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2,009 results on '"Jin, Juan"'

9. High glucose induces podocyte ferroptosis through BAP1/SLC7A11 pathway

Author

Ren Peiyao, Man Xueli, Sun Wenbo, Zheng Danna, Gong Jianguang, Jin Juan, and He Qiang

Subjects
Diabetic nephropathy, Ferroptosis, SLC7A11, Ubiquitination, Science (General), Q1-390, Social sciences (General), H1-99
Abstract

Background: Ferroptosis plays an important role in the development of diabetic nephropathy (DN). However, its specific regulatory mechanisms remain unclear. Methods: MPC5 cells were cultured in high glucose (HG) medium to stimulate the HG environment in vitro. Ferroptosis and oxidative stress were assessed by measuring malondialdehyde (MDA) levels, cystine uptake capacity, and reactive oxygen species (ROS). C91A and wild type (WT) MPC5 cells were constructed to further explore the specific regulatory mechanism of BAP1 on SLC7A11. Results: Erastin-induced ferroptosis was sensitized by HG, leading to a significant reduction in glutathione (GSH) levels, increased oxidative stress, and inhibited cystine uptake in podocytes. HG suppressed the expression of SLC7A11. Overexpression of SLC7A11 improved cystine uptake and reduced oxidative stress. Furthermore, HG increased BAP1 levels. Silencing BAP1 up-regulated SLC7A11 and mitigated ferroptosis. Cell proliferation was reduced after SLC7A11 knockdown. In BAP1 WT cells, but not in its C91A mutant cells, the transcription of SLC7A11 was downregulated and the level of ferroptosis was increased. Conclusion: HG inhibits cystine uptake in podocytes by promoting the expression of BAP1 and inhibiting H2Aub deubiquitination on SLC7A11, leading to lipid peroxide accumulation and ferroptosis in podocytes.

Published
2025
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18. Irisin attenuates type 1 diabetic cardiomyopathy by anti-ferroptosis via SIRT1-mediated deacetylation of p53

Author

Yuan-juan Tang, Zhen Zhang, Tong Yan, Ken Chen, Guo-fan Xu, Shi-qiang Xiong, Dai-qian Wu, Jie Chen, Pedro A. Jose, Chun-yu Zeng, and Jin-juan Fu

Subjects
Type 1 diabetic cardiomyopathy, Ferroptosis, Irisin, p53, SIRT1, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

Abstract Background Diabetic cardiomyopathy (DCM) is a serious complication in patients with type 1 diabetes mellitus (T1DM), which still lacks adequate therapy. Irisin, a cleavage peptide off fibronectin type III domain-containing 5, has been shown to preserve cardiac function in cardiac ischemia–reperfusion injury. Whether or not irisin plays a cardioprotective role in DCM is not known. Methods and results T1DM was induced by multiple low-dose intraperitoneal injections of streptozotocin (STZ). Our current study showed that irisin expression/level was lower in the heart and serum of mice with STZ-induced TIDM. Irisin supplementation by intraperitoneal injection improved the impaired cardiac function in mice with DCM, which was ascribed to the inhibition of ferroptosis, because the increased ferroptosis, associated with increased cardiac malondialdehyde (MDA), decreased reduced glutathione (GSH) and protein expressions of solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4), was ameliorated by irisin. In the presence of erastin, a ferroptosis inducer, the irisin-mediated protective effects were blocked. Mechanistically, irisin treatment increased Sirtuin 1 (SIRT1) and decreased p53 K382 acetylation, which decreased p53 protein expression by increasing its degradation, consequently upregulated SLC7A11 and GPX4 expressions. Thus, irisin-mediated reduction in p53 decreases ferroptosis and protects cardiomyocytes against injury due to high glucose. Conclusion This study demonstrated that irisin could improve cardiac function by suppressing ferroptosis in T1DM via the SIRT1-p53-SLC7A11/GPX4 pathway. Irisin may be a therapeutic approach in the management of T1DM-induced cardiomyopathy.

Published
2024
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19. Integrated 16S rRNA sequencing and metabolomic analysis reveals the potential protective mechanism of Germacrone on diabetic nephropathy in mice

Author

Wang Yunguang, He Xinxin, Xue Mengjiao, Yu Huan, He Qiang, and Jin Juan

Subjects
diabetic nephropathy, Germacrone, gut microbiota, untargeted fecal metabolomics, 16S rRNA sequencing, Biochemistry, QD415-436, Genetics, QH426-470
Abstract

Diabetic nephropathy (DN) is a severe complication of diabetes and the leading cause of end-stage renal disease and death. Germacrone (Ger) possesses anti-inflammatory, antioxidant and anti-DN properties. However, it is unclear whether the improvement in kidney damage caused by Ger in DN mice is related to abnormal compositions and metabolites of the gut microbiota. This study generates a mouse model of DN to explore the potent therapeutic ability and mechanism of Ger in renal function by 16S rRNA sequencing and untargeted fecal metabolomics. Although there is no significant change in microbiota diversity, the structure of the gut microbiota in the DN group is quite different. Serratia_marcescens and Lactobacillus_iners are elevated in the model group but significantly decreased after Ger intervention (P

Published
2024
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26. An AMPK agonist suppresses the progress of colorectal cancer by regulating the polarization of TAM to M1 through inhibition of HIF-1α and mTOR signal pathway

Author

Cao, Yuanyuan, Wo, Mingyi, Xu, Chan, Fei, Xianming, Jin, Juan, and Shan, Zhiming

Subjects
Adenylic acid -- Physiological aspects -- Health aspects, Colorectal cancer -- Care and treatment -- Development and progression, Protein kinases -- Physiological aspects -- Health aspects, Macrophages -- Health aspects
Abstract

Objective: This study aimed to evaluate the impact of an adenosine monophosphate-activated protein kinase (AMPK) agonist, metformin (MET), on the antitumor effects of macrophages and to determine the underlying mechanism involved in the process. Materials and Methods: M0 macrophages were derived from phorbol-12-myristate-13-acetate-stimulated THP-1 cells. Results: The levels of tumor necrosis factor-alpha (TNF-α) and human leukocyte antigen-DR (HLA-DR) were decreased in macrophages incubated with HCT116 cells, whereas those of arginase-1 (Arg-1), CD163, and CD206 were elevated; these effects were reversed by MET. The transfection of small interfering (si) RNA abrogated the influence of MET on the expression of the M1/M2 macrophage biomarkers. MET significantly suppressed the proliferation and migration abilities of HCT116 cells incubated with M0 macrophages; these actions were reversed by siRNA transfection against AMPK. The hypoxia-inducible factor 1-alpha (HIF-1α), phosphorylated protein kinase B (p-AKT), and phosphorylated mammalian target of rapamycin (p-mTOR) levels were reduced by the introduction of MET and promoted by siRNA transfection against AMPK. In addition, the levels of HIF-1α, p-AKT, and p-mTOR suppressed by MET were markedly increased following the transfection of siRNA against AMPK. Conclusion: These findings indicate that MET can repress the progression of colorectal cancer by transforming tumor-associated macrophages to the M1phenotype via inhibition of the HIF-1α and mTOR signaling pathways. Keywords: AMPK, colorectal cancer, macrophages, polarization, Author(s): Yuanyuan Cao [1]; Mingyi Wo [2]; Chan Xu [3]; Xianming Fei [2]; Juan Jin [2]; Zhiming Shan (corresponding author) [2] INTRODUCTION Colorectal cancer (CRC) is a malignant tumor of [...]

Published
2023
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50. Safety and immunogenicity of a mosaic vaccine booster against Omicron and other SARS-CoV-2 variants: a randomized phase 2 trial

Author

Kaabi, Nawal Al, Yang, Yun Kai, Liang, Yu, Xu, Ke, Zhang, Xue Feng, Kang, Yun, Jin, Yu Qin, Hou, Jun Wei, Zhang, Jing, Yang, Tian, Hussein, Salah, ElDein, Mohamed Saif, Lei, Ze Hua, Zhang, Hao, Shao, Shuai, Liu, Zhao Ming, Liu, Ning, Zheng, Xiang, Su, Ji Guo, Yang, Sen Sen, Cong, Xiangfeng, Tan, Yao, Lei, Wenwen, Gao, Xue Jun, Jiang, Zhiwei, Wang, Hui, Li, Meng, Mekki, Hanadi Mekki, Zaher, Walid, Mahmoud, Sally, Zhang, Xue, Qu, Chang, Liu, Dan Ying, Zhang, Jing, Yang, Mengjie, Eltantawy, Islam, Xiao, Peng, Shen, Fu Jie, Wu, Jin Juan, Han, Zi Bo, Du, Li Fang, Tang, Fang, Chen, Shi, Ma, Zhi Jing, Zheng, Fan, Hou, Ya Nan, Li, Xin Yu, Li, Xin, Wang, Zhao Nian, Yin, Jin Liang, Mao, Xiao Yan, Zhang, Jin, Qu, Liang, Zhang, Yun Tao, Yang, Xiao Ming, Wu, Guizhen, and Li, Qi Ming

Published
2023
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