18α-Glycyrrhetinic Acid Induces Phenotypic Changes of Skeletal Muscle Cells to Enter Adipogenesis

Yamanouchi, Keitaro; Yada, Erica; Ishiguro, Nozomu; Nishihara, Masugi

doi:10.1159/000110438

Cited by 27 publications

(25 citation statements)

References 39 publications

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“…For example, inhibition of Cx43 by AGA induces phenotypic changes of skeletal muscle cells to enter adipogenesis (Yamanouchi et al, 2007). Inhibition of gap junctional communication induces the trans-differentiation of osteoblasts to an adipocytic phenotype in vitro (Schiller et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Connexin 43 Mediates White Adipose Tissue Beiging by Facilitating the Propagation of Sympathetic Neuronal Signals

et al. 2016

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“Beige” adipocytes reside in white adipose tissue (WAT) and dissipate energy as heat. Several studies have shown that cold temperature can activate proopiomelanocortin-expressing (POMC) neurons and increase sympathetic neuronal tone to regulate WAT beiging. However, WAT is traditionally known to be sparsely innervated. Details regarding the neuronal innervation and more importantly, the propagation of the signal within the population of “beige” adipocytes are sparse. Here, we demonstrate that beige adipocytes display an increased cell-to-cell coupling via connexin 43 (Cx43) gap junction channels. Blocking of Cx43 channels by 18α-glycyrrhetinic acid decreases POMC activation-induced adipose tissue beiging. Adipocyte-specific deletion of Cx43 reduces WAT beiging to a level similar to that observed in denervated fat pads. In contrast, overexpression of Cx43 is sufficient to promote beiging even with mild cold stimuli. These data reveal the importance of cell-to-cell communication in adipose tissue for the propagation of limited neuronal inputs, resulting in effective beiging.

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Section: Discussionmentioning

confidence: 99%

Connexin 43 Mediates White Adipose Tissue Beiging by Facilitating the Propagation of Sympathetic Neuronal Signals

et al. 2016

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“…SMPCs were isolated from the hindlimb and back muscles of rats according to published procedures [36, 37]. To examine adipogenic potential, SMPCs were cultured in Dulbecco's modified Eagle's medium (DMEM) containing 10% fetal bovine serum (FBS) and penicillin/streptomycin (10% FBS/DMEM) supplemented with insulin (1 μg/ml), dexamethasone (0.1 μg/ml), isobutylmethylxanthine (27.8 μg/ml), and troglitazone (10 μM, kindly donated by Daiichi Sankyo Co., Ltd.) for 2 days, followed by culture for 2 days in 10% FBS/DMEM supplemented with insulin and troglitazone, and culture for 4 days in 10% FBS/DMEM supplemented with troglitazone.…”

Section: Methodsmentioning

confidence: 99%

Age-related resistance of skeletal muscle-derived progenitor cells to SPARC may explain a shift from myogenesis to adipogenesis

Nakamura

Nakano

Miyoshi

et al. 2012

Aging

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Aging causes phenotypic changes in skeletal muscle progenitor cells (SMPCs) that lead to the loss of myogenicity and adipogenesis. Secreted protein acidic and rich in cysteine (SPARC), which is secreted from SMPCs, stimulates myogenesis and inhibits adipogenesis. The present study aimed to examine whether changes in SPARC expression, its signaling pathway, or both are involved in age-related phenotypic changes in SMPCs. SPARC expression levels were comparable in SMPCs derived from young and old rats. However, when SPARC expression was reduced by a SPARC-specific siRNA, SMPCs from young rats showed reduced myogenesis and increased adipogenesis. In striking contrast, old rats showed little changes in these functions. Recombinant SPARC was effective in inhibiting adipogenesis and promoting myogenesis of SMPCs from young rats but had no effect on SMPCs from old rats when endogenous SPARC levels were reduced by the SPARC-siRNA. Further, the level of integrin α5, a subunit of the putative SPARC receptor, was decreased in SMPCs from old rats, and its inhibition in SMPCs from young rats by siRNA reduced adipogenesis in response to SPARC. These results suggest that, although SPARC plays a role in regulating SMPC function, SMPCs become refractory to the action of SPARC with age. Our data may explain an age-related shift from myogenesis to adipogenesis, associated with sarcopenia.

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“…Procedures for isolating skeletal muscle progenitor cells were previously described Yamanouchi et al 2006Yamanouchi et al , 2007. Briefly, rats were killed by inhalation of carbon dioxide gas.…”

Section: Cell Culturementioning

confidence: 99%

Skeletal muscle growth defect in human growth hormone transgenic rat is accompanied by phenotypic changes in progenitor cells

Shibata

Ueno

Ito

et al. 2010

AGE

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Growth hormone (GH) is known to have a pivotal role in the maintenance of skeletal muscle mass. Sarcopenia, the loss of skeletal muscle mass, is a common phenomenon in aging, and it is widely accepted that sarcopenia is largely attributed to agerelated decline in GH secretion. In the present study, we tested if human growth hormone transgenic rats (GH-TG rats) whose plasma GH levels are maintained relatively low could be an appropriate model for sarcopenia. Analyses of GH-TG rats revealed that they exhibit skeletal muscle growth defect as well as atrophy of myofibers. The number of myofibers in tibialis anterior muscle was comparable to that of WT rats, while the proportion of type I slow myofibers in tibialis anterior muscle was increased in GH-TG rats after 5 months. Neither increased expression of ubiquitin ligases, MuRF1 and MAFbx, nor indication of apoptotic cell death was observed. Notably, myogenic differentiation potential of skeletal muscle progenitor cells in GH-TG rats was lower than WT rats, and this was accompanied by increased adipogenic potential. These results indicate that GH-TG rats could be a useful model to elucidate the mechanism of sarcopenia induced by reduced GH action and raised the possibility that decreased GH action may cause an alteration of differentiation potential of skeletal muscle progenitor cells.

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18α-Glycyrrhetinic Acid Induces Phenotypic Changes of Skeletal Muscle Cells to Enter Adipogenesis

Cited by 27 publications

References 39 publications

Connexin 43 Mediates White Adipose Tissue Beiging by Facilitating the Propagation of Sympathetic Neuronal Signals

Connexin 43 Mediates White Adipose Tissue Beiging by Facilitating the Propagation of Sympathetic Neuronal Signals

Age-related resistance of skeletal muscle-derived progenitor cells to SPARC may explain a shift from myogenesis to adipogenesis

Skeletal muscle growth defect in human growth hormone transgenic rat is accompanied by phenotypic changes in progenitor cells

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