期刊
STEM CELL REVIEWS AND REPORTS
卷 15, 期 1, 页码 48-58出版社
SPRINGER
DOI: 10.1007/s12015-018-9850-9
关键词
Mouse myoblast differentiation; Muscle repair; Kinin-B2 receptor; HOE-140
资金
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (Sao Paulo Research Foundation, FAPESP) [2012/50880-4]
- CNPq (Conselho Nacional de Desenvolvimento Cientifico e Tecnologico), Brazil [2015/19128-2]
- NIH [8G12MD007600]
- Universidad Central del Caribe Biomedical Proteomics Facility Grant from the NIH National Institute on Minority Health and Health Disparities (NIMHD) RCMI Program [G12MD007583]
- CAPES (Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior), Brazil
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior - Brazil (CAPES) [001]
The bioactive peptide bradykinin obtained from cleavage of precursor kininogens activates the kinin-B2 receptor functioning in induction of inflammation and vasodilatation. In addition, bradykinin participates in kidney and cardiovascular development and neuronal and muscle differentiation. Here we show that kinin-B2 receptors are expressed throughout differentiation of murine C2C12 myoblasts into myotubes. An autocrine loop between receptor activation and bradykinin secretion is suggested, since bradykinin secretion is significantly reduced in the presence of the kinin-B2 receptor antagonist HOE-140 during differentiation. Expression of skeletal muscle markers and regenerative capacity were decreased after pharmacological inhibition or genetic ablation of the B2 receptor, while its antagonism increased the number of myoblasts in culture. In summary, the present work reveals to date no functions described for the B2 receptor in muscle regeneration due to the control of proliferation and differentiation of muscle precursor cells.
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