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5篇 您的检索式:作者名="Chunlan Long"
    题名 作者 年代 出处 被引量
1Retinoic acid can improve autophagy through depression of the PI3K-Akt-mTOR signaling pathway via RARαto restore spermatogenesis in cryptorchid infertile rats显示文摘Cryptorchidism-caused adult infertility is a common component of idiopathic reasons for male infertility.Retinoic acid(RA)has a vital effect on the spermatogenesis process.Here,we found that the expression of c-Kit,Stra8,and Sycp3 could be up-regulated via the activation of retinoic acid receptorα(RARα)after RA supplementation in neonatal cryptorchid infertile rats.We also demonstrated that the protein expression of PI3K,p-Akt/pan-Akt,and p-mTOR/mTOR was higher in cryptorchid than in normal testes,and could be suppressed with RA in vivo.After RA treatment in infertile cryptorchid testis in vivo,the levels of the autophagy proteins LC3 and Beclin1 increased and those of P62 decreased.Biotin tracer indicated that the permeability of blood-testis barrier(BTB)in cryptorchid rats decreased after RA administration.Additionally,after blocking the RARαwith AR7(an RARαantagonist)in testicle culture in vitro,we observed that compared with normal testes,the PI3K-Akt-mTOR signaling pathway and the autophagy pathway was increased and decreased,respectively,which were coincident with cryptorchisd testes in vivo.Additionally,the appropriate concentrations of RA treatment could depress the PI3K-Akt-mTOR signaling pathway and improve the autophagy pathway.The results confirmed that RA can rehabilitate BTB function and drive key protein levels in spermatogonial differentiation through depressing the PI3K-Akt-mTOR signaling pathway via RARα.Chunlan Long Yu Zhou Lianju Shen Yihang Yu Dong Hu Xing Liu Tao Lin Dawei He Tao Xu Deying Zhang Jing Zhu Guanghui Wei 2022Genes & Diseases2022,9,5:2
2Bioinformatic identification of key genes and molecular pathways in the spermatogenic process of cryptorchidism显示文摘This study aims to determine key genes and pathways that could play important roles in the spermatogenic process of patients with cryptorchidism.The gene expression profile data of GSE25518 was obtained from the Gene Expression Omnibus(GEO)database.Microarray data were analyzed using BRB-Array Tools to identify differentially expressed genes(DEGs)between high azoospermia risk(HAZR)patients and controls.In addition,other analytical methods were deployed,including hierarchical clustering analysis,class comparison between patients with HAZR and the normal control group,gene ontology(GO),Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway enrichment analysis,and the construction of a proteineprotein interaction(PPI)network.In total,1015 upregulated genes and 1650 downregulated genes were identified.GO and KEGG analysis revealed enrichment in terms of changes in the endoplasmic reticulum cellular component and the endoplasmic reticulum protein synthetic process in the HAZR group.Furthermore,the arachidonic acid pathway and mTOR pathway were also identified as important pathways,while RICTOR and GPX8 were indentified as key genes involved in the spermatogenic process of patients with cryptorchidism.In present study,we found that changes in the synthesis of endoplasmic reticulum proteins,arachidonic acid and the mTOR pathway are important in the incidence and spermatogenic process of cryptorchidism.GPX8 and RICTOR were also identified as key genes associated with cryptorchidism.Collectively,these data may provide novel clues with which to explore the precise etiology and mechanism underlying cryptorchidism and cryptorchidism-induced human infertility.Yu Zhou Deying Zhang Bo Liu Dong Hu Lianju Shen Chunlan Long Yihang Yu Tao Lin Xing Liu Dawei He Guanghui Wei 2019Genes & Diseases2019,6,4:1
3No Evidence for the Compensation Hypothesis in the Swelled Vent Frog(Feirana quadranus)显示文摘The compensation hypothesis predicts that if the left testis is defective e.g.due to developmental stress,the increased right testis serves a compensatory role,and thereby displaying testes asymmetry which can be a reliable indicator of male body condition.Here,to test the prediction of the compensation hypothesis,we analyzed difference in size between left testis and right testis and the relationship between testes asymmetry and male body condition in the swelled vent frog(Feirana quadranus).We found that the left testis was larger than right testis,displaying a significant directional asymmetry in testes size.Although testes mass was correlated with body condition,testes asymmetry was not correlated with body condition,which cannot provide evidence that the right testis had a compensatory function.Our findings suggest no evidence for the compensation hypothesis in this species due to lacking the compensatory function in right testis.Yingfeng YUE Long JIN Chunlan MAI Xiaofu HUANG Wenbo LIAO 2020Asian Herpetological Research2020,11,3:0
4Antitumor effect of Escherichia coli-derived outer membrane vesicles on neuroblastoma in vitro and in vivo显示文摘Bacterial outer membrane vesicles(OMVs)are spherical microbubbles that contain biological content and are produced by gram-negative bacteria.The use of OMVs as adjuvants for cancer immunotherapy or as drug carriers for targeted therapies has attracted the interest of many scholars.However,it is unclear whether OMVs can exert direct antitumor effects and whether OMVs can inhibit pediatric tumors.Here,we explore the potential of Escherichia coli-derived OMVs to directly suppress neuroblastoma.Our results demonstrate the antitumor effects of OMVs in vitro and in vivo,and no serious adverse reactions were observed.OMV uptake into the cytoplasm and nucleus directly decreases cell stemness,DNA damage,apoptosis and cell cycle arrest,which may be the mechanisms bywhichOMVs suppress tumors.Ourresultsdemonstrate thepotential of bacterial OMVs to be usedas antitumor adjuvant therapies,increasing the number of candidates for the development of cancer therapies in the future.More relevant studies are urgently needed to demonstrate the efficacy and safety of OMVs.Liming Jin Zhaoxia Zhang Xiaojun Tan Zhaoying Wang Bo Tang Zhang Wang Mujie Li Tao Mi Lianju Shen Chunlan Long Guanghui Wei Dawei He 2022Acta Biochimica et Biophysica Sinica2022,54,9:0
5X-box binding protein 1 caused an imbalance in pyroptosis and mitophagy in immature rats with di-(2-ethylhexyl)phthalate-induced testis toxicity显示文摘As a widely used plasticizer,di-(2-ethylhexyl)phthalate(DEHP)is known to induce significant testicular injury.However,the potential mechanism and effects of pubertal exposure to DEHP on testis development remain unclear.In vivo,postnatal day(PND)21 male rats were gavaged with 0,250,and 500 mg/kg DEHP for ten days.Damage to the seminiferous epithelium and disturbed spermatogenesis were observed after DEHP exposure.Meanwhile,oxidative stress-induced injury and pyroptosis were activated.Both endoplasmic reticulum(ER)stress and mitophagy were involved in this process.Monoethylhexyl phthalate(MEHP)was used as the biometabolite of DEHP in vitro.The GC-1 and GC-2 cell lines were exposed to 0,100μM,200μM,and 400μM MEHP for 24 h.Reactive oxygen species(ROS)generation,oxidative stress damage,ER stress,mitophagy,and pyroptosis were significantly increased after MEHP exposure.The ultrastructure of the ER and mitochondria was destroyed.X-box binding protein 1(XBP1)was observed to be activated and translocated into the nucleus.ROS generation was inhibited by acetylcysteine.The levels of antioxidative stress,ER stress,mitophagy,and pyroptosis were decreased as well.After the administration of the ER stress inhibitor 4-phenyl-butyric acid,both mitophagy and pyroptosis were inhibited.Toyocamycin-induced XBP1 down-regulation decreased the levels of mitophagy and pyroptosis.The equilibrium between pyroptosis and mitophagy was disturbed by XBP1 accumulation.In summary,our findings confirmed that DEHP induced a ROS-mediated imbalance in pyroptosis and mitophagy in immature rat testes via XBP1.Moreover,XBP1 might be the key target in DEHP-related testis dysfunction.Yifan Hong Xiazhu Zhou Qi Li Jing Chen Yuexin Wei Chunlan Long Lianju Shen Xiangqin Zheng Dinggang Li Xia Wang Chenjun Yu Shengde Wu Guanghui Wei 2024Genes & Diseases2024,11,2:0
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