Retinoic Acid Leads to Cytoskeletal Rearrangement through AMPK-Rac1 and Stimulates Glucose Uptake through AMPK-p38 MAPK in Skeletal Muscle Cells
SCIE
SCOPUS
- Title
- Retinoic Acid Leads to Cytoskeletal Rearrangement through AMPK-Rac1 and Stimulates Glucose Uptake through AMPK-p38 MAPK in Skeletal Muscle Cells
- Authors
- Lee, YM; Lee, JO; Jung, JH; Kim, JH; Park, SH; Park, JM; Kim, EK; Suh, PG; Kim, HS
- Date Issued
- 2008-12-05
- Publisher
- AMER SOC BIOCHEMISTRY MOLECULAR BIOLO
- Abstract
- Retinoic acid (RA) is one of the major components of vitamin A. In the present study, we found that retinoic acid activated AMP-activated protein kinase (AMPK). RA induced Rac1-GTP formation and phosphorylation of its downstream target, p21-activated kinase (PAK), whereas the inhibition of AMPK blocked RA-induced Rac1 activation. Moreover, cofilin, an actin polymerization regulator, was activated when incubated with RA. We then showed that inhibition of AMPK by compound C, a selective inhibitor of AMPK, or small interfering RNA of AMPK alpha 1 blocked RA-induced cofilin phosphorylation. Additionally, we found that retinoic acid-stimulated glucose uptake in differentiated C2C12 myoblast cells and activated p38 mitogen-activated protein kinase (MAPK). Finally, the inhibition of AMPK and p38 MAPK blocked retinoic acid-induced glucose uptake. In summary, our results suggest that retinoic acid may have cytoskeletal roles in skeletal muscle cells via stimulation of the AMPK-Rac1-PAK-cofillin pathway and may also have beneficial roles in glucose metabolism via stimulation of the AMPK-p38 MAPK pathway.
- Keywords
- ACTIVATED PROTEIN-KINASE; GROWTH-INHIBITION; CANCER CELLS; FATTY-ACID; ACTIN; EXPRESSION; MOTILITY; DIFFERENTIATION; PATHWAY; CA2+
- URI
- https://oasis.postech.ac.kr/handle/2014.oak/22377
- DOI
- 10.1074/JBC.M8044692
- ISSN
- 0021-9258
- Article Type
- Article
- Citation
- JOURNAL OF BIOLOGICAL CHEMISTRY, vol. 283, no. 49, page. 33969 - 33974, 2008-12-05
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