Hydrogen Sulfide Protects Human Cardiac Fibroblasts Against HO-induced Injury Through Regulating Autophagy-Related Proteins
Autophagy, an intracellular bulk degradation process of proteins and organelles, can be induced by myocardial ischemia in the heart. However, the causative role of autophagy in the survival of human cardiac fibroblasts and the underlying mechanisms are incompletely understood. Oxidative stress can i...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
SAGE Publishing
2018-08-01
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| Series: | Cell Transplantation |
| Online Access: | https://doi.org/10.1177/0963689718779361 |
| _version_ | 1819100121760006144 |
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| author | Ao Feng Chen Ling Lin Xin-duo Wu Bing Wu San-wu Zhan Yu Huang Yu-lan Zhang You-en |
| author_facet | Ao Feng Chen Ling Lin Xin-duo Wu Bing Wu San-wu Zhan Yu Huang Yu-lan Zhang You-en |
| author_sort | Ao Feng |
| collection | DOAJ |
| description | Autophagy, an intracellular bulk degradation process of proteins and organelles, can be induced by myocardial ischemia in the heart. However, the causative role of autophagy in the survival of human cardiac fibroblasts and the underlying mechanisms are incompletely understood. Oxidative stress can induce autophagy in cultured cells upon hydrogen peroxide (H 2 O 2 ) exposure. Because hydrogen sulfide (H 2 S) regulates reactive oxygen species (ROS) and apoptosis, we hypothesize that H 2 S may have a cardioprotective function. To examine our hypothesis, we investigated the regulation of autophagy by the H 2 S donor sodium hydrosulfide (NaHS), using a cell model of human cardiac fibroblasts from adult ventricles (HCF-av) that suffered from endoplasmic reticulum (ER) stress by H 2 O 2 . In the present study, we found that the apoptosis and autophagy were induced along with ER stress by H 2 O 2 in the primary cultured HCF-av cells. In contrast, H 2 S suppressed HCF-av cell apoptosis and autophagic flux, in part directly by inhibiting ROS production and preserving mitochondrial functions. |
| first_indexed | 2024-12-22T00:57:45Z |
| format | Article |
| id | doaj.art-925b8267ffb545c4a42bf5b0ddcf6c54 |
| institution | Directory Open Access Journal |
| issn | 0963-6897 1555-3892 |
| language | English |
| last_indexed | 2024-12-22T00:57:45Z |
| publishDate | 2018-08-01 |
| publisher | SAGE Publishing |
| record_format | Article |
| series | Cell Transplantation |
| spelling | doaj.art-925b8267ffb545c4a42bf5b0ddcf6c542022-12-21T18:44:17ZengSAGE PublishingCell Transplantation0963-68971555-38922018-08-012710.1177/0963689718779361Hydrogen Sulfide Protects Human Cardiac Fibroblasts Against HO-induced Injury Through Regulating Autophagy-Related ProteinsAo Feng0Chen Ling1Lin Xin-duo2Wu Bing3Wu San-wu4Zhan Yu5Huang Yu-lan6Zhang You-en7 Department of Medical Imaging Center, Renmin Hospital, Hubei University of Medicine, Shiyan, China Department of Cardiology, Jinzhou Medical University, Shiyan, China Department of Cardiology, Renmin Hospital, Hubei University of Medicine, Shiyan, China Department of Cardiology, Renmin Hospital, Hubei University of Medicine, Shiyan, China Department of Cardiology, Renmin Hospital, Hubei University of Medicine, Shiyan, China Department of Cardiology, Renmin Hospital, Hubei University of Medicine, Shiyan, China Department of Cardiology, Renmin Hospital, Hubei University of Medicine, Shiyan, China Department of Cardiology, Renmin Hospital, Hubei University of Medicine, Shiyan, ChinaAutophagy, an intracellular bulk degradation process of proteins and organelles, can be induced by myocardial ischemia in the heart. However, the causative role of autophagy in the survival of human cardiac fibroblasts and the underlying mechanisms are incompletely understood. Oxidative stress can induce autophagy in cultured cells upon hydrogen peroxide (H 2 O 2 ) exposure. Because hydrogen sulfide (H 2 S) regulates reactive oxygen species (ROS) and apoptosis, we hypothesize that H 2 S may have a cardioprotective function. To examine our hypothesis, we investigated the regulation of autophagy by the H 2 S donor sodium hydrosulfide (NaHS), using a cell model of human cardiac fibroblasts from adult ventricles (HCF-av) that suffered from endoplasmic reticulum (ER) stress by H 2 O 2 . In the present study, we found that the apoptosis and autophagy were induced along with ER stress by H 2 O 2 in the primary cultured HCF-av cells. In contrast, H 2 S suppressed HCF-av cell apoptosis and autophagic flux, in part directly by inhibiting ROS production and preserving mitochondrial functions.https://doi.org/10.1177/0963689718779361 |
| spellingShingle | Ao Feng Chen Ling Lin Xin-duo Wu Bing Wu San-wu Zhan Yu Huang Yu-lan Zhang You-en Hydrogen Sulfide Protects Human Cardiac Fibroblasts Against HO-induced Injury Through Regulating Autophagy-Related Proteins Cell Transplantation |
| title | Hydrogen Sulfide Protects Human Cardiac Fibroblasts Against HO-induced Injury Through Regulating Autophagy-Related Proteins |
| title_full | Hydrogen Sulfide Protects Human Cardiac Fibroblasts Against HO-induced Injury Through Regulating Autophagy-Related Proteins |
| title_fullStr | Hydrogen Sulfide Protects Human Cardiac Fibroblasts Against HO-induced Injury Through Regulating Autophagy-Related Proteins |
| title_full_unstemmed | Hydrogen Sulfide Protects Human Cardiac Fibroblasts Against HO-induced Injury Through Regulating Autophagy-Related Proteins |
| title_short | Hydrogen Sulfide Protects Human Cardiac Fibroblasts Against HO-induced Injury Through Regulating Autophagy-Related Proteins |
| title_sort | hydrogen sulfide protects human cardiac fibroblasts against ho induced injury through regulating autophagy related proteins |
| url | https://doi.org/10.1177/0963689718779361 |
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