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Salicylates promote mitochondrial biogenesis by regulating the expression of PGC-1α in murine 3T3-L1 pre-adipocytes.
Biochem Biophys Res Commun. 2017 09 16; 491(2):436-441.BB

Abstract

Mitochondrial dysfunction has been associated with insulin resistance and diabetes. Decreased mitochondrial density and mitochondrial copy numbers have been found in insulin-resistant individuals. Restoration of the number of mitochondria and normal mitochondrial function has become an important therapeutic target of diabetes. Salicylate, the main active ingredient in aspirin, has been in medicinal use since ancient times. Little information regarding the effects of salicylate on mitochondrial function has been reported. In this study, we assessed the effects of salicylate on the peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) signaling pathway and mitochondrial biogenesis in pre-adipocytes. Our findings demonstrate that treatment with salicylate promoted the expression of PGC-1α and its downstream targets nuclear respiratory factor 1 (NRF1) and mitochondrial transcription factor A (TFAM). Importantly, salicylate treatment significantly increased the number of mDNA, citrate synthase activity, expression of respiratory chain complex I, and mitochondrial mass, which were suppressed by the specific AMPK inhibitor Compound C. Indeed, salicylate treatment induced the phosphorylation of AMPK, which was involved in the induction of PGC-1α, NRF1, and TFAM. Importantly, inhibition of PGC-1α expression using PGC-1α small RNA interference abolished the effects of salicylate on mitochondrial biogenesis. These results suggest that salicylate has a potential therapeutic capacity against mitochondrial dysfunction in diabetes.

Authors+Show Affiliations

Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, Hubei Province, China.Department of Obstetrics and Gynecology, Xiaogan Central Hospital Affiliated to Wuhan University of Science and Technology, Xiaogan 432000, Hubei Province, China.Department of Endocrinology, Xiaogan Central Hospital Affiliated to Wuhan University of Science and Technology, Xiaogan, 432000, Hubei Province, China.Department of Endocrinology, Xiaogan Central Hospital Affiliated to Wuhan University of Science and Technology, Xiaogan, 432000, Hubei Province, China.Department of Cardiovascular, Xiaogan Central Hospital Affiliated to Wuhan University of Science and Technology, Xiaogan, 432000, Hubei Province, China.Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, Hubei Province, China. Electronic address: xuyc066@yeah.net.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28712868

Citation

Yan, Yimin, et al. "Salicylates Promote Mitochondrial Biogenesis By Regulating the Expression of PGC-1α in Murine 3T3-L1 Pre-adipocytes." Biochemical and Biophysical Research Communications, vol. 491, no. 2, 2017, pp. 436-441.
Yan Y, Yang X, Zhao T, et al. Salicylates promote mitochondrial biogenesis by regulating the expression of PGC-1α in murine 3T3-L1 pre-adipocytes. Biochem Biophys Res Commun. 2017;491(2):436-441.
Yan, Y., Yang, X., Zhao, T., Zou, Y., Li, R., & Xu, Y. (2017). Salicylates promote mitochondrial biogenesis by regulating the expression of PGC-1α in murine 3T3-L1 pre-adipocytes. Biochemical and Biophysical Research Communications, 491(2), 436-441. https://doi.org/10.1016/j.bbrc.2017.07.074
Yan Y, et al. Salicylates Promote Mitochondrial Biogenesis By Regulating the Expression of PGC-1α in Murine 3T3-L1 Pre-adipocytes. Biochem Biophys Res Commun. 2017 09 16;491(2):436-441. PubMed PMID: 28712868.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Salicylates promote mitochondrial biogenesis by regulating the expression of PGC-1α in murine 3T3-L1 pre-adipocytes. AU - Yan,Yimin, AU - Yang,Xiaohong, AU - Zhao,Tao, AU - Zou,Yi, AU - Li,Rui, AU - Xu,Yancheng, Y1 - 2017/07/13/ PY - 2017/07/08/received PY - 2017/07/13/accepted PY - 2017/7/18/pubmed PY - 2017/8/30/medline PY - 2017/7/18/entrez KW - Diabetes KW - Mitochondria biogenesis KW - PGC-1α KW - Salicylate KW - mtDNA SP - 436 EP - 441 JF - Biochemical and biophysical research communications JO - Biochem. Biophys. Res. Commun. VL - 491 IS - 2 N2 - Mitochondrial dysfunction has been associated with insulin resistance and diabetes. Decreased mitochondrial density and mitochondrial copy numbers have been found in insulin-resistant individuals. Restoration of the number of mitochondria and normal mitochondrial function has become an important therapeutic target of diabetes. Salicylate, the main active ingredient in aspirin, has been in medicinal use since ancient times. Little information regarding the effects of salicylate on mitochondrial function has been reported. In this study, we assessed the effects of salicylate on the peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) signaling pathway and mitochondrial biogenesis in pre-adipocytes. Our findings demonstrate that treatment with salicylate promoted the expression of PGC-1α and its downstream targets nuclear respiratory factor 1 (NRF1) and mitochondrial transcription factor A (TFAM). Importantly, salicylate treatment significantly increased the number of mDNA, citrate synthase activity, expression of respiratory chain complex I, and mitochondrial mass, which were suppressed by the specific AMPK inhibitor Compound C. Indeed, salicylate treatment induced the phosphorylation of AMPK, which was involved in the induction of PGC-1α, NRF1, and TFAM. Importantly, inhibition of PGC-1α expression using PGC-1α small RNA interference abolished the effects of salicylate on mitochondrial biogenesis. These results suggest that salicylate has a potential therapeutic capacity against mitochondrial dysfunction in diabetes. SN - 1090-2104 UR - https://www.unboundmedicine.com/medline/citation/28712868/Salicylates_promote_mitochondrial_biogenesis_by_regulating_the_expression_of_PGC_1α_in_murine_3T3_L1_pre_adipocytes_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-291X(17)31424-9 DB - PRIME DP - Unbound Medicine ER -