Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.23 (beta-galactosidase)
14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Skeletal muscle is one of a several adult post-mitotic tissues that retain the capacity to regenerate. This relies on a population of quiescent precursors, termed satellite cells. Here we describe two novel markers of quiescent satellite cells: CD34, an established marker of hematopoietic stem cells, and Myf5, the earliest marker of myogenic commitment. CD34(+ve) myoblasts can be detected in proliferating C2C12 cultures. In differentiating cultures, CD34(+ve) cells do not fuse into myotubes, nor express MyoD. Using isolated myofibers as a model of synchronous precursor cell activation, we show that quiescent satellite cells express CD34. An early feature of their activation is alternate splicing followed by complete transcriptional shutdown of CD34. This data implicates CD34 in the maintenance of satellite cell quiescence. In heterozygous Myf5(nlacZ/+) mice, all CD34(+ve) satellite cells also express beta-galactosidase, a marker of activation of Myf5, showing that quiescent satellite cells are committed to myogenesis. All such cells are positive for the accepted satellite cell marker, M-cadherin. We also show that satellite cells can be identified on isolated myofibers of the myosin light chain 3F-nlacZ-2E mouse as those that do not express the transgene. The numbers of satellite cells detected in this way are significantly greater than those identified by the other three markers. We conclude that the expression of CD34, Myf5, and M-cadherin defines quiescent, committed precursors and speculate that the CD34(-ve), Myf5(-ve) minority may be involved in maintaining the lineage-committed majority.
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PMID:Expression of CD34 and Myf5 defines the majority of quiescent adult skeletal muscle satellite cells. 1112 37

Satellite cells (SC) in adult muscle are quiescent in the G0 phase of the cell cycle. In the present study we determined whether SC after denervation upregulate M-cadherin, an adhesion molecule that is upregulated with differentiation and fusion. We also monitored primary cultures of SC from denervated muscle for expression of the transcription factors of the MyoD family to determine whether SC from denervated muscle can be activated in vitro. Hindlimb muscles of rats were denervated under anesthesia, and rats were killed after 2-28 days. The SC of the denervated limbs were pooled and either assessed for M-cadherin mRNA by using real-time RT-PCR or cultured in vitro. The cultures were processed for RT-PCR or immunofluorescence for expression of the transcription factors of the MyoD family. Hindlimb muscles of M-cadherin knockout mice were denervated under anesthesia, mice were killed after 2-28 days, and cells were stained for beta-galactosidase activity by X-gal histochemistry. In vitro, primary SC cultures from rat muscle denervated for 2-28 days expressed transcripts of myf5, MyoD, myogenin, and MRF4 as SC from normal innervated muscle. In vivo, M-cadherin transcription was not upregulated in SC from denervated rat muscle when compared with normal muscle. Moreover, beta-galactosidase activity was not detected in denervated mouse muscle. The finding that SC do not upregulate M-cadherin after denervation supports the notion that they remain in the G(0) phase of the cell cycle in vivo. However, the cells retain the capacity to pass through the proliferative and differentiative program when robustly stimulated to do so in vitro.
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PMID:M-cadherin transcription in satellite cells from normal and denervated muscle. 1476 88