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| 1 | Endoplasmic reticulum oxidoreductin 1α mediates hepatic endoplasmic reticulum stress in homocysteine-induced atherosclerosis显示文摘Endoplasmic 蜂窝胃(嗯) 应力作为不同病理学的过程的一个重要调节的人并且作为贡献导致的 homocysteine (Hcy ) 的机制正在出现 hepar 损害。然而,分子的事件导致 Hcy 嗯在在动脉粥样硬化背景下面的 hepar 的应力当前是未知的。Endoplasmic 蜂窝胃 oxidoreductin (ERO1 ) 1 在维持起一个关键作用嗯压力功能。在这研究,我们在 hepacytes 在 hyperhomocysteinemia 和 ERO1 的效果在 hepar 决定了 ERO1 的表示嗯应力面对 Hcy。HHcy 模型被在 apolipoprotein-E-deficient (ApoE-/-) 喂蛋氨酸食谱建立老鼠,和 hepatocytes 与 Hcy 的叶酸、不同的集中被孵化。我们的结果证明 Hcy 被触发嗯应力描绘了由一调整葡萄糖的蛋白质的增加的内容 78 (GRP78 ) ,蛋白质 kinase 象 RNA 一样嗯 kinase (津贴) ,激活抄写因素(ATF ) 6 并且 X 盒子有约束力的 protein-1 (XBP-1 ) 。在 HHcy 老鼠和对待 Hcy 的 hepatocytes 的 ERO1 表情在 ApoE-/- 组和控制 hepacytes 与那些相比被减少(P < 0.05 ) 分别地。有小介入的 RNA 的 ERO1 的表示显著地扩充了的敲门下面导致 Hcy 嗯应力。同时,表情嗯压力相关的因素包括 GRP78,津贴, ATF6 和 XBP-1,当 ERO1 基因在 hepacytes 是过去表示的时,显著地被减少。我们的结果建议 ERO1 可以涉及导致 Hcy 的 hepar 嗯 ERO1 表示的应力,和抑制能加速这进程。 | Xiaoling Yang Hua Xu Yinju Hao Li Zhao Xin Cai Jue Tian Minghao Zhang Xuebo Han Shengchao Ma Jun Cao Yideng Jiang | 2014 | Acta Biochimica et Biophysica Sinica2014，46，10： | 14 |
| 2 | Protective effect of oxysophoridine on cerebral ischemia/reperfusion injury in mice显示文摘Oxysophoridine, a new alkaloid extracted from Sophora alopecuroides L., has been shown to have a protective effect against ischemic brain damage. In this study, a focal cerebral ischemia/reperfusion injury model was established using middle cerebral artery occlusion in mice. Both 62.5, 125, and 250 mg/kg oxysophoridine, via intraperitoneal injection, and 6 mg/kg nimodipine, via intragastric administration, were administered daily for 7 days before modeling. After 24 hours of reperfusion, mice were tested for neurological deficit, cerebral infarct size was assessed and brain tissue was collected. Results showed that oxysophoridine at 125, 250 mg/kg and 6 mg/kg nimodipine could reduce neurological deficit scores, cerebral infarct size and brain water content in mice. These results provided evidence that oxysophoridine plays a protective role in cerebral ischemia/reperfusion injury. In addition, oxysophoridine at 62.5, 125, and 250 mg/kg and 6 mg/kg nimodipine increased adenosine-triphosphate content, and decreased malondialdehyde and nitric oxide content. These compounds enhanced the activities of glutathione-peroxidase, superoxide dismutase, catalase, and lactate dehydrogenase, and decreased the activity of nitric oxide synthase. Protein and mRNA expression levels of N-methyl-D-aspartate receptor subunit NR1 were markedly inhibited in the presence of 250 mg/kg oxysophoridine and 6 mg/kg nimodipine. Our experimental findings indicated that oxysophoridine has a neuroprotective effect against cerebral ischemia/reperfusion injury in mice, and that the effect may be due to its ability to inhibit oxidative stress and expression of the N-methyl-D-aspartate receptor subunit NR1. | Hongbo Wang Yuxiang Li Ning Jiang Xiaoping Chen Yi Zhang Kuai Zhang Tengfei Wang Yinju Hao Lin Ma Chengjun Zhao Yanrong Wang Tao Sun Jianqiang Yu | 2013 | Neural Regeneration Research2013，8，15： | 5 |
| 3 | Homocysteine accelerates hepatocyte autophagy by upregulating TFEB via DNMT3b-mediated DNA hypomethylation显示文摘Autophagy plays a critical role in the physiology and pathophysiology of hepatocytes.High level of homocysteine(Hcy)promotes autophagy in hepatocytes,but the underlying mechanism is still unknown.Here,we investigate the relationship between Hcy-induced autophagy level and the expression of nuclear transcription factor EB(TFEB).The results show that Hcy-induced autophagy level is mediated by upregulation of TFEB.Silencing of TFEB decreases the level of autophagy-related protein LC3BII/I and increases p62 expression level in hepatocytes after exposure to Hcy.Moreover,the effect of Hcy on the expression of TFEB is regulated by hypomethylation of the TFEB promoter catalyzed by DNA methyltransferase 3b(DNMT3b).In summary,this study shows that Hcy can activate autophagy by inhibiting DNMT3b-mediated DNA methylation and upregulating TFEB expression.These findings provide another new mechanism for Hcy-induced autophagy in hepatocytes. | Anning Yang Wen Zeng Hongwen Zhang Yinju Hao Qingqing Wang Yue Sun Shangkun Quan Ning Ding Xiaoling Yang Jianmin Sun Huiping Zhang Bin Liu Yun Jiao Kai Wu Yideng Jiang | 2023 | Acta Biochimica et Biophysica Sinica2023，55，8： | 0 |
| 4 | LncRNA FPASL suppresses fibroblast proliferation through its DNA methylation via DNMT3b in hypertrophic scar显示文摘Long noncoding RNAs(lncRNAs)are increasingly being implicated as key regulators of cell proliferation,apoptosis,and differentiation.However,the molecular mechanisms of specific lncRNAs in the context of hypertrophic scar remain largely unclear.Here,we find that the lncRNA FPASL(fibroblast proliferation-associated LncRNA)is downregulated in HS,and FPASL reduces fibroblast proliferation and colony formation and blocks cell cycle progression.Using GO annotation enrichment analysis along with AZC(a specific inhibitor of DNA methylation),we identify that DNA methylation is responsible for downregulating FPASL in hypertrophic scar.Subsequent studies demonstrate that high expression of DNMT3b inhibits FPASL expression in HS.Mechanistic study reveals a significant increase in fibroblast proliferation after transfection with LNA-FPASL,which is further inhibited by knockdown of DNMT3b.Thus,our study reveals that DNMT3b mediates hypermethylation of the lncRNA FPASL promoter and the downregulation of lncRNA FPASL promotes fibroblast proliferation in hypertrophic scar. | Kai Wu Fang Ma Jiangyong Shen Hui Zhang Yu Wan Xi He Anning Yang Jiantuan Xiong Yun jiao Zhigang Bai Shengchao Ma Yideng Jiang Huiping Zhang Yinju Hao | 2022 | Acta Biochimica et Biophysica Sinica2022，54，12： | 0 |
| 5 | HSFAS mediates fibroblast proliferation, migration, trans-differentiation and apoptosis in hypertrophic scars via interacting with ADAMTS8显示文摘Hypertrophic scar(HS)is one of the most common sequelae of patients,especially after burns and trauma.The roles of regulatory long noncoding RNAs(lncRNAs)in mediating HS remain underexplored.Human hypertrophic scarderived fibroblasts(HSFBs)have been shown to exert more potent promoting effects on extracellular matrix(ECM)accumulation than normal skin-derived fibroblasts(NSFBs)and are associated with enhanced HS formation.The purpose of this study is to search for lncRNAs enriched in HSFBs and investigate their roles and mechanisms.LncRNA MSTRG.59347.16 is one of the most highly expressed lncRNAs in HS detected by lncRNA-seq and qRT-PCR and named as hypertrophic scar fibroblast-associated lncRNA(HSFAS).HSFAS overexpression significantly induces fibroblast proliferation,migration,and myofibroblast trans-differentiation and inhibits apoptosis in HSFBs,while knockdown of HSFAS results in augmented apoptosis and attenuated proliferation,migration,and myofibroblast trans-differentiation of HSFBs.Mechanistically,HSFAS suppresses the expression of A disintegrin and metalloproteinase with thrombospondin motifs 8(ADAMTS8).ADAMTS8 knockdown rescues downregulated HSFAS-mediated fibroblast proliferation,migration,myofibroblast trans-differentiation and apoptosis.Thus,our findings uncover a previously unknown lncRNA-dependent regulatory pathway for fibroblast function.Targeted intervention in the HSFAS-ADAMTS8 pathway is a potential therapy for HS. | Fang Ma Honglin Liu Tongtong Xia Zhenghao Zhang Shengchao Ma Yinju Hao Jiangyong Shen Yideng Jiang Nan Li | 2024 | Acta Biochimica et Biophysica Sinica2024，56，3： | 0 |
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