Endoplasmic reticulum stress caused by traumatic injury promotes cardiomyocyte apoptosis through acetylation modification of GRP78
Cardiomyocyte apoptosis is an important cause of trauma-induced secondary cardiac injury (TISCI), in which the endoplasmic reticulum stress (ERS)-mediated apoptosis signaling pathway is known to be first activated, but the mechanism remains unclear. In this study, rat models of traumatic injury are...
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| Format: | Article |
| Language: | English |
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China Science Publishing & Media Ltd.
2023-12-01
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| Series: | Acta Biochimica et Biophysica Sinica |
| Subjects: | |
| Online Access: | https://www.sciengine.com/doi/10.3724/abbs.2023277 |
| _version_ | 1797347131555577856 |
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| author | Yan Zi Liu Yufeng Yang Bowen Zhao Wenhui Wang Yan Wang Deping Li Jianguo Jiao Xiangying Cao Jimin |
| author_facet | Yan Zi Liu Yufeng Yang Bowen Zhao Wenhui Wang Yan Wang Deping Li Jianguo Jiao Xiangying Cao Jimin |
| author_sort | Yan Zi |
| collection | DOAJ |
| description | Cardiomyocyte apoptosis is an important cause of trauma-induced secondary cardiac injury (TISCI), in which the endoplasmic reticulum stress (ERS)-mediated apoptosis signaling pathway is known to be first activated, but the mechanism remains unclear. In this study, rat models of traumatic injury are established by using the Noble-Collip trauma device. The expression of glucose-regulating protein 78 (GRP78, a molecular chaperone of the cardiomyocyte ER), acetylation modification of GRP78 and apoptosis of cardiomyocytes are determined. The results show that ERS-induced GRP78 elevation does not induce cardiomyocyte apoptosis in the early stage of trauma. However, with prolonged ERS, the GRP78 acetylation level is elevated, and the apoptosis of cardiomyocytes also increases significantly. In addition, in the early stage of trauma, the expression of histone acetyl-transferase (HAT) P300 is increased and that of histone deacetylase 6 (HDAC6) is decreased in cardiomyocytes. Inhibition of HDAC function could induce the apoptosis of traumatic cardiomyocytes by increasing the acetylation level of GRP78. Our present study demonstrates for the first time that post-traumatic protracted ERS can promote cardiomyocyte apoptosis by increasing the acetylation level of GRP78, which may provide an experimental basis for seeking early molecular events of TISCI. |
| first_indexed | 2024-03-08T11:43:14Z |
| format | Article |
| id | doaj.art-28f3679b5b7f48a3b9d46a0702103513 |
| institution | Directory Open Access Journal |
| issn | 1672-9145 |
| language | English |
| last_indexed | 2024-03-08T11:43:14Z |
| publishDate | 2023-12-01 |
| publisher | China Science Publishing & Media Ltd. |
| record_format | Article |
| series | Acta Biochimica et Biophysica Sinica |
| spelling | doaj.art-28f3679b5b7f48a3b9d46a07021035132024-01-25T01:50:24ZengChina Science Publishing & Media Ltd.Acta Biochimica et Biophysica Sinica1672-91452023-12-01569610510.3724/abbs.202327720d259ccEndoplasmic reticulum stress caused by traumatic injury promotes cardiomyocyte apoptosis through acetylation modification of GRP78Yan Zi0Liu Yufeng1Yang Bowen2Zhao Wenhui3Wang Yan4Wang Deping5Li Jianguo6Jiao Xiangying7Cao Jimin8["Department of Physiology, Shanxi Medical University, Taiyuan 030001, China","State Key Laboratory of Cellular Physiology, Shanxi Medical University, Taiyuan 030001, China"]["Department of Physiology, Shanxi Medical University, Taiyuan 030001, China"]["Department of Physiology, Shanxi Medical University, Taiyuan 030001, China"]["Department of Physiology, Shanxi Medical University, Taiyuan 030001, China"]["the First Clinical Medical College, Shanxi Medical University, Taiyuan 030001, China"]["Department of Physiology, Shanxi Medical University, Taiyuan 030001, China","State Key Laboratory of Cellular Physiology, Shanxi Medical University, Taiyuan 030001, China"]["Department of Physiology, Shanxi Medical University, Taiyuan 030001, China","State Key Laboratory of Cellular Physiology, Shanxi Medical University, Taiyuan 030001, China","Guangdong Province Key Laboratory of Psychiatric Disorders, Guangzhou 510515, China"]["Department of Physiology, Shanxi Medical University, Taiyuan 030001, China","State Key Laboratory of Cellular Physiology, Shanxi Medical University, Taiyuan 030001, China"]["Department of Physiology, Shanxi Medical University, Taiyuan 030001, China","State Key Laboratory of Cellular Physiology, Shanxi Medical University, Taiyuan 030001, China"]Cardiomyocyte apoptosis is an important cause of trauma-induced secondary cardiac injury (TISCI), in which the endoplasmic reticulum stress (ERS)-mediated apoptosis signaling pathway is known to be first activated, but the mechanism remains unclear. In this study, rat models of traumatic injury are established by using the Noble-Collip trauma device. The expression of glucose-regulating protein 78 (GRP78, a molecular chaperone of the cardiomyocyte ER), acetylation modification of GRP78 and apoptosis of cardiomyocytes are determined. The results show that ERS-induced GRP78 elevation does not induce cardiomyocyte apoptosis in the early stage of trauma. However, with prolonged ERS, the GRP78 acetylation level is elevated, and the apoptosis of cardiomyocytes also increases significantly. In addition, in the early stage of trauma, the expression of histone acetyl-transferase (HAT) P300 is increased and that of histone deacetylase 6 (HDAC6) is decreased in cardiomyocytes. Inhibition of HDAC function could induce the apoptosis of traumatic cardiomyocytes by increasing the acetylation level of GRP78. Our present study demonstrates for the first time that post-traumatic protracted ERS can promote cardiomyocyte apoptosis by increasing the acetylation level of GRP78, which may provide an experimental basis for seeking early molecular events of TISCI.https://www.sciengine.com/doi/10.3724/abbs.2023277acetylationapoptosiscardiomyocytesGRP78trauma |
| spellingShingle | Yan Zi Liu Yufeng Yang Bowen Zhao Wenhui Wang Yan Wang Deping Li Jianguo Jiao Xiangying Cao Jimin Endoplasmic reticulum stress caused by traumatic injury promotes cardiomyocyte apoptosis through acetylation modification of GRP78 Acta Biochimica et Biophysica Sinica acetylation apoptosis cardiomyocytes GRP78 trauma |
| title | Endoplasmic reticulum stress caused by traumatic injury promotes cardiomyocyte apoptosis through acetylation modification of GRP78 |
| title_full | Endoplasmic reticulum stress caused by traumatic injury promotes cardiomyocyte apoptosis through acetylation modification of GRP78 |
| title_fullStr | Endoplasmic reticulum stress caused by traumatic injury promotes cardiomyocyte apoptosis through acetylation modification of GRP78 |
| title_full_unstemmed | Endoplasmic reticulum stress caused by traumatic injury promotes cardiomyocyte apoptosis through acetylation modification of GRP78 |
| title_short | Endoplasmic reticulum stress caused by traumatic injury promotes cardiomyocyte apoptosis through acetylation modification of GRP78 |
| title_sort | endoplasmic reticulum stress caused by traumatic injury promotes cardiomyocyte apoptosis through acetylation modification of grp78 |
| topic | acetylation apoptosis cardiomyocytes GRP78 trauma |
| url | https://www.sciengine.com/doi/10.3724/abbs.2023277 |
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