Hsp22 ameliorates lipopolysaccharide-induced myocardial injury by inhibiting inflammation, oxidative stress, and apoptosis
Sepsis-induced myocardial dysfunction (SIMD) is ubiquitous in septic shock patients and is associated with high morbidity and mortality rates. Heat shock protein 22 (Hsp22), which belongs to the small HSP family of proteins, is involved in several biological functions. However, the function of Hsp22...
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Taylor & Francis Group
2021
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oai:doaj.org-article:600ddc6ca74c4cc5a83a08b710a1f0e62021-12-01T14:41:00ZHsp22 ameliorates lipopolysaccharide-induced myocardial injury by inhibiting inflammation, oxidative stress, and apoptosis2165-59792165-598710.1080/21655979.2021.2010315https://doaj.org/article/600ddc6ca74c4cc5a83a08b710a1f0e62021-11-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.2010315https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987Sepsis-induced myocardial dysfunction (SIMD) is ubiquitous in septic shock patients and is associated with high morbidity and mortality rates. Heat shock protein 22 (Hsp22), which belongs to the small HSP family of proteins, is involved in several biological functions. However, the function of Hsp22 in lipopolysaccharide (LPS)-induced myocardial injury is not yet established. This study was aimed at investigating the underlying mechanistic aspects of Hsp22 in myocardial injury induced by LPS. In this study, following the random assignment of male C57BL/6 mice into control, LPS-treated, and LPS + Hsp22 treated groups, relevant echocardiograms and staining were performed to scrutinise the cardiac pathology. Plausible mechanisms were proposed based on the findings of the enzyme-linked immunosorbent assay and western blotting assay. A protective role of Hsp22 against LPS-induced myocardial injury emerged, as evidenced from decreased levels of creatinine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and enhanced cardiac function. The post-LPS administration-caused spike in inflammatory cytokines (IL-1β, IL-6, TNF-α and NLRP3) was attenuated by the Hsp22 pre-treatment. In addition, superoxide dismutase (SOD) activity and B-cell lymphoma-2 (Bcl2) levels were augmented by Hsp22 treatment resulting in lowering of LPS-induced oxidative stress and cardiomyocyte apoptosis. In summary, the suppression of LPS-induced myocardial injury by Hsp22 overexpression via targeting of inflammation, oxidative stress, and apoptosis in cardiomyocytes paves the way for this protein to be employed in the therapy of SIMD.Yun YuLong-long HuLiang LiuLing-ling YuJun-pei LiJing-an RaoLing-juan ZhuHui-hui BaoXiao-shu ChengTaylor & Francis Grouparticlesepsis-induced myocardial dysfunctionheat shock protein 22lipopolysaccharideinflammatoryoxidative stressapoptosisBiotechnologyTP248.13-248.65ENBioengineered, Vol 0, Iss 0 (2021) |
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DOAJ |
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DOAJ |
| language |
EN |
| topic |
sepsis-induced myocardial dysfunction heat shock protein 22 lipopolysaccharide inflammatory oxidative stress apoptosis Biotechnology TP248.13-248.65 |
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sepsis-induced myocardial dysfunction heat shock protein 22 lipopolysaccharide inflammatory oxidative stress apoptosis Biotechnology TP248.13-248.65 Yun Yu Long-long Hu Liang Liu Ling-ling Yu Jun-pei Li Jing-an Rao Ling-juan Zhu Hui-hui Bao Xiao-shu Cheng Hsp22 ameliorates lipopolysaccharide-induced myocardial injury by inhibiting inflammation, oxidative stress, and apoptosis |
| description |
Sepsis-induced myocardial dysfunction (SIMD) is ubiquitous in septic shock patients and is associated with high morbidity and mortality rates. Heat shock protein 22 (Hsp22), which belongs to the small HSP family of proteins, is involved in several biological functions. However, the function of Hsp22 in lipopolysaccharide (LPS)-induced myocardial injury is not yet established. This study was aimed at investigating the underlying mechanistic aspects of Hsp22 in myocardial injury induced by LPS. In this study, following the random assignment of male C57BL/6 mice into control, LPS-treated, and LPS + Hsp22 treated groups, relevant echocardiograms and staining were performed to scrutinise the cardiac pathology. Plausible mechanisms were proposed based on the findings of the enzyme-linked immunosorbent assay and western blotting assay. A protective role of Hsp22 against LPS-induced myocardial injury emerged, as evidenced from decreased levels of creatinine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and enhanced cardiac function. The post-LPS administration-caused spike in inflammatory cytokines (IL-1β, IL-6, TNF-α and NLRP3) was attenuated by the Hsp22 pre-treatment. In addition, superoxide dismutase (SOD) activity and B-cell lymphoma-2 (Bcl2) levels were augmented by Hsp22 treatment resulting in lowering of LPS-induced oxidative stress and cardiomyocyte apoptosis. In summary, the suppression of LPS-induced myocardial injury by Hsp22 overexpression via targeting of inflammation, oxidative stress, and apoptosis in cardiomyocytes paves the way for this protein to be employed in the therapy of SIMD. |
| format |
article |
| author |
Yun Yu Long-long Hu Liang Liu Ling-ling Yu Jun-pei Li Jing-an Rao Ling-juan Zhu Hui-hui Bao Xiao-shu Cheng |
| author_facet |
Yun Yu Long-long Hu Liang Liu Ling-ling Yu Jun-pei Li Jing-an Rao Ling-juan Zhu Hui-hui Bao Xiao-shu Cheng |
| author_sort |
Yun Yu |
| title |
Hsp22 ameliorates lipopolysaccharide-induced myocardial injury by inhibiting inflammation, oxidative stress, and apoptosis |
| title_short |
Hsp22 ameliorates lipopolysaccharide-induced myocardial injury by inhibiting inflammation, oxidative stress, and apoptosis |
| title_full |
Hsp22 ameliorates lipopolysaccharide-induced myocardial injury by inhibiting inflammation, oxidative stress, and apoptosis |
| title_fullStr |
Hsp22 ameliorates lipopolysaccharide-induced myocardial injury by inhibiting inflammation, oxidative stress, and apoptosis |
| title_full_unstemmed |
Hsp22 ameliorates lipopolysaccharide-induced myocardial injury by inhibiting inflammation, oxidative stress, and apoptosis |
| title_sort |
hsp22 ameliorates lipopolysaccharide-induced myocardial injury by inhibiting inflammation, oxidative stress, and apoptosis |
| publisher |
Taylor & Francis Group |
| publishDate |
2021 |
| url |
https://doaj.org/article/600ddc6ca74c4cc5a83a08b710a1f0e6 |
| work_keys_str_mv |
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| _version_ |
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