DRAM1 increases the secretion of PKM2-enriched EVs from hepatocytes to promote macrophage activation and disease progression in ALD
DNA damage-regulated autophagy modulator 1 (DRAM1) could play important roles in inflammation and hepatic apoptosis, while its roles in alcohol-related liver disease (ALD), which is characterized by hepatic inflammation and apoptosis, are still unclear. In this study, we explored the expression, rol...
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Published in | Molecular therapy. Nucleic acids Vol. 27; pp. 375 - 389 |
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Main Authors | , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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United States
Elsevier Inc
08.03.2022
American Society of Gene & Cell Therapy Elsevier |
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Abstract | DNA damage-regulated autophagy modulator 1 (DRAM1) could play important roles in inflammation and hepatic apoptosis, while its roles in alcohol-related liver disease (ALD), which is characterized by hepatic inflammation and apoptosis, are still unclear. In this study, we explored the expression, role, and mechanism of DRAM1 in ALD. Firstly, our results showed that DRAM1 was significantly increased in liver tissues of mice at the early stage of alcohol treatment. In addition, DRAM1 knockout reduced, and liver-specific overexpression of DRAM1 aggravated, alcohol-induced hepatic steatosis, injury, and expressions of M1 macrophage markers in mice. Furthermore, ethanol-induced DRAM1 of hepatic cells increased pyruvate kinase M2 (PKM2)-enriched extracellular vesicles (EVs), and ectosomes derived from hepatic cells with DRAM1 overexpression promoted macrophage activation. Mechanistic investigations showed that DRAM1 interacted with PKM2 and increased the PKM2 level in plasma membrane. At last, DRAM1 was significantly increased in liver tissues of ALD patients, and it was positively correlated with M1 macrophage markers. Taken together, this study revealed that ethanol-induced DRAM1 of hepatic cells could increase the PKM2-enriched EVs, promote macrophage activation, and aggravate the disease progression of ALD. These findings suggested that DRAM1 might be a potentially promising target for the therapy of ALD.
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In this study, ethanol-induced DRAM1 could increase the level of PKM2 in extracellular vesicles released from hepatic cells, promote macrophage activation, and aggravate the progression of alcohol-related liver disease (ALD). These suggested that DRAM1 might be a potential target for the treatment of patients with ALD. |
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AbstractList | DNA damage-regulated autophagy modulator 1 (DRAM1) could play important roles in inflammation and hepatic apoptosis, while its roles in alcohol-related liver disease (ALD), which is characterized by hepatic inflammation and apoptosis, are still unclear. In this study, we explored the expression, role, and mechanism of DRAM1 in ALD. Firstly, our results showed that DRAM1 was significantly increased in liver tissues of mice at the early stage of alcohol treatment. In addition, DRAM1 knockout reduced, and liver-specific overexpression of DRAM1 aggravated, alcohol-induced hepatic steatosis, injury, and expressions of M1 macrophage markers in mice. Furthermore, ethanol-induced DRAM1 of hepatic cells increased pyruvate kinase M2 (PKM2)-enriched extracellular vesicles (EVs), and ectosomes derived from hepatic cells with DRAM1 overexpression promoted macrophage activation. Mechanistic investigations showed that DRAM1 interacted with PKM2 and increased the PKM2 level in plasma membrane. At last, DRAM1 was significantly increased in liver tissues of ALD patients, and it was positively correlated with M1 macrophage markers. Taken together, this study revealed that ethanol-induced DRAM1 of hepatic cells could increase the PKM2-enriched EVs, promote macrophage activation, and aggravate the disease progression of ALD. These findings suggested that DRAM1 might be a potentially promising target for the therapy of ALD. DNA damage-regulated autophagy modulator 1 (DRAM1) could play important roles in inflammation and hepatic apoptosis, while its roles in alcohol-related liver disease (ALD), which is characterized by hepatic inflammation and apoptosis, are still unclear. In this study, we explored the expression, role, and mechanism of DRAM1 in ALD. Firstly, our results showed that DRAM1 was significantly increased in liver tissues of mice at the early stage of alcohol treatment. In addition, DRAM1 knockout reduced, and liver-specific overexpression of DRAM1 aggravated, alcohol-induced hepatic steatosis, injury, and expressions of M1 macrophage markers in mice. Furthermore, ethanol-induced DRAM1 of hepatic cells increased pyruvate kinase M2 (PKM2)-enriched extracellular vesicles (EVs), and ectosomes derived from hepatic cells with DRAM1 overexpression promoted macrophage activation. Mechanistic investigations showed that DRAM1 interacted with PKM2 and increased the PKM2 level in plasma membrane. At last, DRAM1 was significantly increased in liver tissues of ALD patients, and it was positively correlated with M1 macrophage markers. Taken together, this study revealed that ethanol-induced DRAM1 of hepatic cells could increase the PKM2-enriched EVs, promote macrophage activation, and aggravate the disease progression of ALD. These findings suggested that DRAM1 might be a potentially promising target for the therapy of ALD. [Display omitted] In this study, ethanol-induced DRAM1 could increase the level of PKM2 in extracellular vesicles released from hepatic cells, promote macrophage activation, and aggravate the progression of alcohol-related liver disease (ALD). These suggested that DRAM1 might be a potential target for the treatment of patients with ALD. DNA damage-regulated autophagy modulator 1 (DRAM1) could play important roles in inflammation and hepatic apoptosis, while its roles in alcohol-related liver disease (ALD), which is characterized by hepatic inflammation and apoptosis, are still unclear. In this study, we explored the expression, role, and mechanism of DRAM1 in ALD. Firstly, our results showed that DRAM1 was significantly increased in liver tissues of mice at the early stage of alcohol treatment. In addition, DRAM1 knockout reduced, and liver-specific overexpression of DRAM1 aggravated, alcohol-induced hepatic steatosis, injury, and expressions of M1 macrophage markers in mice. Furthermore, ethanol-induced DRAM1 of hepatic cells increased pyruvate kinase M2 (PKM2)-enriched extracellular vesicles (EVs), and ectosomes derived from hepatic cells with DRAM1 overexpression promoted macrophage activation. Mechanistic investigations showed that DRAM1 interacted with PKM2 and increased the PKM2 level in plasma membrane. At last, DRAM1 was significantly increased in liver tissues of ALD patients, and it was positively correlated with M1 macrophage markers. Taken together, this study revealed that ethanol-induced DRAM1 of hepatic cells could increase the PKM2-enriched EVs, promote macrophage activation, and aggravate the disease progression of ALD. These findings suggested that DRAM1 might be a potentially promising target for the therapy of ALD. In this study, ethanol-induced DRAM1 could increase the level of PKM2 in extracellular vesicles released from hepatic cells, promote macrophage activation, and aggravate the progression of alcohol-related liver disease (ALD). These suggested that DRAM1 might be a potential target for the treatment of patients with ALD. |
Author | Chen, Lizhen Wang, Mengke Zhuang, Likun Sun, Baokai Ma, Xuefeng Dong, Mengzhen Liu, Kai Liu, Shousheng Zhao, Zhenzhen Jin, Wenwen Wang, Yifen Zhang, Jie Xin, Yongning Tan, Jie |
Author_xml | – sequence: 1 givenname: Jie surname: Tan fullname: Tan, Jie organization: Department of Infectious Diseases, Qingdao Municipal Hospital, Qingdao University, Qingdao 266011, China – sequence: 2 givenname: Jie surname: Zhang fullname: Zhang, Jie organization: Department of Infectious Diseases, Qingdao Municipal Hospital, Qingdao University, Qingdao 266011, China – sequence: 3 givenname: Mengke surname: Wang fullname: Wang, Mengke organization: Department of Infectious Diseases, Qingdao Municipal Hospital, Qingdao University, Qingdao 266011, China – sequence: 4 givenname: Yifen surname: Wang fullname: Wang, Yifen organization: Department of Infectious Diseases, Qingdao Municipal Hospital, Qingdao University, Qingdao 266011, China – sequence: 5 givenname: Mengzhen surname: Dong fullname: Dong, Mengzhen organization: Department of Infectious Diseases, Qingdao Municipal Hospital, Qingdao University, Qingdao 266011, China – sequence: 6 givenname: Xuefeng surname: Ma fullname: Ma, Xuefeng organization: Department of Infectious Diseases, Qingdao Municipal Hospital, Qingdao University, Qingdao 266011, China – sequence: 7 givenname: Baokai surname: Sun fullname: Sun, Baokai organization: Department of Infectious Diseases, Qingdao Municipal Hospital, Qingdao University, Qingdao 266011, China – sequence: 8 givenname: Shousheng surname: Liu fullname: Liu, Shousheng organization: Clinical Research Center, Qingdao Municipal Hospital, Qingdao University, Qingdao 266071, China – sequence: 9 givenname: Zhenzhen surname: Zhao fullname: Zhao, Zhenzhen organization: Clinical Research Center, Qingdao Municipal Hospital, Qingdao University, Qingdao 266071, China – sequence: 10 givenname: Lizhen surname: Chen fullname: Chen, Lizhen organization: Department of Infectious Diseases, Qingdao Municipal Hospital, Qingdao University, Qingdao 266011, China – sequence: 11 givenname: Wenwen surname: Jin fullname: Jin, Wenwen organization: Department of Infectious Diseases, Qingdao Municipal Hospital, Qingdao University, Qingdao 266011, China – sequence: 12 givenname: Kai surname: Liu fullname: Liu, Kai organization: Beijing Institute of Hepatology, Beijing Youan Hospital, Capital Medical University, Beijing 100069, China – sequence: 13 givenname: Yongning surname: Xin fullname: Xin, Yongning email: xinyongning9812@163.com organization: Department of Infectious Diseases, Qingdao Municipal Hospital, Qingdao University, Qingdao 266011, China – sequence: 14 givenname: Likun orcidid: 0000-0003-3002-2406 surname: Zhuang fullname: Zhuang, Likun email: zlk0823@163.com organization: Clinical Research Center, Qingdao Municipal Hospital, Qingdao University, Qingdao 266071, China |
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Keywords | Extracellular vesicles Macrophage activation DRAM1 PKM2 Alcohol-related liver disease |
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Title | DRAM1 increases the secretion of PKM2-enriched EVs from hepatocytes to promote macrophage activation and disease progression in ALD |
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