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Effect of Heme Oxygenase-1 on Mitofusin-1 protein in LPS-induced ALI/ARDS in rats.

Authors: Yu, Jianbo  Wang, Ying  Li, Zhen  Dong, Shuan  Wang, Dan  Gong, Lirong  Shi, Jia  Zhang, Yuan  Liu, Daquan  Mu, Rui 
Citation: Yu J, etal., Sci Rep. 2016 Nov 10;6:36530. doi: 10.1038/srep36530.
Pubmed: (View Article at PubMed) PMID:27830717
DOI: Full-text: DOI:10.1038/srep36530

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a common and important oxidative stress in the lung. Mitochondrial fusion responds to the normal morphology and function of cells and is finely regulated by mitochondrial fusion proteins, such as mitofusin-1 protein (Mfn1), mitofusin-2 protein (Mfn2) and optical atrophy 1 (OPA1). Additionally, Mfn1 has been identified as the most important protein in mitochondrial fusion. Heme oxygenase-1 (HO-1) is a stress-inducible protein that plays a critical role in protecting against oxidative stress. However, whether the protection of HO-1 is related to mitochondrial fusion is still a question. Thus, our in vitro and in vivo experiments aimed to identify the relationship between HO-1 and Mfn1. Here, we used Hemin and ZnPP-IX as treatments in an in vivo experiment. Then, HO-1 and Mfn1 were measured using RT-PCR and Western blotting. Supernatants were analyzed for MDA, SOD, and ROS. Our results implied that HO-1 upregulation suppressed oxidative stress induced by LPS, and the possible mechanism could be associated with Mfn1 and the PI3K/Akt pathway.

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RGD Object Information
RGD ID: 12910765
Created: 2017-06-23
Species: All species
Last Modified: 2017-06-23
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.