PMID- 30652078 OWN - NLM STAT- MEDLINE DCOM- 20200219 LR - 20200309 IS - 2211-5463 (Print) IS - 2211-5463 (Electronic) IS - 2211-5463 (Linking) VI - 9 IP - 1 DP - 2019 Jan TI - Heat induces myogenic transcription factors of myoblast cells via transient receptor potential vanilloid 1 (Trpv1). PG - 101-113 LID - 10.1002/2211-5463.12550 [doi] AB - Exercise generates heat, blood flow, and metabolic changes, thereby inducing hypertrophy of skeletal muscle cells. However, the mechanism by which heat incudes hypertrophy in response to heat is not well known. Here, we hypothesized that heat would induce differentiation of myoblast cells. We investigated the underlying mechanism by which myoblast cells respond to heat. When mouse myoblast cells were exposed to 42 degrees C for over 30 min, the phosphorylation level of protein kinase C (PKC) and heat shock factor 1 (Hsf1) increased, and the mRNA and protein expression level of heat shock protein 70 (Hsp70) increased. Inhibitors of transient receptor potential vanilloid 1 (Trpv1), calmodulin, PKC, and Hsf1, and the small interfering RNA-mediated knockdown of Trpv1 diminished those heat responses. Heat exposure increased the phosphorylation levels of thymoma viral proto-oncogene 1 (Akt), mammalian target of rapamycin (mTOR), eukaryotic translation initiation factor 4E binding protein 1 (Eif4ebp1), and ribosomal protein S6 kinase, polypeptide 1 (S6K1). The knockdown of Trpv1 decreased these heat-induced responses. Antagonists of Hsp70 inhibited the phosphorylation level of Akt. Finally, heat increased the protein expression level of skeletal muscle markers such as myocyte enhancer factor 2D, myogenic factor 5, myogenic factor 6, and myogenic differentiation 1. Heat also increased myotube formation. Knockdown of Trpv1 diminished heat-induced increases of those proteins and myotube formation. These results indicate that heat induces myogenic transcription factors of myoblast cells through the Trpv1, calmodulin, PKC, Hsf1, Hsp70, Akt, mTOR, Eif4ebp1, and S6K1 pathway. Moreover, heat increases myotube formation through Trpv1. FAU - Obi, Syotaro AU - Obi S AD - Research Support Center Dokkyo Medical University Tochigi Japan. AD - Department of Cardiovascular Medicine Dokkyo Medical University Tochigi Japan. FAU - Nakajima, Toshiaki AU - Nakajima T AD - Department of Cardiovascular Medicine Dokkyo Medical University Tochigi Japan. AD - Heart Center Dokkyo Medical University Hospital Tochigi Japan. FAU - Hasegawa, Takaaki AU - Hasegawa T AD - Department of Cardiovascular Medicine Dokkyo Medical University Tochigi Japan. FAU - Nakamura, Fumitaka AU - Nakamura F AD - Third Department of Internal Medicine Teikyo University Chiba Medical Center Japan. FAU - Sakuma, Masashi AU - Sakuma M AD - Department of Cardiovascular Medicine Dokkyo Medical University Tochigi Japan. FAU - Toyoda, Shigeru AU - Toyoda S AD - Department of Cardiovascular Medicine Dokkyo Medical University Tochigi Japan. AD - Heart Center Dokkyo Medical University Hospital Tochigi Japan. FAU - Tei, Chuwa AU - Tei C AD - Department of Cardiovascular Medicine Dokkyo Medical University Tochigi Japan. FAU - Inoue, Teruo AU - Inoue T AD - Research Support Center Dokkyo Medical University Tochigi Japan. AD - Department of Cardiovascular Medicine Dokkyo Medical University Tochigi Japan. AD - Heart Center Dokkyo Medical University Hospital Tochigi Japan. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20181203 PL - England TA - FEBS Open Bio JT - FEBS open bio JID - 101580716 RN - 0 (TRPV Cation Channels) RN - 0 (TRPV1 protein, mouse) RN - 0 (Transcription Factors) SB - IM MH - *Hot Temperature MH - *Muscle Development MH - Muscle, Skeletal/metabolism MH - Myoblasts/cytology/*metabolism MH - Signal Transduction MH - TRPV Cation Channels/*metabolism MH - Transcription Factors/*metabolism PMC - PMC6325605 OTO - NOTNLM OT - heat response signaling OT - skeletal muscle OT - translation EDAT- 2019/01/18 06:00 MHDA- 2019/01/18 06:01 PMCR- 2018/12/03 CRDT- 2019/01/18 06:00 PHST- 2018/04/13 00:00 [received] PHST- 2018/09/25 00:00 [revised] PHST- 2018/10/30 00:00 [accepted] PHST- 2019/01/18 06:00 [entrez] PHST- 2019/01/18 06:00 [pubmed] PHST- 2019/01/18 06:01 [medline] PHST- 2018/12/03 00:00 [pmc-release] AID - FEB412550 [pii] AID - 10.1002/2211-5463.12550 [doi] PST - epublish SO - FEBS Open Bio. 2018 Dec 3;9(1):101-113. doi: 10.1002/2211-5463.12550. eCollection 2019 Jan.