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Adiponectin ameliorates the apoptotic effects of paraquat on alveolar type Ⅱ cells via improvements in mitochondrial function.
Mol Med Rep. 2016 Jul; 14(1):746-52.MM

Abstract

Previous studies have demonstrated that excessive reactive oxygen/nitrogen species (ROS/RNS)‑induced apoptosis is an important feature of the injury to the lung epithelium in paraquat (PQ) poisoning. However the precise mechanisms of PQ‑induced dysfunction of the mitochondria, where ROS/RNS are predominantly produced, remain to be fully elucidated. Whether globular adiponectin (gAd), a potent molecule protective to mitochondria, regulates the mitochondrial function of alveolar type II cells to reduce PQ‑induced ROS/RNS production remains to be investigated. The current study aimed to investigate the precise mechanisms of PQ poisoning in the mitochondria of alveolar type II cells, and to elucidate the role of gAd in protecting against PQ‑induced lung epithelium injury. Therefore, lung epithelial injury was induced by PQ co‑culture of alveolar type II A549 cells for 24 h. gAd was administrated to and removed from the injured cells in after 24 h. PQ was observed to reduce cell viability and increase apoptosis by ~1.5 fold in A549 cells. The oxidative/nitrative stress, resulting from ROS/RNS and disordered mitochondrial function were evidenced by increased O2‑., NO production and reduced mitochondrial membrane potential (ΔΨ), adenosine 5'‑triphosphate (ATP) content in PQ‑poisoned A549 cells. gAd treatment significantly reversed the PQ‑induced cell injury and mitochondrial dysfunction in A549 cells. The protective effects of gAd were partly abrogated by an adenosine 5'‑monophosphate‑activated protein kinase (AMPK) inhibitor, compound C. The results suggest that reduced ΔΨ and ATP content may result in PQ‑induced mitochondrial dysfunction of the lung epithelium, which constitutes a novel mechanism for gAd exerting pulmonary protection against PQ poisoning via AMPK activation.

Authors+Show Affiliations

Emergency Medicine Department, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China.Emergency Medicine Department, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China.Emergency Medicine Department, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China.Emergency Medicine Department, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China.Emergency Medicine Department, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China.Emergency Medicine Department, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China.Emergency Medicine Department, Thomas Jefferson University Hospital, Philadelphia, PA 19107, USA.National Engineering Research Center for Biomaterials, Sichuan University, Chengdu, Sichuan 610064, P.R. China.Laboratory of Ethnopharmacology, Institute for Nanobiomedical Technology and Membrane Biology, Regenerative Medicine Research Center, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China.Emergency Medicine Department, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China.Emergency Medicine Department, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27220901

Citation

He, Yarong, et al. "Adiponectin Ameliorates the Apoptotic Effects of Paraquat On Alveolar Type Ⅱ Cells Via Improvements in Mitochondrial Function." Molecular Medicine Reports, vol. 14, no. 1, 2016, pp. 746-52.
He Y, Zou L, Zhou Y, et al. Adiponectin ameliorates the apoptotic effects of paraquat on alveolar type Ⅱ cells via improvements in mitochondrial function. Mol Med Rep. 2016;14(1):746-52.
He, Y., Zou, L., Zhou, Y., Hu, H., Yao, R., Jiang, Y., Lau, W. B., Yuan, T., Huang, W., Zeng, Z., & Cao, Y. (2016). Adiponectin ameliorates the apoptotic effects of paraquat on alveolar type Ⅱ cells via improvements in mitochondrial function. Molecular Medicine Reports, 14(1), 746-52. https://doi.org/10.3892/mmr.2016.5328
He Y, et al. Adiponectin Ameliorates the Apoptotic Effects of Paraquat On Alveolar Type Ⅱ Cells Via Improvements in Mitochondrial Function. Mol Med Rep. 2016;14(1):746-52. PubMed PMID: 27220901.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Adiponectin ameliorates the apoptotic effects of paraquat on alveolar type Ⅱ cells via improvements in mitochondrial function. AU - He,Yarong, AU - Zou,Liqun, AU - Zhou,Yaxiong, AU - Hu,Hai, AU - Yao,Rong, AU - Jiang,Yaowen, AU - Lau,Wayne Bond, AU - Yuan,Tun, AU - Huang,Wen, AU - Zeng,Zhi, AU - Cao,Yu, Y1 - 2016/05/23/ PY - 2015/06/11/received PY - 2016/04/19/accepted PY - 2016/5/26/entrez PY - 2016/5/26/pubmed PY - 2017/4/7/medline SP - 746 EP - 52 JF - Molecular medicine reports JO - Mol Med Rep VL - 14 IS - 1 N2 - Previous studies have demonstrated that excessive reactive oxygen/nitrogen species (ROS/RNS)‑induced apoptosis is an important feature of the injury to the lung epithelium in paraquat (PQ) poisoning. However the precise mechanisms of PQ‑induced dysfunction of the mitochondria, where ROS/RNS are predominantly produced, remain to be fully elucidated. Whether globular adiponectin (gAd), a potent molecule protective to mitochondria, regulates the mitochondrial function of alveolar type II cells to reduce PQ‑induced ROS/RNS production remains to be investigated. The current study aimed to investigate the precise mechanisms of PQ poisoning in the mitochondria of alveolar type II cells, and to elucidate the role of gAd in protecting against PQ‑induced lung epithelium injury. Therefore, lung epithelial injury was induced by PQ co‑culture of alveolar type II A549 cells for 24 h. gAd was administrated to and removed from the injured cells in after 24 h. PQ was observed to reduce cell viability and increase apoptosis by ~1.5 fold in A549 cells. The oxidative/nitrative stress, resulting from ROS/RNS and disordered mitochondrial function were evidenced by increased O2‑., NO production and reduced mitochondrial membrane potential (ΔΨ), adenosine 5'‑triphosphate (ATP) content in PQ‑poisoned A549 cells. gAd treatment significantly reversed the PQ‑induced cell injury and mitochondrial dysfunction in A549 cells. The protective effects of gAd were partly abrogated by an adenosine 5'‑monophosphate‑activated protein kinase (AMPK) inhibitor, compound C. The results suggest that reduced ΔΨ and ATP content may result in PQ‑induced mitochondrial dysfunction of the lung epithelium, which constitutes a novel mechanism for gAd exerting pulmonary protection against PQ poisoning via AMPK activation. SN - 1791-3004 UR - https://www.unboundmedicine.com/medline/citation/27220901/Adiponectin_ameliorates_the_apoptotic_effects_of_paraquat_on_alveolar_type_Ⅱ_cells_via_improvements_in_mitochondrial_function_ L2 - http://www.spandidos-publications.com/mmr/14/1/746 DB - PRIME DP - Unbound Medicine ER -