CaMK II Inhibition Attenuates ROS Dependent Necroptosis in Acinar Cells and Protects against Acute Pancreatitis in Mice

As a calcium-regulated protein, CaMK II is closely related to cell death, and it participates in the development of pathological processes such as reperfusion injury, myocardial infarction, and oligodendrocyte death. The function of CaMK II activation in acute pancreatitis (AP) remains unclear. In o...

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Autores principales:	Qingtian Zhu, Lu Hao, Qinhao Shen, Jiajia Pan, Weili Liu, Weijuan Gong, Lianghao Hu, Weiming Xiao, Mei Wang, Xinnong Liu, Yanbing Ding, Guotao Lu
Formato:	article
Lenguaje:	EN
Publicado:	Hindawi Limited 2021
Materias:	Cytology QH573-671
Acceso en línea:	https://doaj.org/article/e37f532b4270439d930e8af1b7acd0b0
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spelling	oai:doaj.org-article:e37f532b4270439d930e8af1b7acd0b02021-11-29T00:55:54ZCaMK II Inhibition Attenuates ROS Dependent Necroptosis in Acinar Cells and Protects against Acute Pancreatitis in Mice1942-099410.1155/2021/4187398https://doaj.org/article/e37f532b4270439d930e8af1b7acd0b02021-01-01T00:00:00Zhttp://dx.doi.org/10.1155/2021/4187398https://doaj.org/toc/1942-0994As a calcium-regulated protein, CaMK II is closely related to cell death, and it participates in the development of pathological processes such as reperfusion injury, myocardial infarction, and oligodendrocyte death. The function of CaMK II activation in acute pancreatitis (AP) remains unclear. In our study, we confirmed that the expression of p-CaMK II was increased significantly and consistently in injured pancreatic tissues after caerulein-induced AP. Then, we found that KN93, an inhibitor of CaMK II, could mitigate the histopathological manifestations in pancreatic tissues, reduce serum levels of enzymology, and decrease oxidative stress products. Accordingly, we elucidated the effect of KN93 in vitro and found that KN93 had a protective effect on the pancreatic acinar cell necroptosis pathway by inhibiting the production of ROS and decreasing the expression of RIP3 and p-MLKL. In addition, we identified the protective effect of KN93 on AP through another mouse model induced by pancreatic duct ligation (PDL). Together, these data demonstrated that CaMK II participates in the development of AP and that inhibiting CaMK II activation could protect against AP by reducing acinar cell necroptosis, which may provide a new idea target for the prevention and treatment of AP in the clinic.Qingtian ZhuLu HaoQinhao ShenJiajia PanWeili LiuWeijuan GongLianghao HuWeiming XiaoMei WangXinnong LiuYanbing DingGuotao LuHindawi LimitedarticleCytologyQH573-671ENOxidative Medicine and Cellular Longevity, Vol 2021 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Cytology QH573-671
spellingShingle	Cytology QH573-671 Qingtian Zhu Lu Hao Qinhao Shen Jiajia Pan Weili Liu Weijuan Gong Lianghao Hu Weiming Xiao Mei Wang Xinnong Liu Yanbing Ding Guotao Lu CaMK II Inhibition Attenuates ROS Dependent Necroptosis in Acinar Cells and Protects against Acute Pancreatitis in Mice
description	As a calcium-regulated protein, CaMK II is closely related to cell death, and it participates in the development of pathological processes such as reperfusion injury, myocardial infarction, and oligodendrocyte death. The function of CaMK II activation in acute pancreatitis (AP) remains unclear. In our study, we confirmed that the expression of p-CaMK II was increased significantly and consistently in injured pancreatic tissues after caerulein-induced AP. Then, we found that KN93, an inhibitor of CaMK II, could mitigate the histopathological manifestations in pancreatic tissues, reduce serum levels of enzymology, and decrease oxidative stress products. Accordingly, we elucidated the effect of KN93 in vitro and found that KN93 had a protective effect on the pancreatic acinar cell necroptosis pathway by inhibiting the production of ROS and decreasing the expression of RIP3 and p-MLKL. In addition, we identified the protective effect of KN93 on AP through another mouse model induced by pancreatic duct ligation (PDL). Together, these data demonstrated that CaMK II participates in the development of AP and that inhibiting CaMK II activation could protect against AP by reducing acinar cell necroptosis, which may provide a new idea target for the prevention and treatment of AP in the clinic.
format	article
author	Qingtian Zhu Lu Hao Qinhao Shen Jiajia Pan Weili Liu Weijuan Gong Lianghao Hu Weiming Xiao Mei Wang Xinnong Liu Yanbing Ding Guotao Lu
author_facet	Qingtian Zhu Lu Hao Qinhao Shen Jiajia Pan Weili Liu Weijuan Gong Lianghao Hu Weiming Xiao Mei Wang Xinnong Liu Yanbing Ding Guotao Lu
author_sort	Qingtian Zhu
title	CaMK II Inhibition Attenuates ROS Dependent Necroptosis in Acinar Cells and Protects against Acute Pancreatitis in Mice
title_short	CaMK II Inhibition Attenuates ROS Dependent Necroptosis in Acinar Cells and Protects against Acute Pancreatitis in Mice
title_full	CaMK II Inhibition Attenuates ROS Dependent Necroptosis in Acinar Cells and Protects against Acute Pancreatitis in Mice
title_fullStr	CaMK II Inhibition Attenuates ROS Dependent Necroptosis in Acinar Cells and Protects against Acute Pancreatitis in Mice
title_full_unstemmed	CaMK II Inhibition Attenuates ROS Dependent Necroptosis in Acinar Cells and Protects against Acute Pancreatitis in Mice
title_sort	camk ii inhibition attenuates ros dependent necroptosis in acinar cells and protects against acute pancreatitis in mice
publisher	Hindawi Limited
publishDate	2021
url	https://doaj.org/article/e37f532b4270439d930e8af1b7acd0b0
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CaMK II Inhibition Attenuates ROS Dependent Necroptosis in Acinar Cells and Protects against Acute Pancreatitis in Mice

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