TACE release of TNF-α mediates mechanotransduction-induced activation of p38 MAPK and myogenesis

Zhan, Mel; Jin, Bingwen; Chen, Shuen-Ei; Reecy, James M.; Li, Yi Ping

doi:10.1242/jcs.03372

Cited by 79 publications

(110 citation statements)

References 84 publications

(113 reference statements)

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“…1D). Consequently, stretch activation of p38 MAPK, which was previously shown dependent on the activation of TACE-mediated TNFa release (Zhan et al, 2007), was abolished by PP2 (Fig. 1E).…”

Section: Src Mediates Mechanical Activation Of Tace In Myoblastssupporting

confidence: 65%

“…We previously showed that mechanical stretch of myoblasts rapidly activates TACE (Zhan et al, 2007). To assess whether Src mediates TACE activation by mechanical stretch, we first investigated whether there is a causal relationship between Src activity and TACE phosphorylation and activation in mechanically stretched myoblasts.…”

Section: Src Mediates Mechanical Activation Of Tace In Myoblastsmentioning

confidence: 99%

“…(E) PP2 blocks mechanical activation of myogenic marker p38 MAPK. On the basis of the previously determined time course of stretchactivation of p38 (Zhan et al, 2007), C2C12 myoblasts were stretched for 120 minutes with or without 10 mM PP2 or PP3. Cell lysate was analyzed for p38 activation using western blotting.…”

Section: Src Mediates Mechanical Activation Of Tace In Myoblastsmentioning

confidence: 99%

“…To gain insights into the related mechanism of mechanotransduction, we showed previously that, in response to mechanical stimulation, myoblasts release autocrine TNFa, which is crucial to myogenic activation of the MKK6 (also known as MAP2K6) to p38 MAPK pathway and ensuing myogenic differentiation (Zhan et al, 2007). Moreover, we found that TNFa-converting enzyme (TACE, also known as ADAM17), the disintegrin metalloproteinase (Black, 2002) that cleaves plasma membrane-anchored pro-TNFa (26 kDa) to release free TNFa (17 kDa), is rapidly activated by mechanical stimulation and is rate limiting for mechano-activation of p38 MAPK (Zhan et al, 2007). These findings revealed a new signaling paradigm through which myogenic cues are transduced to activate myogenic gene expression via the activation of TACE release of autocrine TNFa.…”

Section: Introductionmentioning

confidence: 99%

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Src mediates the mechanical activation of myogenesis by activating TNFα-converting enzyme

Niu

Wen

Liu

et al. 2013

Journal of Cell Science

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SummaryMechanical stimulation affects many biological aspects in living cells through mechanotransduction. In myogenic precursor cells (MPCs), mechanical stimulation activates p38 mitogen-activated protein kinase (MAPK), a key regulator of myogenesis, via activating TNFa-converting enzyme (TACE, also known as ADAM17), to release autocrine TNFa. However, the signaling mechanism of mechanical activation of TACE is unknown. Because TACE possesses the structural features of substrates of the non-receptor tyrosine kinase Src, we tested the hypothesis that Src mediates mechanical activation of TACE in MPCs. We observed that mechanical stretch of C2C12 or primary rat myoblasts rapidly activates Src, which in turn interacts and colocalizes with TACE, resulting in tyrosine phosphorylation and activation of TACE. Particularly, Src activates TACE via the phosphorylation of amino acid residue Tyr702 in the intracellular tail of TACE, resulting in increased TNFa release and p38 activation. Src inhibition or deficiency blocks stretch activation of the TACE-p38-MAPK signaling, resulting in impaired myogenic gene expression. In response to functional overloading, Src and TACE are activated in mouse soleus muscle. Further, overloading-induced myogenesis and regeneration are impaired in the soleus of Src +/2 mice. Therefore, Src mediates mechano-activation of TACE and myogenesis.

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“…1D). Consequently, stretch activation of p38 MAPK, which was previously shown dependent on the activation of TACE-mediated TNFa release (Zhan et al, 2007), was abolished by PP2 (Fig. 1E).…”

Section: Src Mediates Mechanical Activation Of Tace In Myoblastssupporting

confidence: 65%

Section: Src Mediates Mechanical Activation Of Tace In Myoblastsmentioning

confidence: 99%

Section: Src Mediates Mechanical Activation Of Tace In Myoblastsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Src mediates the mechanical activation of myogenesis by activating TNFα-converting enzyme

Niu

Wen

Liu

et al. 2013

Journal of Cell Science

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“…It is also established that TNFα stimulates differentiation of muscle precursor cells 14,15 by activating the mitogen-activated protein kinase p38. 15,16 Expectedly, we found that PrP-KO muscles displayed significantly reduced amounts of active [phosphorylated (P-)] p38 than WT samples. P-p38 regulates muscle differentiation in multiple ways; it directly activates pioneer muscle regulatory factors (MRFs), such as MyoD and Myf5, but it also regulates the ATP-dependent SWI/SNF chromatin remodeling complex that allows access and binding of muscle transcription factors (MEF-2 and MRFs) to their specific loci.…”

Section: The Prion Protein In Pathology and Physiologymentioning

confidence: 69%

Prion and TNFα: TAC(E)it agreement between the prion protein and cell signaling

Stella

Massimino²,

Sorgato

et al. 2010

Cell Cycle

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Crosstalk Between MLO‐Y4 Osteocytes and C2C12 Muscle Cells Is Mediated by the Wnt/β‐Catenin Pathway

et al. 2017

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We examined the effects of osteocyte secreted factors on myogenesis and muscle function. MLO-Y4 osteocyte-like cell conditioned media (CM) (10%) increased ex vivo soleus muscle contractile force by ~25%. MLO-Y4 and primary osteocyte CM (1–10%) stimulated myogenic differentiation of C2C12 myoblasts, but 10% osteoblast CMs did not enhance C2C12 cell differentiation. Since WNT3a and WNT1 are secreted by osteocytes, and the expression level of Wnt3a is increased in MLO-Y4 cells by fluid flow shear stress, both were compared, showing WNT3a more potent than WNT1 in inducing myogenesis. Treatment of C2C12 myoblasts with WNT3a at concentrations as low as 0.5ng/mL mirrored the effects of both primary osteocyte and MLO-Y4 CM by inducing nuclear translocation of β-catenin with myogenic differentiation, suggesting that Wnts might be potential factors secreted by osteocytes that signal to muscle cells. Knocking down Wnt3a in MLO-Y4 osteocytes inhibited the effect of CM on C2C12 myogenic differentiation. Sclerostin (100ng/mL) inhibited both the effects of MLO-Y4 CM and WNT3a on C2C12 cell differentiation. RT-PCR array results supported the activation of the Wnt/β-catenin pathway by MLO-Y4 CM and WNT3a. These results were confirmed by qPCR showing up-regulation of myogenic markers and two Wnt/β-catenin downstream genes, Numb and Flh1. We postulated that MLO-Y4 CM/WNT3a could modulate intracellular calcium homeostasis as the trigger mechanism for the enhanced myogenesis and contractile force. MLO-Y4 CM and WNT3a increased caffeine-induced Ca2+ release from the sarcoplasmic reticulum (SR) of C2C12 myotubes and the expression of genes directly associated with intracellular Ca2+ signaling and homeostasis. Together, these data show that in vitro and ex vivo, osteocytes can stimulate myogenesis and enhance muscle contractile function and suggest that Wnts could be mediators of bone to muscle signaling, likely via modulation of intracellular Ca2+ signaling and the Wnt/β-Catenin pathway.

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TACE release of TNF-α mediates mechanotransduction-induced activation of p38 MAPK and myogenesis

Cited by 79 publications

References 84 publications

Src mediates the mechanical activation of myogenesis by activating TNFα-converting enzyme

Src mediates the mechanical activation of myogenesis by activating TNFα-converting enzyme

Prion and TNFα: TAC(E)it agreement between the prion protein and cell signaling

Crosstalk Between MLO‐Y4 Osteocytes and C2C12 Muscle Cells Is Mediated by the Wnt/β‐Catenin Pathway

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