Adiponectin modulates oxidative stress-induced mitophagy and protects C2C12 myoblasts against apoptosis
Abstract Adiponectin (APN), also known as apM1, Acrp30, GBP28 and adipoQ, is a circulating hormone that is predominantly produced by adipose tissue. Many pharmacological studies have demonstrated that this protein possesses potent anti-diabetic, anti-atherogenic and anti-inflammatory properties. Alt...
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Nature Portfolio
2017
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oai:doaj.org-article:3ede853f23c84c0bbf8571975760e2332021-12-02T12:32:40ZAdiponectin modulates oxidative stress-induced mitophagy and protects C2C12 myoblasts against apoptosis10.1038/s41598-017-03319-22045-2322https://doaj.org/article/3ede853f23c84c0bbf8571975760e2332017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-03319-2https://doaj.org/toc/2045-2322Abstract Adiponectin (APN), also known as apM1, Acrp30, GBP28 and adipoQ, is a circulating hormone that is predominantly produced by adipose tissue. Many pharmacological studies have demonstrated that this protein possesses potent anti-diabetic, anti-atherogenic and anti-inflammatory properties. Although several studies have demonstrated the antioxidative activity of this protein, the regulatory mechanisms have not yet been defined in skeletal muscles. The aim of the present study was to examine the cytoprotective effects of APN against damage induced by oxidative stress in mouse-derived C2C12 myoblasts. APN attenuated H2O2-induced growth inhibition and exhibited scavenging activity against intracellular reactive oxygen species that were induced by H2O2. Furthermore, treating C2C12 cells with APN significantly induced heme oxygenase-1 (HO-1) and nuclear factor-erythroid 2 related factor 2 (Nrf2). APN also suppressed H2O2-induced mitophagy and partially inhibited the colocalization of mitochondria with autophagosomes/lysosomes, correlating with the expression of Pink1 and Parkin and mtDNA. Moreover, APN protected C2C12 myoblasts against oxidative stress-induced apoptosis. Furthermore, APN significantly reduced the mRNA and protein expression levels of Bax. These data suggest that APN has a moderate regulatory role in oxidative stress-induced mitophagy and suppresses apoptosis. These findings demonstrate the antioxidant potential of APN in oxidative stress-associated skeletal muscle diseases.Yinghui RenYan LiJun YanMingkun MaDongmei ZhouZhenyi XueZimu ZhangHongkun LiuHuipeng YangLong JiaLijuan ZhangQi ZhangShuqin MuRongxin ZhangYurong DaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-12 (2017) |
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Medicine R Science Q Yinghui Ren Yan Li Jun Yan Mingkun Ma Dongmei Zhou Zhenyi Xue Zimu Zhang Hongkun Liu Huipeng Yang Long Jia Lijuan Zhang Qi Zhang Shuqin Mu Rongxin Zhang Yurong Da Adiponectin modulates oxidative stress-induced mitophagy and protects C2C12 myoblasts against apoptosis |
| description |
Abstract Adiponectin (APN), also known as apM1, Acrp30, GBP28 and adipoQ, is a circulating hormone that is predominantly produced by adipose tissue. Many pharmacological studies have demonstrated that this protein possesses potent anti-diabetic, anti-atherogenic and anti-inflammatory properties. Although several studies have demonstrated the antioxidative activity of this protein, the regulatory mechanisms have not yet been defined in skeletal muscles. The aim of the present study was to examine the cytoprotective effects of APN against damage induced by oxidative stress in mouse-derived C2C12 myoblasts. APN attenuated H2O2-induced growth inhibition and exhibited scavenging activity against intracellular reactive oxygen species that were induced by H2O2. Furthermore, treating C2C12 cells with APN significantly induced heme oxygenase-1 (HO-1) and nuclear factor-erythroid 2 related factor 2 (Nrf2). APN also suppressed H2O2-induced mitophagy and partially inhibited the colocalization of mitochondria with autophagosomes/lysosomes, correlating with the expression of Pink1 and Parkin and mtDNA. Moreover, APN protected C2C12 myoblasts against oxidative stress-induced apoptosis. Furthermore, APN significantly reduced the mRNA and protein expression levels of Bax. These data suggest that APN has a moderate regulatory role in oxidative stress-induced mitophagy and suppresses apoptosis. These findings demonstrate the antioxidant potential of APN in oxidative stress-associated skeletal muscle diseases. |
| format |
article |
| author |
Yinghui Ren Yan Li Jun Yan Mingkun Ma Dongmei Zhou Zhenyi Xue Zimu Zhang Hongkun Liu Huipeng Yang Long Jia Lijuan Zhang Qi Zhang Shuqin Mu Rongxin Zhang Yurong Da |
| author_facet |
Yinghui Ren Yan Li Jun Yan Mingkun Ma Dongmei Zhou Zhenyi Xue Zimu Zhang Hongkun Liu Huipeng Yang Long Jia Lijuan Zhang Qi Zhang Shuqin Mu Rongxin Zhang Yurong Da |
| author_sort |
Yinghui Ren |
| title |
Adiponectin modulates oxidative stress-induced mitophagy and protects C2C12 myoblasts against apoptosis |
| title_short |
Adiponectin modulates oxidative stress-induced mitophagy and protects C2C12 myoblasts against apoptosis |
| title_full |
Adiponectin modulates oxidative stress-induced mitophagy and protects C2C12 myoblasts against apoptosis |
| title_fullStr |
Adiponectin modulates oxidative stress-induced mitophagy and protects C2C12 myoblasts against apoptosis |
| title_full_unstemmed |
Adiponectin modulates oxidative stress-induced mitophagy and protects C2C12 myoblasts against apoptosis |
| title_sort |
adiponectin modulates oxidative stress-induced mitophagy and protects c2c12 myoblasts against apoptosis |
| publisher |
Nature Portfolio |
| publishDate |
2017 |
| url |
https://doaj.org/article/3ede853f23c84c0bbf8571975760e233 |
| work_keys_str_mv |
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