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RISS 인기검색어
- 검색키워드
- 저자 : Jing-Miao Ding (검색결과 4 건)
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Qian Ding,Xiao-Li Xie,Miao-Miao Wang,Jie Yin,Jin-Mei Tian,Xiao-Yu Jiang,Di Zhang,Jing Han,Yun Bai,Zi-Jin Cui,Hui-Qing Jiang 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-
The clearance of activated hepatic stellate cells (HSCs) by apoptosis is critical for the reversibility of hepatic fibrosis. Mitochondrial homeostasis is regulated by mitophagy, which is an efficient way of clearing injured mitochondria that plays an important role in apoptosis. However, the role of mitophagy in apoptosis in HSCs and hepatic fibrosis is still unclear. Here, we show that mitophagy is enhanced in parallel with increased apoptosis in hepatic stellate cells during the reversal of hepatic fibrosis. The inhibition of mitophagy suppressed apoptosis in HSCs and aggravated hepatic fibrosis in mice. In contrast, the activation of mitophagy induced apoptosis in HSCs. Furthermore, we confirmed that BCL-B, which is a member of the BCL-2 family, is a regulator mediating mitophagy-related apoptosis. The knockdown of BCL-B resulted in increased apoptosis and mitophagy in HSCs, while the overexpression of BCL-B caused the opposite effects. BCL-B inhibited the phosphorylation of Parkin (a key regulator of mitophagy) and directly bound phospho-Parkin. Altogether, enhanced mitophagy promotes apoptosis in HSCs during the reversal of hepatic fibrosis. BCL-B suppresses mitophagy in HSCs by binding and suppressing phospho-Parkin, thereby inhibiting apoptosis. BCLB- dependent mitophagy is a new pathway for the regulation of apoptosis in HSCs during the regression of hepatic fibrosis
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Yang Yang,Shi Yao,Jing-Miao Ding,Wei Chen,Yan Guo 대한당뇨병학회 2021 Diabetes and Metabolism Journal Vol.45 No.2
Background: Genetic interactions are known to play an important role in the missing heritability problem for type 2 diabetes mellitus (T2DM). Interactions between enhancers and their target genes play important roles in gene regulation and disease pathogenesis. In the present study, we aimed to identify genetic interactions between enhancers and their target genes associated with T2DM. Methods: We performed genetic interaction analyses of enhancers and protein-coding genes for T2DM in 2,696 T2DM patients and 3,548 controls of European ancestry. A linear regression model was used to identify single nucleotide polymorphism (SNP) pairs that could affect the expression of the protein-coding genes. Differential expression analyses were used to identify differentially expressed susceptibility genes in diabetic and nondiabetic subjects. Results: We identified one SNP pair, rs4947941×rs7785013, significantly associated with T2DM (combined P=4.84×10−10). The SNP rs4947941 was annotated as an enhancer, and rs7785013 was located in the epidermal growth factor receptor (EGFR) gene. This SNP pair was significantly associated with EGFR expression in the pancreas (P=0.033), and the minor allele “A” of rs7785013 decreased EGFR gene expression and the risk of T2DM with an increase in the dosage of “T” of rs4947941. EGFR expression was significantly upregulated in T2DM patients, which was consistent with the effect of rs4947941×rs7785013 on T2DM and EGFR expression. A functional validation study using the Mouse Genome Informatics (MGI) database showed that EGFR was associated with diabetes-relevant phenotypes. Conclusion: Genetic interaction analyses of enhancers and protein-coding genes suggested that EGFR may be a novel susceptibility gene for T2DM.
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Stanniocalcin-1 protects bovine intestinal epithelial cells from oxidative stress-induced damage
Li-ming Wu,Rui Guo,Lin Hui,Yong-gang Ye,Jing-mei Xiang,Chun-yun Wan,Miao Zou,Rui Ma,Xiao-zhuan Sun,Shi-jin Yang,Ding-zong Guo 대한수의학회 2014 JOURNAL OF VETERINARY SCIENCE Vol.15 No.4
Chronic enteritis can produce an excess of reactive oxygenspecies resulting in cellular damage. Stanniocalcin-1(STC-1)reportedly possesses anti-oxidative activity, the aim of thisstudy was to define more clearly the direct contribution ofSTC-1 to anti-oxidative stress in cattle. In this study, primaryintestinal epithelial cells (IECs) were exposed to hydrogenperoxide (H2O2) for different time intervals to mimic chronicenteritis-induced cellular damage. Prior to treatment with 200μM H2O2, the cells were transfected with a recombinantplasmid for 48 h to over-express STC-1. Acridine orange/ethidium bromide (AO/EB) double staining and trypan blueexclusion assays were then performed to measure cell viabilityand apoptosis of the cells, respectively. The expression of STC-1and apoptosis-related proteins in the cells was monitored byreal-time PCR and Western blotting. The results indicated thatboth STC-1 mRNA and protein expression levels positivelycorrelated with the duration of H2O2 treatment. H2O2 damagedthe bovine IECs in a time-dependent manner, and this effectwas attenuated by STC-1 over-expression. Furthermore, overexpressionof STC-1 up-regulated Bcl-2 protein expression andslightly down-regulated caspase-3 production in the damagedcells. Findings from this study suggested that STC-1 plays aprotective role in intestinal cells through an antioxidant mechanism.
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Outcomes of Anti-CD19 CAR-T Treatment of Pediatric B-ALL with Bone Marrow and Extramedullary Relapse
Xinyu Wan,Xiaomin Yang,Fan Yang,Tianyi Wang,Lixia Ding,Lili Song,Yan Miao,Xiang Wang,Yani Ma,Chengjuan Luo,Jingyan Tang,Longjun Gu,Jing Chen,Yanjing Tang,Jun Lu,Benshang Li 대한암학회 2022 Cancer Research and Treatment Vol.54 No.3
PurposeAnti-CD19 chimeric antigen receptor T-cell immunotherapy (19CAR-T) has achieved impressive clinical results in adult and pediatric relapsed/refractory (r/r) B-lineage acute lymphoblastic leukemia (B-ALL). However, the application and effect of CAR-T therapy in B-ALL patients with extramedullary relapse are rarely issued even disqualified in some clinical trials. Here, we examined the efficacy of 19CAR-T in patients with both bone marrow and extramedullary involvement.Materials and MethodsCAR-T cells were generated by transfection of primary human T lymphocytes with a lentiviral vector expressing anti-CD19 single chain antibody fragments (scFvs) with the cytoplasmic domains of 4-1BB and CD3ζ, and used to infuse patients diagnosed as having r/r B-ALL with extramedullary origination. Clinical responses were evaluated by the use of bone marrow aspiration, imaging, and flow cytometry. ResultsEight patients received 19CAR-T infusion and all attained complete remission (CR). Only one patient was bridged to hematopoietic stem cell transplantation (HSCT). Although three patients relapsed after infusion, they received 19/22CAR-T infusion sequentially and attained a second remission. To date, five patients are in continuous CR and all eight patients are still alive. The mean follow-up time was 21.9 months, while the 24-month estimated event-free survival is 51.4%. Conclusion19CAR-T therapy can lead to clinical remission for extramedullary relapsed pediatric B-ALL patients. However, the problem of CD19+ relapses after CAR-T remained to be solved. For patients relapsing after CAR-T, a second CAR-T therapy creates another opportunity for remission for subsequent HSCT.
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