JNK是MAPK超家族成员之一,c-Jun是JNK的主要下游因子,是一种受JNK调控的即早基因。JNK和c-Jun是创伤、应激、细胞凋亡相关的调节因子,参与调控多种疾病的发生发展过程。近年来,研究发现,JNK/c-Jun信号通路在IgA肾病、抗GBM肾小球肾炎、...JNK是MAPK超家族成员之一,c-Jun是JNK的主要下游因子,是一种受JNK调控的即早基因。JNK和c-Jun是创伤、应激、细胞凋亡相关的调节因子,参与调控多种疾病的发生发展过程。近年来,研究发现,JNK/c-Jun信号通路在IgA肾病、抗GBM肾小球肾炎、肾纤维化、急性肾损伤等多种肾脏疾病中表现为异常活化,调控着相关肾脏疾病的发生和发展过程。本文就JNK/c-Jun信号通路在肾脏疾病发生发展过程中的调控作用作简要综述。JNK is one of the members of the MAPK superfamily, and c-Jun is the main downstream factor of JNK, which is an early gene regulated by JNK. JNK and c-Jun are regulators related to trauma, stress and apoptosis, and are involved in regulating the occurrence and development of a variety of diseases. In recent years, studies have found that the JNK/c-Jun signaling pathway is abnormally activated in a variety of kidney diseases, such as IgA nephropathy, anti-GBM glomerulonephritis, renal fibrosis, and acute kidney injury, which regulates the occurrence and development of related kidney diseases. This article briefly reviews the regulatory role of JNK/c-Jun signaling pathway in the occurrence and development of kidney diseases.展开更多
Research has shown that long-chain noncoding RNAs(lncRNAs) are involved in the regulation of a variety of biological processes, including peripheral nerve regeneration, in part by acting as competing endogenous RNAs. ...Research has shown that long-chain noncoding RNAs(lncRNAs) are involved in the regulation of a variety of biological processes, including peripheral nerve regeneration, in part by acting as competing endogenous RNAs. c-Jun plays a key role in the repair of peripheral nerve injury. However, the precise underlying mechanism of c-Jun remains unclear. In this study, we performed microarray and bioinformatics analysis of mouse crush-injured sciatic nerves and found that the lncRNA Pvt1 was overexpressed in Schwann cells after peripheral nerve injury. Mechanistic studies revealed that Pvt1 increased c-Jun expression through sponging miRNA-214. We overexpressed Pvt1 in Schwann cells cultured in vitro and found that the proliferation and migration of Schwann cells were enhanced, and overexpression of miRNA-214 counteracted the effects of Pvt1 overexpression on Schwann cell proliferation and migration. We conducted in vivo analyses and injected Schwann cells overexpressing Pvt1 into injured sciatic nerves of mice. Schwann cells overexpressing Pvt1 enhanced the regeneration of injured sciatic nerves following peripheral nerve injury and the locomotor function of mice was improved. Our findings reveal the role of lncRNAs in the repair of peripheral nerve injury and highlight lncRNA Pvt1 as a novel potential treatment target for peripheral nerve injury.展开更多
文摘JNK是MAPK超家族成员之一,c-Jun是JNK的主要下游因子,是一种受JNK调控的即早基因。JNK和c-Jun是创伤、应激、细胞凋亡相关的调节因子,参与调控多种疾病的发生发展过程。近年来,研究发现,JNK/c-Jun信号通路在IgA肾病、抗GBM肾小球肾炎、肾纤维化、急性肾损伤等多种肾脏疾病中表现为异常活化,调控着相关肾脏疾病的发生和发展过程。本文就JNK/c-Jun信号通路在肾脏疾病发生发展过程中的调控作用作简要综述。JNK is one of the members of the MAPK superfamily, and c-Jun is the main downstream factor of JNK, which is an early gene regulated by JNK. JNK and c-Jun are regulators related to trauma, stress and apoptosis, and are involved in regulating the occurrence and development of a variety of diseases. In recent years, studies have found that the JNK/c-Jun signaling pathway is abnormally activated in a variety of kidney diseases, such as IgA nephropathy, anti-GBM glomerulonephritis, renal fibrosis, and acute kidney injury, which regulates the occurrence and development of related kidney diseases. This article briefly reviews the regulatory role of JNK/c-Jun signaling pathway in the occurrence and development of kidney diseases.
基金supported by the National Natural Science Foundation of China,No. 81801213 (to BP)Xuzhou Special Fund for Promoting Scientific and Technological Innovation,Nos. KC21177 (to BP),KC21195 (to HF)Science and Technology Project of Yili Kazak Autonomous Prefecture,No. YZ2019D006 (to HF)。
文摘Research has shown that long-chain noncoding RNAs(lncRNAs) are involved in the regulation of a variety of biological processes, including peripheral nerve regeneration, in part by acting as competing endogenous RNAs. c-Jun plays a key role in the repair of peripheral nerve injury. However, the precise underlying mechanism of c-Jun remains unclear. In this study, we performed microarray and bioinformatics analysis of mouse crush-injured sciatic nerves and found that the lncRNA Pvt1 was overexpressed in Schwann cells after peripheral nerve injury. Mechanistic studies revealed that Pvt1 increased c-Jun expression through sponging miRNA-214. We overexpressed Pvt1 in Schwann cells cultured in vitro and found that the proliferation and migration of Schwann cells were enhanced, and overexpression of miRNA-214 counteracted the effects of Pvt1 overexpression on Schwann cell proliferation and migration. We conducted in vivo analyses and injected Schwann cells overexpressing Pvt1 into injured sciatic nerves of mice. Schwann cells overexpressing Pvt1 enhanced the regeneration of injured sciatic nerves following peripheral nerve injury and the locomotor function of mice was improved. Our findings reveal the role of lncRNAs in the repair of peripheral nerve injury and highlight lncRNA Pvt1 as a novel potential treatment target for peripheral nerve injury.
