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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Luo, Tao Ren, Hongmei Jiang, Weihua Esser, Karyn A. Zhuang, Xun Zhu, Jing Zhang, Xiping |
| Description | Author Affiliation: Jiang W ( From the Division of Cardiovascular Medicine, Department of Internal Medicine, Saha Cardiovascular Center.); Zhu J ( From the Division of Cardiovascular Medicine, Department of Internal Medicine, Saha Cardiovascular Center.); Zhuang X ( From the Division of Cardiovascular Medicine, Department of Internal Medicine, Saha Cardiovascular Center.); Zhang X ( Department of Physiology, University of Kentucky, Lexington, Kentucky 40536.); Luo T ( From the Division of Cardiovascular Medicine, Department of Internal Medicine, Saha Cardiovascular Center.); Esser KA ( Department of Physiology, University of Kentucky, Lexington, Kentucky 40536.); Ren H ( From the Division of Cardiovascular Medicine, Department of Internal Medicine, Saha Cardiovascular Center, hongmei.ren@uky.edu.) |
| Abstract | Lipin1, an intracellular protein, plays critical roles in controlling lipid synthesis and energy metabolism through its enzymatic activity and nuclear transcriptional functions. Several mouse models of skeletal muscle wasting are associated with lipin1 mutation or altered expression. Recent human studies have suggested that children with homozygous null mutations in the LPIN1 gene suffer from rhabdomyolysis. However, the underlying pathophysiologic mechanism is still poorly understood. In the present study we examined whether lipin1 contributes to regulating muscle regeneration. We characterized the time course of skeletal muscle regeneration in lipin1-deficient fld mice after injury. We found that fld mice exhibited smaller regenerated muscle fiber cross-sectional areas compared with wild-type mice in response to injury. Our results from a series of in vitro experiments suggest that lipin1 is up-regulated and translocated to the nucleus during myoblast differentiation and plays a key role in myogenesis by regulating the cytosolic activation of ERK1/2 to form a complex and a downstream effector cyclin D3-mediated cell cycle withdrawal. Overall, our study reveals a previously unknown role of lipin1 in skeletal muscle regeneration and expands our understanding of the cellular and molecular mechanisms underlying skeletal muscle regeneration. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 39 |
| Volume Number | 290 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2015-09-25 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Cell Cycle Cell Differentiation Physiology Cyclin D Metabolism Extracellular Signal-Regulated MAP Kinases Muscle, Skeletal Cytology Nuclear Proteins Phosphatidate Phosphatase Animals Cyclin-Dependent Kinase 6 Mice Enzymology Myoblasts Organ Size Phosphorylation Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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