Why the study?
Does genetic ablation of MKP-1 and MKP-5 impair regenerative myogenesis in mice?
Does genetic ablation of MKP-1 and MKP-5 impair regenerative myogenesis in mice?
The positive regulatory actions of MKP-1 on myogenesis predominate over the negative regulatory actions of MKP-5, demonstrating their non-overlapping roles in skeletal muscle homeostasis.
Should not inform clinical myogenesis strategies; leaves open non-overlapping MKP-1/5 roles in satellite cell regeneration and inflammation.
The relative contribution of the MAP kinase phosphatases (MKPs) in the integration of MAP kinase-dependent signaling during regenerative myogenesis has yet to be fully investigated. MKP-1 and MKP-5 maintain skeletal muscle homeostasis by providing positive and negative effects on regenerative myogenesis, respectively. In order to define the hierarchical contributions of MKP-1 and MKP-5 in the regulation of regenerative myogenesis we genetically ablated both MKPs in mice. MKP-1/MKP 5-deficient double-knockout (MKP1/5- DKO) mice were viable, and upon skeletal muscle injury, were severely impaired in their capacity to regenerate skeletal muscle. Satellite cells were fewer in number in MKP1/5-DKO mice and displayed a reduced proliferative capacity as compared with those derived from wild-type mice. MKP1/5-DKO mice exhibited increased inflammation and the macrophage M1 to M2 transition during the resolution of inflammation was impaired following injury. These results demonstrate that the actions of MKP-1 to positively regulate myogenesis predominate over those of MKP-5, which negatively regulates myogenesis. Hence, MKP-1 and MKP-5 function to maintain skeletal muscle homeostasis through non-overlapping and opposing signaling pathways.
No takes yet. Share an insight, caveat, or question.
Hao Shi (2015) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: