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Presence of VDR and CYP27B1 in mouse C2C12 cells and skeletal muscle reveal the action of 25(OH)D3 on suppression of myoblast proliferation
Author(s) -
Srikuea Ratchakrit,
Zhang Xiping,
McCarthy John J.,
Esser Karyn A.,
Park-Sarge Ok-Kyong
Publication year - 2012
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.26.1_supplement.1143.6
Subject(s) - calcitriol receptor , c2c12 , myogenesis , skeletal muscle , myocyte , endocrinology , medicine , biology , chemistry , microbiology and biotechnology , vitamin d and neurology
1α,25(OH) 2 D 3 , an active form of vitamin D 3 was demonstrated to regulate myoblast proliferation via its nuclear vitamin D receptor (VDR). Local production of 1α,25(OH) 2 D 3 was reported in the cells that express VDR and CYP27B1, the latter is used to convert 25(OH)D 3 to 1α,25(OH) 2 D 3 . However, whether skeletal muscle expresses CYP27B1 and 25(OH)D 3 can be used as a precursor for the local synthesis of 1α,25(OH) 2 D 3 in skeletal muscle and regulate muscle cell functions are currently unknown. In this study, we investigated 1) VDR and CYP27B1 mRNA transcripts in C2C12 cells (mouse muscle cell line) and skeletal muscle tissue 2) the expression of VDR and CYP27B1 protein in C2C12 cells 3) the effect of 25(OH)D 3 on C2C12 cell proliferation. Here, we demonstrated that C2C12 cells and skeletal muscle expressed VDR and CYP27B1 mRNA transcripts. Both genes were significantly up‐regulated at the mRNA level after skeletal muscle was overloaded. Nuclear VDR and mitochondrial CYP27B1 were expressed in C2C12 myoblasts but not myotubes. 25(OH)D 3 treatment increased nuclear VDR expression and inhibited C2C12 myoblast proliferation. This effect was abolished by CYP27B1 knockdown, suggesting CYP27B1 is required for 25(OH)D 3 action in myoblasts. Taken together, the presence of VDR and CYP27B1 in C2C12 cells and skeletal muscle revealed the possible contribution of 25(OH)D 3 on the regulation of skeletal muscle function, in part on controlling of muscle cell proliferation. This work was supported by NIH R01AR45617 to KAE and PGY funds to OKPS