - 95 JF - Journal of applied physiology (Bethesda, Md. : 1985) JO - J. Appl. Physiol. VL - 111 IS - 3 N2 - Receptor interacting protein 1 (RIP140) has recently been demonstrated to be a key player in the regulation of skeletal muscle mitochondrial content. We have shown that β-guanadinopropionic acid (β-GPA) feeding reduces RIP140 protein content and mRNA levels concomitant with increases in mitochondrial content (Williams DB, Sutherland LN, Bomhof MR, Basaraba SA, Thrush AB, Dyck DJ, Field CJ, Wright DC. Am J Physiol Endocrinol Metab 296: E1400-E1408, 2009). Since β-GPA feeding reduces high-energy phosphate levels and activates AMPK, alterations reminiscent of exercise, we hypothesized that exercise training would reduce RIP140 protein content. We further postulated that an acute bout of exercise, or interventions known to induce the expression of mitochondrial enzymes or genes involved in mitochondrial biogenesis, would result in decreases in nuclear RIP140 content. Two weeks of daily swim training increased markers of mitochondrial content in rat skeletal muscle independent of reductions in RIP140 protein. Similarly, high-intensity exercise training in humans failed to reduce RIP140 content despite increasing skeletal muscle mitochondrial enzymes. We found that 6 wk of daily 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR) injections had no effect on RIP140 protein content in rat skeletal muscle while RIP140 content from LKB1 knockout mice was unaltered despite reductions in mitochondria. An acute bout of exercise, AICAR treatment, and epinephrine injections increased the mRNA levels of PGC-1α, COXIV, and lipin1 independent of decreases in nuclear RIP140 protein. Surprisingly these interventions increased RIP140 mRNA expression. In conclusion our results demonstrate that decreases in RIP140 protein content are not required for exercise and AMPK-dependent increases in skeletal muscle mitochondrial content, nor do acute perturbations alter the cellular localization of RIP140 in parallel with the induction of genes involved in mitochondrial biogenesis. SN - 1522-1601 UR - https://www.unboundmedicine.com/medline/citation/21700896/Reductions_in_RIP140_are_not_required_for_exercise__and_AICAR_mediated_increases_in_skeletal_muscle_mitochondrial_content_ L2 - http://www.physiology.org/doi/full/10.1152/japplphysiol.00279.2011?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -