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作 者:周晓煦 聂涵 赵越[2] 田文[1] ZHOU Xiao-xu;NIE Han;ZHAO Yue;TIAN Wen(Department of Geriatrie Cardiology,the First Affiliated Hospital of China Medical University,Shenyang 110001;Department of Cell Biology,Key Laboratory of Cell Biology of Ministry of Public Health,School of Life Sciences,China Medical University,Shenyang 110122,China)
机构地区:[1]中国医科大学附属第一医院老年心血管病科,沈阳110001 [2]中国医科大学生命科学学院细胞生物学系卫生部细胞生物学重点实验室,沈阳110122
出 处:《解剖科学进展》2022年第2期125-128,共4页Progress of Anatomical Sciences
基 金:沈阳市科技计划项目(19-112-4-063)。
摘 要:目的 探究USP22在血管钙化过程中的作用及其机制。方法 使用人主动脉平滑肌细胞(HASMCs)构建高磷诱导血管钙化模型,通过免疫荧光实验观察USP22在钙化HASMCs中的表达;通过茜素红染色观察USP22对HASMCs钙化影响,Western blot方法检测USP22对成骨分化标志物及NF-κB信号通路的影响。结果 USP22在钙化的HASMCs中高表达且定位于细胞核,促进HASMCs的成骨分化及高磷诱导的HASMCs的钙化,促进NF-κB激活,NF-κB抑制剂PDTC逆转了USP22对HASMCs的促钙化作用。结论 USP22通过NF-κB信号通路促进高磷诱导的血管钙化。Objective To investigate the role of USP22 in the process of vascular calcification and its possible mechanism. Methods The vascular calcification model induced by high concentration of phosphorus was constructed using human aortic vascular smooth muscle cells(HASMCs), and the expression of USP22 in calcified HASMCs was investigated by immunofluorescence. The USP22 plasmid was transfected and the effect of USP22 overexpression on vascular calcification was determined by alizarin red staining and Western blot. And the changes of NF-κB pathway were detected by Western blot. PDTC, an inhibitor of NF-κB signaling, was added to verify whether the effect of USP22 on calcification was blocked. Results USP22 increasedly expressed in calcified HASMCs and located in cellular nucleus. Overexpression of USP22 with pcDNA3.1-USP22 plasmid in HASMCs promotes vascular calcification accompanied by activation of NF-κB. The activated process of vascular calcification can be ameliorated by PDTC. Conclusion USP22 promotes phosphorus-induced vascular calcification through the NF-κB signaling pathway.
分 类 号:R543.5[医药卫生—心血管疾病]
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