Traumatic brain injury （TBI） results in a range of neuroinflam- matory events that vary depending on the type and extent of in- jury. Central to this is the activation of tissue resident microglia and infiltration o...Traumatic brain injury （TBI） results in a range of neuroinflam- matory events that vary depending on the type and extent of in- jury. Central to this is the activation of tissue resident microglia and infiltration of peripheral macrophages, which phagocytose debris and/or secrete a range of cytokines, chemokines and oth- er factors which modify the injured environment to promote or inhibit repair （Schwartz et al., 2013）. The reactive macro- phages/microglia are broadly divided into two categories.展开更多
Background:Hepatocellular carcinoma(HCC)is one of the most prevalent human cancers with high mortality.Long non-coding RNA heart and neural crest derivatives expressed 2 anti-sense 1(HAND2-AS1)is down-regulated in sev...Background:Hepatocellular carcinoma(HCC)is one of the most prevalent human cancers with high mortality.Long non-coding RNA heart and neural crest derivatives expressed 2 anti-sense 1(HAND2-AS1)is down-regulated in several cancers including HCC,yet the precise mechanisms how HAND2-AS1 regulates cell survival in HCC remains poorly understood.Methods:The expression levels of HAND2-AS1 and miR-300 were measured using quantitative real-time PCR.The protein levels of suppressor of cytokine signaling 5(SOCS5),Bcl-2,Bax and cleaved caspase-3 were determined by Western blot.Cell viability and cell proliferation were assessed using cell counting kit-8 and clone formation assay,respectively.Cell apoptosis was detected using flow cytometry.The interactions between HAND2-AS1 and miR-300,miR-300 and SOCS5 were validated using luciferase reporter assay.Results:HAND2-AS1 was down-regulated in HCC tissues and cell lines,and the expression level of HAND2-AS1 was positively correlated to patient survival.HAND2-AS1 over-expression reduced viability and proliferation in HCC cells.Elevated HAND2-AS1 level induced apoptosis in HCC cells,accompanied with increased Bax and cleaved caspase-3 levels and decreased Bcl-2 level.We also validated that HAND2-AS1 acted as a sponge of miR-300,and there was a negative correlation between expression levels of HAND2-AS1 and miR-300 in HCC tissues.Furthermore,we found that SOCS5 was a downstream target of miR-300.In addition,miR-300 mimics abolished HAND2-AS1-mediated inhibition of cell viability and proliferation.miR-300 mimics also reversed the HAND2-AS1-induced apoptosis in HCC cells.Conclusion:lncRNA HAND2-AS1 inhibits proliferation in HCC through regulating miR-300/SOCS5 axis.展开更多
目的探讨细胞因子信号传导抑制蛋白2(SOCS2)和SOCS5在儿童过敏性紫癜(HSP)中的表达及其意义。方法应用逆转录聚合酶链反应检测HSP患儿(36例)和正常健康对照儿童(17例)外周血单个核细胞中SOCS2和SOCS5 m RNA表达水平。结果 HSP患儿SOCS2...目的探讨细胞因子信号传导抑制蛋白2(SOCS2)和SOCS5在儿童过敏性紫癜(HSP)中的表达及其意义。方法应用逆转录聚合酶链反应检测HSP患儿(36例)和正常健康对照儿童(17例)外周血单个核细胞中SOCS2和SOCS5 m RNA表达水平。结果 HSP患儿SOCS2和SOCS5 m RNA表达水平高于对照儿童(P<0.05)。混合型HSP患儿SOCS2和SOCS5 m RNA表达水平较单纯型患儿升高(P<0.05)。HSP患儿SOCS2和SOCS5 m RNA表达水平无性别差异(P>0.05)。结论 SOCS2、SOCS5可能参与儿童HSP的发病。展开更多
目的:研究肥胖小鼠及正常小鼠不同周龄下丘脑组织SH2B1(adapter protein with a Src-homology 2 domain),细胞因子信号转导抑制蛋白3(the suppressor of cytokine signaling-3,SOCS3),蛋白质酪氨酸磷酸酶1B(proteintyrosine phosphatase...目的:研究肥胖小鼠及正常小鼠不同周龄下丘脑组织SH2B1(adapter protein with a Src-homology 2 domain),细胞因子信号转导抑制蛋白3(the suppressor of cytokine signaling-3,SOCS3),蛋白质酪氨酸磷酸酶1B(proteintyrosine phosphatase 1B,PTP1B)和神经肽Y(neturopetide Y,NPY)表达的变化规律及其与血清瘦素及胰岛素水平的关系。方法:选用健康C57BL/6乳鼠制作肥胖动物模型,计算Lee’s指数及稳态模型胰岛素抵抗指数。荧光定量RT-PCR法检测下丘脑SH2B1,SOCS3及PTP1B mRNA表达量,Western印迹检测下丘脑SH2B1和NPY蛋白表达量。结果:与同周龄对照组小鼠相比,肥胖组小鼠下丘脑组织SH2B1 mRNA表达减少,SOCS3及PTP1B mRNA表达增加;Western印迹结果显示:肥胖组小鼠SH2B1蛋白表达水平较对照组下降,NPY表达升高。直线相关分析显示:血清瘦素和血清空腹胰岛素水平与SH2B1 mRNA表达呈负相关,与SOCS3及PTP1B mRNA表达正相关。结论:SH2B1,SOCS3,PTP1B及NPY是肥胖发生、发展过程中的关键因子。展开更多
基金supported by the National Health and Medical Research Council of AustraliaProject grant 1045125 and Fellowship(to AMT)628344support from Stem Cells Australia
文摘Traumatic brain injury （TBI） results in a range of neuroinflam- matory events that vary depending on the type and extent of in- jury. Central to this is the activation of tissue resident microglia and infiltration of peripheral macrophages, which phagocytose debris and/or secrete a range of cytokines, chemokines and oth- er factors which modify the injured environment to promote or inhibit repair （Schwartz et al., 2013）. The reactive macro- phages/microglia are broadly divided into two categories.
文摘Background:Hepatocellular carcinoma(HCC)is one of the most prevalent human cancers with high mortality.Long non-coding RNA heart and neural crest derivatives expressed 2 anti-sense 1(HAND2-AS1)is down-regulated in several cancers including HCC,yet the precise mechanisms how HAND2-AS1 regulates cell survival in HCC remains poorly understood.Methods:The expression levels of HAND2-AS1 and miR-300 were measured using quantitative real-time PCR.The protein levels of suppressor of cytokine signaling 5(SOCS5),Bcl-2,Bax and cleaved caspase-3 were determined by Western blot.Cell viability and cell proliferation were assessed using cell counting kit-8 and clone formation assay,respectively.Cell apoptosis was detected using flow cytometry.The interactions between HAND2-AS1 and miR-300,miR-300 and SOCS5 were validated using luciferase reporter assay.Results:HAND2-AS1 was down-regulated in HCC tissues and cell lines,and the expression level of HAND2-AS1 was positively correlated to patient survival.HAND2-AS1 over-expression reduced viability and proliferation in HCC cells.Elevated HAND2-AS1 level induced apoptosis in HCC cells,accompanied with increased Bax and cleaved caspase-3 levels and decreased Bcl-2 level.We also validated that HAND2-AS1 acted as a sponge of miR-300,and there was a negative correlation between expression levels of HAND2-AS1 and miR-300 in HCC tissues.Furthermore,we found that SOCS5 was a downstream target of miR-300.In addition,miR-300 mimics abolished HAND2-AS1-mediated inhibition of cell viability and proliferation.miR-300 mimics also reversed the HAND2-AS1-induced apoptosis in HCC cells.Conclusion:lncRNA HAND2-AS1 inhibits proliferation in HCC through regulating miR-300/SOCS5 axis.
文摘目的探讨细胞因子信号传导抑制蛋白2(SOCS2)和SOCS5在儿童过敏性紫癜(HSP)中的表达及其意义。方法应用逆转录聚合酶链反应检测HSP患儿(36例)和正常健康对照儿童(17例)外周血单个核细胞中SOCS2和SOCS5 m RNA表达水平。结果 HSP患儿SOCS2和SOCS5 m RNA表达水平高于对照儿童(P<0.05)。混合型HSP患儿SOCS2和SOCS5 m RNA表达水平较单纯型患儿升高(P<0.05)。HSP患儿SOCS2和SOCS5 m RNA表达水平无性别差异(P>0.05)。结论 SOCS2、SOCS5可能参与儿童HSP的发病。
文摘目的:研究肥胖小鼠及正常小鼠不同周龄下丘脑组织SH2B1(adapter protein with a Src-homology 2 domain),细胞因子信号转导抑制蛋白3(the suppressor of cytokine signaling-3,SOCS3),蛋白质酪氨酸磷酸酶1B(proteintyrosine phosphatase 1B,PTP1B)和神经肽Y(neturopetide Y,NPY)表达的变化规律及其与血清瘦素及胰岛素水平的关系。方法:选用健康C57BL/6乳鼠制作肥胖动物模型,计算Lee’s指数及稳态模型胰岛素抵抗指数。荧光定量RT-PCR法检测下丘脑SH2B1,SOCS3及PTP1B mRNA表达量,Western印迹检测下丘脑SH2B1和NPY蛋白表达量。结果:与同周龄对照组小鼠相比,肥胖组小鼠下丘脑组织SH2B1 mRNA表达减少,SOCS3及PTP1B mRNA表达增加;Western印迹结果显示:肥胖组小鼠SH2B1蛋白表达水平较对照组下降,NPY表达升高。直线相关分析显示:血清瘦素和血清空腹胰岛素水平与SH2B1 mRNA表达呈负相关,与SOCS3及PTP1B mRNA表达正相关。结论:SH2B1,SOCS3,PTP1B及NPY是肥胖发生、发展过程中的关键因子。
