| First Author | Dominov JA | Year | 2001 |
| Journal | Dev Dyn | Volume | 220 |
| Issue | 1 | Pages | 18-26 |
| PubMed ID | 11146504 | Mgi Jnum | J:66494 |
| Mgi Id | MGI:1928555 | Doi | 10.1002/1097-0177(2000)9999:9999<::AID-DVDY1088>3.0.CO;2-# |
| Citation | Dominov JA, et al. (2001) Pro- and anti-apoptotic members of the bcl-2 family in skeletal muscle: A distinct role for bcl-2 in later stages of myogenesis. Dev Dyn 220(1):18-26 |
| abstractText | Apoptotic myonuclei appear during myogenesis and in diseased muscles. To investigate cell death regulation in skeletal muscle, we examined how members of the Bcl-2 family of apoptosis regulators are expressed and function in the C2C12 muscle cell line and in primary muscle cells at different stages of development. Both anti-apoptotic (Bcl-W, Bcl-X(L)) and pro-apoptotic (Bad, Bak, Bax) members of the Bcl-2 family were expressed in developing skeletal muscle in vivo. Each was also expressed in embryonic (E11-12), fetal (E15-16), and neonatal muscle stem cells, myoblasts, and myotubes in vitro. In contrast, Bcl-2 expression was limited to a small group of mononucleate, desmin-positive, myogenin-negative muscle cells that were seen in fetal and neonatal, but not embryonic, muscle cell cultures. The cell surface protein Sca-1, which is associated with muscle and blood stem cells, was found on approximately 1/2 of these Bcl-2-positive cells. Loss of Bcl-2 did not affect expression of other family members, because neonatal muscles of wild-type and Bcl-2-null mice had similar amounts of Bcl-X(L), Bcl-W, Bad, Bak, and Bax mRNAs. Loss of Bcl-2 did have functional consequences; however, because neonatal muscles of Bcl-2-null mice had only approximately 2/3 as many fast muscle fibers as muscles in wild-type mice. Thus, Bcl-2 function is required for particular stages of fetal and postnatal myogenesis. Copyright 2001 Wiley-Liss, Inc. |
