Expression of the rat connexin 39 (rCx39) gene in myoblasts and myotubes in developing and regenerating skeletal muscles: An in situ hybridization study
Department of Experimental Medicine, Section of Human Physiology, Laboratory of Neurobiology, University of Palermo, Italy. Cell and Tissue Research
(Impact Factor: 3.57).
06/2005; 320(2):299-310. DOI: 10.1007/s00441-005-1087-7
We report a detailed analysis of the expression pattern of the recently identified rat connexin gene, named rat connexin 39 (rCx39), both during embryonic development and in adult life. Qualitative and quantitative reverse transcription/polymerase chain reaction analysis showed intense expression of rCx39 restricted to differentiating skeletal muscles, with a peak of expression detected at 18 days of embryonic life, followed by a rapid decline to undetectable levels within the first week of postnatal life. A combination of the in situ hybridization technique for the detection of rCx39 mRNA and immunohistochemistry for myogenin, a myoblast-specific marker, allowed us to establish that the mRNA for this connexin was expressed in myogenin-positive myoblasts and early myotubes but disappeared in mature myotubes. Moreover, in adult animals, rCx39 mRNA was expressed in myogenic cells involved in skeletal myofiber regeneration following a crush injury. This is the first case of a connexin being mainly expressed in the myogenic cell lineage. The information presented should pave the way to novel molecular approaches in studies on the role of connexin-based gap-junctional communication in skeletal muscle differentiation and regeneration.
Available from: Jose Luis Vega Pizarro
- "In adult rat skeletal muscle we did not find immunoreactivity for connexin32, connexin43, or connexin45 (Data not shown). As noted above, connexin39 is not expressed in adult skeletal myofibers (Belluardo et al., 2005; von Maltzahn et al., 2004). Thus, we conclude that connexin HCs are unlikely to be expressed in normal adult rat skeletal myofibers mediating changes in permeability of the sarcolema. "
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ABSTRACT: During repetitive stimulation of skeletal muscle, extracellular ATP levels raise, activating purinergic receptors, increasing Ca(2+) influx, and enhancing contractile force, a response called potentiation. We found that ATP appears to be released through pannexin 1 hemichannels (Panx1 HCs). Immunocytochemical analyses and function were consistent with pannexin1 localization to T-tubules intercalated with dihydropyridine and ryanodine receptors in slow (soleus) and fast (extensor digitorum longus, EDL) muscles. Isolated myofibers took up ethidium (Etd(+)) and released small molecules (as ATP) during electrical stimulation. Consistent with two glucose uptake pathways, induced uptake of 2-NBDG, a fluorescent glucose derivative, was decreased by inhibition of HCs or glucose transporter (GLUT4), and blocked by dual blockade. Adult skeletal muscles apparently do not express connexins, making it unlikely that connexin hemichannels contribute to the uptake and release of small molecules. ATP release, Etd(+) uptake, and potentiation induced by repetitive electrical stimulation were blocked by HC blockers and did not occur in muscles of pannexin1 knockout mice. MRS 2179, a P2Y1R blocker, prevented potentiation in EDL, but not soleus muscles, suggesting that in fast muscles ATP activates P2Y1 but not P2X receptors. Phosphorylation on Ser and Thr residues of pannexin1 was increased during potentiation, possibly mediating HC opening. Opening of Panx1 HCs during repetitive activation allows efflux of ATP, influx of glucose and possibly Ca(2+) too, which are required for potentiation of contraction.
Neuropharmacology 04/2013; 75. DOI:10.1016/j.neuropharm.2013.03.022 · 5.11 Impact Factor
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ABSTRACT: Extensive numerical simulations of anisotropic etching of exact and vicinal Si(111) are performed for the first time using the target rate kinetic Monte-Carlo (TR-KMC) algorithm. The results show that the removal of layers on Si(111) is largely controlled by step propagation and that pit nucleation has a vanishingly small role. In turn, step flow itself is largely controlled by kink propagation and, only to a minor extent, by kink nucleation.
Micro-Nanomechatronics and Human Science, 2004 and The Fourth Symposium Micro-Nanomechatronics for Information-Based Society, 2004. Proceedings of the 2004 International Symposium on; 01/2004
Available from: Roberta Squecco
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ABSTRACT: Although sphingosine 1-phosphate (S1P) has been considered a potent regulator of skeletal muscle biology, acting as a physiological anti-mitogenic and prodifferentiating agent, its downstream effectors are poorly known. In the present study, we provide experimental evidence for a novel mechanism by which S1P regulates skeletal muscle differentiation through the regulation of gap junctional protein connexin (Cx) 43. Indeed, the treatment with S1P greatly enhanced Cx43 expression and gap junctional intercellular communication during the early phases of myoblast differentiation, whereas the down-regulation of Cx43 by transfection with short interfering RNA blocked myogenesis elicited by S1P. Moreover, calcium and p38 MAPK-dependent pathways were required for S1P-induced increase in Cx43 expression. Interestingly, enforced expression of mutated Cx43(Delta130-136) reduced gap junction communication and totally inhibited S1P-induced expression of the myogenic markers, myogenin, myosin heavy chain, caveolin-3, and myotube formation. Notably, in S1P-stimulated myoblasts, endogenous or wild-type Cx43 protein, but not the mutated form, coimmunoprecipitated and colocalized with F-actin and cortactin in a p38 MAPK-dependent manner. These data, together with the known role of actin remodeling in cell differentiation, strongly support the important contribution of gap junctional communication, Cx43 expression and Cx43/cytoskeleton interaction in skeletal myogenesis elicited by S1P.
Molecular Biology of the Cell 12/2006; 17(11):4896-910. DOI:10.1091/mbc.E06-03-0243 · 4.47 Impact Factor
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