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RISS 인기검색어
- 검색키워드
- 저자 : Xin-Ke Zhai (검색결과 2 건)
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Xiang Zhai,Xin-yang Li,Yu-jing Wang,Ke-ru Qin,Jin-rui Hu,Mei-ning Li,Hai-long Wang,Rui Guo 대한내분비학회 2022 Endocrinology and metabolism Vol.37 No.3
Background: It is well-established that serum testosterone in men decreases with age, yet the underlying mechanism of this changeremains elusive. Methods: The expression patterns of Fancd2 opposite-strand (Fancd2os) in BALB/c male mice and testicular tissue derived celllines (GC-1, GC-2, TM3, and TM4) were assessed using real-time polymerase chain reaction (RT-PCR), Western blot and immunofluorescence. The Fancd2os-overexpressing or knockdown TM3 cells were constructed by infecting them with lentivirus particlesand were used to evaluated the function of Fancd2os. The testosterone production was measured using enzyme linked immunosorbent assay (ELISA) and the steroidogenic enzymes such as steroidogenic acute regulatory protein (StAR), P450 cholesterol sidechain cleavage (P450scc), and 3β-hydroxysteroid dehydrogenase (3β-HSD) were analysed using RT-PCR. The apoptosis of TM3cells induced by ultraviolet light or testicular tissues was detected using flow cytometry, Western blot or dUTP-biotin nick end labeling (TUNEL) assays. Pearson correlation analysis was used to assess the correlation between the Fancd2os expression and TUNELpositive staining in mouse testicular Leydig cells. Results: The Fancd2os protein was predominantly expressed in mouse testicular Leydig cells and its expression increased with age. Fancd2os overexpression inhibited testosterone levels in TM3 Leydig cells, whereas knockdown of Fancd2os elevated testosteroneproduction. Fancd2os overexpression downregulated the levels of StAR, P450scc and 3β-HSD, while Fancd2os knockdown reversed this effect. Fancd2os overexpression promoted ultraviolet light-induced apoptosis of TM3 cells. In contrast, Fancd2os knockdown restrained apoptosis in TM3 cells. In vivo assays revealed that higher Fancd2os levels and mouse age were associated with increased apoptosis in Leydig cells and decreased serum testosterone levels. Pearson correlation analysis exhibited a strong positivecorrelation between the expression of Fancd2os and TUNEL-positive staining in mouse testicular Leydig cells. Conclusion: Our findings suggest that Fancd2os regulates testosterone synthesis via both steroidogenic enzymes and the apoptoticpathway.
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Hai-Xia Li,Yan Ma,Yu-Xiao Yan,Xin-Ke Zhai,Meng-Yu Xin,Tian Wang,Dong-Cao Xu,Yu-Tong Song,Chun-Dong Song,Cheng-Xue Pan 고려인삼학회 2023 Journal of Ginseng Research Vol.47 No.6
Background: Caveolin-1, the scaffolding protein of cholesterol-rich invaginations, plays an important rolein store-operated Ca2þ influx and its phosphorylation at Tyr14 (p-caveolin-1) is vital to mobilize protectionagainst myocardial ischemia (MI) injury. SOCE, comprising STIM1, ORAI1 and TRPC1, contributesto intracellular Ca2þ ([Ca2þ]i) accumulation in cardiomyocytes. The purified extract of steamed Panaxginseng (EPG) attenuated [Ca2þ]i overload against MI injury. Thus, the aim of this study was to investigatethe possibility of EPG affecting p-caveolin-1 to further mediate SOCE/[Ca2þ]i against MI injury in neonatalrat cardiomyocytes and a rat model. Methods: PP2, an inhibitor of p-caveolin-1, was used. Cell viability, [Ca2þ]i concentration were analyzedin cardiomyocytes. In rats, myocardial infarct size, pathological damages, apoptosis and cardiac fibrosiswere evaluated, p-caveolin-1 and STIM1 were detected by immunofluorescence, and the levels ofcaveolin-1, STIM1, ORAI1 and TRPC1 were determined by RT-PCR and Western blot. And, release of LDH,cTnI and BNP was measured. Results: EPG, ginsenosides accounting for 57.96%, suppressed release of LDH, cTnI and BNP, and protectedcardiomyocytes by inhibiting Ca2þ influx. And, EPG significantly relieved myocardial infarct size, cardiacapoptosis, fibrosis, and ultrastructure abnormality. Moreover, EPG negatively regulated SOCE viaincreasing p-caveolin-1 protein, decreasing ORAI1 mRNA and protein levels of ORAI1, TRPC1 and STIM1. More importantly, inhibition of the p-caveolin-1 significantly suppressed all of the above cardioprotectionof EPG. Conclusions: Caveolin-1 phosphorylation is involved in the protective effects of EPG against MI injury viaincreasing p-caveolin-1 to negatively regulate SOCE/[Ca2þ]i.
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