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作 者:李园园 党红星[2] Li Yuanyuan;Dang Hongxing(People's Hospital of Changshou,Chongqing Chongqing 401220;Department of PICU,Children's Hospital ofChongqing Medical University,Chongqing Key Laboratory of Pediatrics,Ministry of Education Key Labortory of Child Development and Disorders,National Clinical Research Center for Child Health and Disorders,China Intermational Science and Technology Cooperation base ofChild development and Critical Disorders,Chonging,400014)
机构地区:[1]重庆市长寿区人民医院,重庆401220 [2]儿童发育重大疾病国家国际科技合作基地,国家儿童健康与疾病临床医学研究中心,儿童发育疾病研究教育部重点实验室,儿科学重庆市重点实验室,重庆医科大学附属儿童医院重症医学科,重庆400014
出 处:《基因组学与应用生物学》2020年第2期929-933,共5页Genomics and Applied Biology
摘 要:婴儿血管瘤是一种血管瘤,表现出独特的快速生长的特征,然后随着时间而消退。血管瘤来自CD133+干细胞,当植入免疫缺陷小鼠时,它们分化成内皮细胞。同样克隆扩增的干细胞也产生脂肪细胞,从而重现血管瘤的消退期。本研究主要阐明了使用血管瘤来源的干细胞(hemSC)增殖和分化的内在机制。本研究发现血小板衍生生长因子(PDGF)在增殖期升高并可能抑制脂肪细胞分化。hemSC表达高水平的PDGF-b并且在基础(未刺激)条件下显示PDGF受体的持续酪氨酸磷酸化。PDGF受体信号传导的抑制导致hemSCs中的脂肪生成增强。此外,hemSCs暴露于外源性PDGF-b降低了脂肪含量和脂肪细胞特异性转录因子的表达。总之,本研究将PDGF信号传导鉴定为血管瘤退化的内在负调节因子,并强调了破坏PDGF信号传导治疗血管瘤的治疗潜力。Infant hemangioma is a kind of hemangioma,which shows unique characteristics of rapid growth and then subsides over time.Hemangiomas are derived from CD133+stem cells,which differentiate into endothelial cells when implanted into immunodeficient mice.Likewise,cloned and amplified stem cells also produce adipocytes,thus reproducing the regression phase of hemangioma.In this study,we mainly elucidated the intrinsic mechanism of proliferation and differentiation of hemSC derived from hemangioma.The research found that platelet-derived growth factor(PDGF)increased in the proliferative phase and may inhibit adipocyte differentiation.HemSC expressed high levels of PDGF-b and showed persistent tyrosine phosphorylation of PDGF receptors under basic(unstimulated)conditions.Inhibition of PDGF receptor signaling leads to increased fat production in hemSCs.In addition,hemSCs exposure to exogenous PDGF-b reduced fat content and adipocyte-specific transcription factor expression.In conclusion,this study identified PDGF signal transduction as an intrinsic negative regulator of hemangioma degeneration and highlighted the therapeutic potential of destroying PDGF signal transduction in the treatment of hemangioma.
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