Histamine Deficiency Delays Ischemic Skeletal Muscle Regeneration Via Inducing Aberrant Inflammatory Responses and Repressing Myoblast Proliferation

2018 ◽  
Author(s):  
Mieradilijiang Abudupataer ◽  
Weihong Zou ◽  
Weiwei Zhang ◽  
Suling Ding ◽  
Zheliang Zhou ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Inflammatory Responses ◽  
Skeletal Muscle Regeneration ◽  
Myoblast Proliferation

scholarly journals Simvastatin impairs myoblast proliferation and myotube formation of C2C12 myoblasts and in mouse skeletal muscle

2021 ◽  
Author(s):  
Gerda M Sanvee ◽  
Jamal Bouitbir ◽  
Stephan Kraehenbuehl
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Skeletal Muscle Regeneration ◽  
Plasma Membrane Permeability ◽  
Ki 67 ◽  
C2c12 Myoblasts ◽  
Mouse Skeletal Muscle ◽  
Myotube Formation ◽  
Myoblast Proliferation ◽  
Adam 12

Abstract Statins reduce cardiovascular complications in patients with high LDL-cholesterol but are associated with myopathy. We investigated the possibility that statins impair skeletal muscle regeneration by assessing simvastatin toxicity on C2C12 myoblasts and myotubes and mouse skeletal muscle. Simvastatin increased plasma membrane permeability and decreased the cellular ATP content in both myoblasts and myotubes, but with a stronger effect on myoblasts. While insulin prevented cytotoxicity up to 8 hours after addition of simvastatin to myotubes, prevention in myoblasts required simultaneous addition. Mevalonate and geranylgeraniol also prevented simvastatin-associated cytotoxicity on myoblasts and myotubes. Simvastatin impaired the phosphorylation of the insulin receptor (IR β), Akt ser473 and S6rp, and increased phosphorylation of AMPK thr172 in both myotubes and myoblasts, which was prevented by insulin and mevalonate. Simvastatin impaired oxygen consumption and increased superoxide production by myoblasts and myotubes and induced apoptosis via cytochromc c release. In addition, simvastatin impaired proliferation and fusion of myoblasts to myotubes by inhibiting the expression of the nuclear transcription factor MyoD and of the metalloprotease ADAM-12. Decreased expression of the proliferation factor Ki-67 and of ADAM-12 were also observed in gastrocnemius of mice treated with simvastatin. In conclusion, myoblasts were more susceptible to the toxic effects of simvastatin and simvastatin impaired myoblast proliferation and myotube formation. Impaired muscle regeneration represents a new mechanism of statin myotoxicity and may be important in statin-associated myopathy.

scholarly journals Roles of IL-1α/β in regeneration of cardiotoxin-injured muscle and satellite cell function

2018 ◽  
Vol 315 (1) ◽  
pp. R90-R103 ◽  
Author(s):  
Chayanit Chaweewannakorn ◽  
Masahiro Tsuchiya ◽  
Masashi Koide ◽  
Hiroyasu Hatakeyama ◽  
Yukinori Tanaka ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cells ◽  
Muscle Regeneration ◽  
Cell Function ◽  
Inflammatory Responses ◽  
Cell Types ◽  
Skeletal Muscle Regeneration ◽  
Double Knockout ◽  
Positive Role

Skeletal muscle regeneration after injury is a complex process involving interactions between inflammatory microenvironments and satellite cells. Interleukin (IL)-1 is a key mediator of inflammatory responses and exerts pleiotropic impacts on various cell types. Thus, we aimed to investigate the role of IL-1 during skeletal muscle regeneration. We herein show that IL-1α/β-double knockout (IL-1KO) mice exhibit delayed muscle regeneration after cardiotoxin (CTX) injection, characterized by delayed infiltrations of immune cells accompanied by suppressed local production of proinflammatory factors including IL-6 and delayed increase of paired box 7 (PAX7)-positive satellite cells postinjury compared with those of wild-type (WT) mice. A series of in vitro experiments using satellite cells obtained from the IL-1KO mice unexpectedly revealed that IL-1KO myoblasts have impairments in terms of both proliferation and differentiation, both of which were reversed by exogenous IL-1β administration in culture. Intriguingly, the delay in myogenesis was not attributable to the myogenic transcriptional program since MyoD and myogenin were highly upregulated in IL-1KO cells, instead appearing, at least in part, to be due to dysregulation of cellular fusion events, possibly resulting from aberrant actin regulatory systems. We conclude that IL-1 plays a positive role in muscle regeneration by coordinating the initial interactions among inflammatory microenvironments and satellite cells. Our findings also provide compelling evidence that IL-1 is intimately engaged in regulating the fundamental function of myocytes.

scholarly journals FOXO1 delays skeletal muscle regeneration and suppresses myoblast proliferation

2016 ◽  
Vol 80 (8) ◽  
pp. 1531-1535 ◽  
Author(s):  
Atsushi Yamashita ◽  
Yukino Hatazawa ◽  
Yuma Hirose ◽  
Yusuke Ono ◽  
Yasutomi Kamei
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Skeletal Muscle Regeneration ◽  
Myoblast Proliferation
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