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作 者:Cui-Hao Song Rui Wang Zhen-Kai Zhao Yuan Zhang Jie Sun Xu Zhang Xiang-Yu Ding Jia Bai Xiao-Qiang Liang Xuan-Jin Wei Xiao-Ling Liu Tao Yang Xin-Lin Liang Cheng-Xin Li Bi-Wen Lin
机构地区:[1]Department of Dermatology,PLA General Hospital,Beijing 100853,China [2]Department of Clinical Laboratory,PLA General Hospital,Beijing 100853,China [3]Department of Dermatology,Southern Medical University,Guangzhou,Guangdong 510515,China
出 处:《International Journal of Dermatology and Venereology》2024年第3期121-130,共10页国际皮肤性病学杂志(英文)
基 金:supported by Beijing Natural Science Foundation(No.7212097).
摘 要:Objective:Psoriasis is associated with a high prevalence of metabolic syndrome(MS),and patients with concomitant psoriasis and MS are more severely affected and less responsive to treatment.However,the molecular mechanisms behind these effects are unknown.Recent studies have shown that leptin may serve as a molecular link between psoriasis and MS,suggesting that high leptin concentrations may exacerbate psoriasis.However,the molecular mechanism of this effect is still unclear.We aimed to investigate the effect of leptin on autophagy in patients with psoriasis.Methods:From January 2021 to June 2022 in PLA General Hospital,we enrolled 51 patients with psoriasis,including 21 patients with MS and 30 without MS,and 30 healthy controls who had undergone nevus surgery.We measured the epidermal leptin,P62,and LC3B concentrations of patients by immunohistochemistry,and measured the serum leptin concentration by enzyme-linked immunosorbent assay.We then performed correlation analyses to compare these proteins’concentrations between patients with concomitant psoriasis and MS,patients with psoriasis alone,and healthy control groups.Additionally,we performed western blotting after in vitro culture of HaCaT cells with different concentrations of leptin and measured the expression levels of the autophagy markers Beclin1,LC3B,and P62;the differentiation markers K10,K16,and K17;and PI3K/AKT/mTOR signaling pathway-related proteins of HaCat cells.Next,we transfected ATG5 into HaCaT cells to revert autophagy and used the specific PI3K inhibitor LY294002 to block PI3K/AKT/mTOR signaling.The expression levels of K10,K16,and K17 of HaCat cells were again measured.One-way analysis of variance was used for the comparison of means of multiple samples,and LSD-t post hoc test was used for comparison between the 2 groups.The counting data were analyzed by the chisquare test.Correlations were evaluated by Pearson correlation analysis.Results:The serum leptin concentration was significantly higher in patients with concomitant psoriasis and M
关 键 词:PSORIASIS metabolic syndrome LEPTIN AUTOPHAGY keratinocyte differentiation signal pathway PI3K/AKT/mTOR
分 类 号:R758.63[医药卫生—皮肤病学与性病学]
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