Regulation of P300 and HDAC1 on endoplasmic reticulum stress in isoniazid‐induced HL‐7702 hepatocyte injury. Issue 9 (20th February 2019)

• Record Type: Journal Article
• Authors: Li, Jin‐Feng; Li, Ying‐Shu; Zhang, Yi‐Yang; Sun, Shu‐Feng; Han, Tie‐Sheng; Li, Yu‐Hong; Feng, Fu‐Min
• Is Part Of: Journal of cellular physiology. Volume 234:Issue 9(2019:Sep.)
• Page Start: 15299
• Page End: 15307
• Publication Date: 2019-02-20
• Subjects: endoplasmic reticulum stress -- HDAC1 -- isoniazid‐induced HL‐7702 hepatocyte injury -- P300; Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.28175
• Languages: English
• ISSNs: 0021-9541

Abstract

Abstract: P300 and HDAC1 can be involved in the development of various liver diseases by regulating gene transcription. Endoplasmic reticulum stress (ERS) is one of the main pathways of apoptosis and is activated during inflammatory responses, but the roles of P300 and HDAC1 in ERS in antituberculosis drug‐induced liver injury (ADLI) are not clear. This study confirms that isoniazid can change the states of P300 and HDAC1 in HL‐7702 hepatocyte metabolism and induce ERS, causing hepatocyte injury and apoptosis. When combined with C646, however, P300 can be reduced. HL‐7702 cells were flattened, and the cytoplasm became crinkled. To a certain extent, ERS was relieved, but hepatocytes suffered worse damage, and the rate of cell apoptosis markedly increased. When MS‐275 was applied, HDAC1 level was increased, cell fusion appeared, and fluorescence intensity of endoplasmic reticulum was weakened. In addition, ERS was aggravated, but liver injury was relieved, and the apoptosis rate significantly decreased. Therefore, alteration of P300 and HDAC1 status and ERS are involved in ADLI, and changes in P300 and HDAC1 can regulate ERS and then affect cell damage. Abstract : In this work, we evaluated that the alteration of E1A binding protein p300 (P300) and histone deacetylase 1 (HDAC1) status and the occurrence of endoplasmic reticulum stress (ERS) are involved in antituberculosis drug‐induced liver injury (ADLI), and changes in P300 and HDAC1 level can regulate ERS and then affect cell damage.