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Multiple‐staged Regulation of Myogenic Differentiation by Prostaglandin E2
Author(s) -
Mo Chenglin,
Romero-Suarez Sandra,
Igwe Orisa,
Brotto Marco
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.1143.1
Subject(s) - myogenesis , myod , myogenin , c2c12 , myocyte , chemistry , microbiology and biotechnology , prostaglandin e2 , endocrinology , medicine , biology
We showed that conditioned media from osteocytes accelerates myogenesis in C2C12 myoblasts, which suggests signaling from bone to muscle cells. Since osteocytes secrete Prostaglandin E2 (PGE 2 ), one of the major PGs synthesized from arachidonic acid through cyclooxygenase pathways, we started a systematic investigation of PGE 2 roles in myogenesis. C2C12 myoblasts were used to investigate the effect and related molecular mechanisms of PGE 2 on myogenic differentiation. Expression of PGE 2 receptors (EP1‐EP4) was determined by real‐time PCR. EP1 and EP4 were highly expressed, whereas EP2 and EP3 were not detectable. Specific inhibitors SC 51322 for EP1 or L161,982 for EP4 significantly attenuated myogenesis. EP1 inhibition reduced the number of early myotubes, and subsequently affected the development of mature myotubes. On the other hand, EP4 inhibition did not affect the generation of early myotubes, but the fusion of early myotubes was dramatically inhibited. Interestingly, expression of two key myogenic regulatory factors, MyoD and Myogenin, was downregulated by EP1, but not by EP4 inhibition. These data provide evidence for the regulation of myogenesis by PGE 2 via EP1 and EP4. The different effects of EP1 and EP4 inhibition suggest PGE 2 signaling in myogenic differentiation is complex and multiple‐faceted. Support: NIH RC2 AR058962, Missouri Life Sciences Research Board(MB), and NIDCR DE021888(OJI).