Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/81571
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dc.contributor.authorChandrashekar, Preetien
dc.contributor.authorManickam, Ravikumaren
dc.contributor.authorGe, Xiaojiaen
dc.contributor.authorBonala, Sabeeraen
dc.contributor.authorMcFarlane, Craigen
dc.contributor.authorSharma, Mridulaen
dc.contributor.authorWahli, Walteren
dc.contributor.authorKambadur, Ravien
dc.date.accessioned2016-01-06T07:25:05Zen
dc.date.accessioned2019-12-06T14:34:00Z-
dc.date.available2016-01-06T07:25:05Zen
dc.date.available2019-12-06T14:34:00Z-
dc.date.issued2015en
dc.identifier.citationChandrashekar, P., Manickam, R., Ge, X., Bonala, S., McFarlane, C., Sharma, M., et al. (2015). Inactivation of PPARβ/δ adversely affects satellite cells and reduces postnatal myogenesis. American Journal of Physiology - Endocrinology And Metabolism, 309(2), 122-131.en
dc.identifier.issn0193-1849en
dc.identifier.urihttps://hdl.handle.net/10356/81571-
dc.description.abstractPeroxisome proliferator-activated receptor β/δ (PPARβ/δ) is a ubiquitously expressed gene with higher levels observed in skeletal muscle. Recently, our laboratory showed (Bonala S, Lokireddy S, Arigela H, Teng S, Wahli W, Sharma M, McFarlane C, Kambadur R. J Biol Chem 287: 12935–12951, 2012) that PPARβ/δ modulates myostatin activity to induce myogenesis in skeletal muscle. In the present study, we show that PPARβ/δ-null mice display reduced body weight, skeletal muscle weight, and myofiber atrophy during postnatal development. In addition, a significant reduction in satellite cell number was observed in PPARβ/δ-null mice, suggesting a role for PPARβ/δ in muscle regeneration. To investigate this, tibialis anterior muscles were injured with notexin, and muscle regeneration was monitored on days 3, 5, 7, and 28 postinjury. Immunohistochemical analysis revealed an increased inflammatory response and reduced myoblast proliferation in regenerating muscle from PPARβ/δ-null mice. Histological analysis confirmed that the regenerated muscle fibers of PPARβ/δ-null mice maintained an atrophy phenotype with reduced numbers of centrally placed nuclei. Even though satellite cell numbers were reduced before injury, satellite cell self-renewal was found to be unaffected in PPARβ/δ-null mice after regeneration. Previously, our laboratory had showed (Bonala S, Lokireddy S, Arigela H, Teng S, Wahli W, Sharma M, McFarlane C, Kambadur R. J Biol Chem 287: 12935–12951, 2012) that inactivation of PPARβ/δ increases myostatin signaling and inhibits myogenesis. Our results here indeed confirm that inactivation of myostatin signaling rescues the atrophy phenotype and improves muscle fiber cross-sectional area in both uninjured and regenerated tibialis anterior muscle from PPARβ/δ-null mice. Taken together, these data suggest that absence of PPARβ/δ leads to loss of satellite cells, impaired skeletal muscle regeneration, and postnatal myogenesis. Furthermore, our results also demonstrate that functional antagonism of myostatin has utility in rescuing these effects.en
dc.format.extent10 p.en
dc.language.isoenen
dc.relation.ispartofseriesAmerican Journal of Physiology - Endocrinology And Metabolismen
dc.rights© 2015 The American Physiological Society.en
dc.subjectMyostatinen
dc.subjectPPARβ/δen
dc.subjectSkeletal muscle regenerationen
dc.titleInactivation of PPARβ/δ adversely affects satellite cells and reduces postnatal myogenesisen
dc.typeJournal Articleen
dc.contributor.schoolSchool of Biological Sciencesen
dc.contributor.schoolLee Kong Chian School of Medicine (LKCMedicine)en
dc.identifier.doi10.1152/ajpendo.00586.2014en
item.grantfulltextnone-
item.fulltextNo Fulltext-
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