Connexin39 deficient mice display accelerated myogenesis and regeneration of skeletal muscle

Wulf, Volker; Matern, Gabi; Willecke, Klaus

doi:10.1016/j.yexcr.2011.01.017

Cited by 15 publications

(10 citation statements)

References 41 publications

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“…Transient expression of Cx40 has been described in axial skeletal muscles of mouse embryos during myoblast fusion (Dahl et al , 1995). Other Cx species found in muscle include Cx39 and Cx45 (von Maltzahn et al , 2004, von Maltzahn et al , 2011). Denervation of fast skeletal muscle cells activates NF-κB and elevates mRNA levels of TNF-α and IL-1β, which clearly shows the onset of inflammation after denervation.…”

Section: Connexin Signaling and Inflammationmentioning

confidence: 99%

Connexins and their channels in inflammation

Willebrords

Yanguas

Maes

et al. 2016

Critical Reviews in Biochemistry and Molecular Biology

115

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Inflammation may be caused by a variety of factors and is a hallmark of a plethora of acute and chronic diseases. The purpose of inflammation is to eliminate the initial cell injury trigger, to clear out dead cells from damaged tissue and to initiate tissue regeneration. Despite the wealth of knowledge regarding the involvement of cellular communication in inflammation, studies on the role of connexin-based channels in this process have only begun to emerge in the last few years. In this paper, a state-of-the-art overview of the effects of inflammation on connexin signaling is provided. Vice versa, the involvement of connexins and their channels in inflammation will be discussed by relying on studies that use a variety of experimental tools, such as genetically modified animals, small interfering RNA and connexin-based channel blockers. A better understanding of the importance of connexin signaling in inflammation may open up towards clinical perspectives.

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Section: Connexin Signaling and Inflammationmentioning

confidence: 99%

Connexins and their channels in inflammation

Willebrords

Yanguas

Maes

et al. 2016

Critical Reviews in Biochemistry and Molecular Biology

115

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“…This condition is called hypertrophy and multiple studies identified different roles for canonical and non-canonical Wnt signaling in muscle fiber hypertrophy (Armstrong and Esser, 2005;Bernardi et al, 2011;Han et al, 2011;Rochat et al, 2004;von Maltzahn et al, 2011). Furthermore, expression of β-catenin is a prerequisite for the physiological growth of adult skeletal muscle, underscoring the importance of canonical Wnt signaling (Armstrong et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Wnt/β-catenin signaling via Axin2 is required for myogenesis and, together with YAP/Taz and Tead1, active in IIa/IIx muscle fibers

et al. 2016

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Canonical Wnt/β-catenin signaling plays an important role in myogenic differentiation, but its physiological role in muscle fibers remains elusive. Here, we studied activation of Wnt/β-catenin signaling in adult muscle fibers and muscle stem cells in an Axin2 reporter mouse. Axin2 is a negative regulator and a target of Wnt/β-catenin signaling. In adult muscle fibers, Wnt/β-catenin signaling is only detectable in a subset of fast fibers that have a significantly smaller diameter than other fast fibers. In the same fibers, immunofluorescence staining for YAP/Taz and Tead1 was detected. Wnt/β-catenin signaling was absent in quiescent and activated satellite cells. Upon injury, Wnt/β-catenin signaling was detected in muscle fibers with centrally located nuclei. During differentiation of myoblasts expression of Axin2, but not of Axin1, increased together with Tead1 target gene expression. Furthermore, absence of Axin1 and Axin2 interfered with myoblast proliferation and myotube formation, respectively. Treatment with the canonical Wnt3a ligand also inhibited myotube formation. Wnt3a activated TOPflash and Tead1 reporter activity, whereas neither reporter was activated in the presence of Dkk1, an inhibitor of canonical Wnt signaling. We propose that Axin2-dependent Wnt/β-catenin signaling is involved in myotube formation and, together with YAP/Taz/Tead1, associated with reduced muscle fiber diameter of a subset of fast fibers.

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“…Several recent studies have demonstrated that during myogenesis in development or regeneration, myoblasts or satellite cells express at least 3 other Cx species in addition to Cx40, including Cx39, Cx43 and Cx45 [36][37][38][39][40][41]. It has been possible to study the consequences of a lack of each of these Cxs during myogenesis.…”

Section: Connexin-based Channels In Myogenesismentioning

confidence: 99%

“…However, Cx39 is expressed in murine myotubes, but not in myoblast cells or adult myofibers [41], suggesting that this Cx is involved in skeletal muscle differentiation, but not in the process of commitment to myogenic differentiation. In addition, the lack of Cx39 accelerates skeletal muscle differentiation [40]. Moreover, the reduced expression of myogenin, creatine kinase activity and the decrease in cell fusion found in myoblasts after induced deletion of Cx43 suggests a role of Cx43 in myoblast terminal differentiation [37].…”

Section: Connexin-based Channels In Myogenesismentioning

confidence: 99%

Regulation of pannexin and connexin channels and their functional role in skeletal muscles

Sáez

Cisterna

Vargas

et al. 2015

Cell. Mol. Life Sci.

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Myogenic precursor cells express connexins (Cx) and pannexins (Panx), proteins that form different membrane channels involved in cell-cell communication. Cx channels connect either the cytoplasm of adjacent cells, called gap junction channels (GJC), or link the cytoplasm with the extracellular space, termed hemichannels (HC), while Panx channels only support the latter. In myoblasts, Panx1 HCs play a critical role in myogenic differentiation, and Cx GJCs and possibly Cx HCs coordinate metabolic responses during later steps of myogenesis. After innervation, myofibers do not express Cxs, but still express Panx1. In myotubes and innervated myofibers, Panx1 HCs allow release of adenosine triphosphate and thus they might be involved in skeletal muscle plasticity. In addition, Panx1 HCs present in adult myofibers mediate adenosine triphosphate release and glucose uptake required for potentiation of muscle contraction. Under pathological conditions, such as upon denervation and spinal cord injury, levels of Panx1 are upregulated. However, Panx1(-/-) mice show similar degree of atrophy as denervated wild-type muscles. Skeletal muscles also express Cx HCs in the sarcolemma after denervation or spinal cord injury, plus other non-selective membrane channels, including purinergic P2X7 receptors and transient receptor potential type V2 channels. The absence of Cx43 and Cx45 is sufficient to drastically reduce denervation atrophy. Moreover, inflammatory cytokines also induce the expression of Cxs in myofibers, suggesting the expression of these Cxs as a common factor for myofiber degeneration under diverse pathological conditions. Inhibitors of skeletal muscle Cx HCs could be promising tools to prevent muscle wasting induced by conditions associated with synaptic dysfunction and inflammation.

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Connexin39 deficient mice display accelerated myogenesis and regeneration of skeletal muscle

Cited by 15 publications

References 41 publications

Connexins and their channels in inflammation

Connexins and their channels in inflammation

Wnt/β-catenin signaling via Axin2 is required for myogenesis and, together with YAP/Taz and Tead1, active in IIa/IIx muscle fibers

Regulation of pannexin and connexin channels and their functional role in skeletal muscles

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