Epidemiological studies have shown a high prevalence of low serum testosterone levels in men with cardiovascular disease. Moreover, the tyrosine kinase receptor Axl, the ligand of which is growth arrest-specific prote...Epidemiological studies have shown a high prevalence of low serum testosterone levels in men with cardiovascular disease. Moreover, the tyrosine kinase receptor Axl, the ligand of which is growth arrest-specific protein 6 （GAS6）, is expressed in the vasculature, and serum GAS6 levels are associated with endothelial dysfunction and cardiovascular events. Testosterone regulates GAS6 gene transcription directly, which inhibits calcification of vascular smooth muscle cells and provides a mechanistic insight into the cardioprotective action of androgens. This study was designed to determine the correlation between serum GAS6 and testosterone levels in male patients with coronary heart disease （CHD）. We recruited 225 patients with CHD and 102 apparently healthy controls, Serum concentrations of GAS6 and soluble Axl were quantified by an enzyme-linked immunosorbent assay. Levels of high-sensitivity C-reactive protein, testosterone, estradiol, and other routine biochemical markers were also measured. Testosterone decreased from 432.69 ± 14.40 to 300.76± 6.23 ng d1-1 （P 〈 0.001） and GAS6 decreased from 16.20± 0.31 to 12.51 ± 0.19 ng ml-1 （P 〈 0.001） in patients with CHD, compared with control subjects. Multiple linear regression analysis showed that serum testosterone and GAS6 levels were positively associated in male patients with CHD. Alterations in GAS6 levels may influence the development of CHD. Downregulation of GAS6/Axl signaling in the presence of low sex hormone levels during disease progression is a potential mechanism by which GAS6 affects CHD. This study provides novel results regarding the influence of sex hormones on serum GAS6 levels in patients with CHD.展开更多
目的探讨生长停滞特异性蛋白6(growth arrest-specifi c protein 6,Gas6)调控巨噬细胞极化在创面修复中的作用。方法采用清洁级雄性B6小鼠随机(随机数字法)分为正常组、皮肤缺损组、皮肤缺损组+生理盐水组、皮肤缺损+Gas6(1μg)组、皮...目的探讨生长停滞特异性蛋白6(growth arrest-specifi c protein 6,Gas6)调控巨噬细胞极化在创面修复中的作用。方法采用清洁级雄性B6小鼠随机(随机数字法)分为正常组、皮肤缺损组、皮肤缺损组+生理盐水组、皮肤缺损+Gas6(1μg)组、皮肤缺损+Gas6(5μg)组和皮肤缺损+Gas6(10μg)组,每组16只,其中10只用来观察各组小鼠皮肤创面愈合情况,剩余6只于造模后第5天分离创面组织巨噬细胞,酶联免疫吸附法(ELISA)检测IL-6,IL-10水平,RTPCR检测精氨酸酶-1(Arg-1)、诱导性一氧化氮合酶(iNOS)的mRNA表达水平,流式细胞术检测巨噬细胞M1型标记物CD197和M2型标记物CD163、F4/80的表达,HE染色检测皮肤创面病理改变,Masson染色分析创面肉芽组织及胶原沉积情况。结果皮肤缺损造模后第3天伤口表面开始结痂。Gas6治疗组伤口面积小于PBS组,伤口愈合情况优于PBS组。与正常组相比,皮肤缺损组小鼠第5天巨噬细胞CD197的比例升高明显(P=0.0049)、CD163和F4/80双阳性的比例明显降低(P=0.0086)、IL-6水平明显升高(P=0.0013)、IL-10水平明显升高(P=0.0014)、iNOS mRNA水平明显升高(P=0.008)、Arg-1 mRNA水平明显降低(P=0.0121)、组织炎症浸润加重。与PBS对照组相比,Gas6治疗组CD197的比例明显下降(P=0.000)、CD163和F4/80双阳性比例明显升高(P=0.000)、IL-6水平明显降低(P=0.000)、IL-10水平明显升高(P=0.0003)、iNOS mRNA水平明显降低(P=0.0018)、Arg-1 mRNA水平明显升高(P=0.001)、组织炎性细胞减少,胶原纤维增多。结论Gas6可促使皮肤缺损小鼠巨噬细胞由M1向M2转化,加快缺损皮肤创面愈合。展开更多
目的:探讨血浆CA125、纤维蛋白原(fibrinogen,FIB)、D-二聚体(D-dimer,D-D)及血清生长停滞特异性蛋白6(growth arrest-specific protein 6,Gas6)检测在子痫前期并发胎盘早剥患者中的临床意义。方法:本文为回顾性研究,将2017年12月-2019...目的:探讨血浆CA125、纤维蛋白原(fibrinogen,FIB)、D-二聚体(D-dimer,D-D)及血清生长停滞特异性蛋白6(growth arrest-specific protein 6,Gas6)检测在子痫前期并发胎盘早剥患者中的临床意义。方法:本文为回顾性研究,将2017年12月-2019年12月在笔者所在医院妇产科门诊或住院治疗的76例子痫前期并发胎盘早剥患者设为并发胎盘早剥组,将2017年12月-2019年12月在笔者所在医院妇产科门诊或住院治疗的104例子痫前期未并发胎盘早剥患者设为未并发胎盘早剥组。另选取正常妊娠且孕周满37周的30例孕妇作为对照组。比较三组血浆CA125、FIB、D-D水平、血清Gas6水平,分析子痫前期患者血浆CA125、FIB、D-D水平、血清Gas6水平异常与并发胎盘早剥情况;依据子痫前期严重程度将患者分为轻度组(n=68)和重度组(n=112),比较两组CA125、FIB、D-D、Gas6水平及并发胎盘早剥情况,采用Pearson相关性分析CA125、FIB、D-D、Gas6与子痫前期并发胎盘早剥的相关性。结果:三组血浆CA125、FIB、D-D及血清Gas6水平比较,差异均有统计学意义(P<0.001);并发胎盘早剥组和未并发胎盘早剥组血浆CA125、FIB、D-D水平均明显高于对照组,血清Gas6水平明显低于对照组(P<0.001),且并发胎盘早剥组血浆CA125、FIB、D-D水平均明显高于未并发胎盘早剥组,血清Gas6水平明显低于未并发胎盘早剥组,差异有统计学意义(P<0.001)。三项指标同时异常者,胎盘早剥发生率高达87.50%,上述4项指标同时异常者胎盘早剥发生率高达90.91%,而单一指标异常者胎盘早剥发生率较低。重度组血浆CA125、FIB、D-D水平均明显高于轻度组,血清Gas6水平明显低于轻度组,差异有统计学意义(P<0.05)。重度组血浆CA125、D-D水平及血清Gas6水平异常率及胎盘早剥发生率均高于轻度组,差异有统计学意义(P<0.01)。Pearson相关性分析显示,血浆CA125、FIB、D-D水平与子痫前期并发胎盘早剥呈正相关,�展开更多
目的研究重组人生长停滞特异性蛋白6(Gas6)对大鼠肾上腺嗜铬细胞瘤PC12细胞氧糖剥夺/复糖复氧是否有保护作用及可能机制。方法体外培养PC12细胞,随机分为3组:正常对照组(Control组)、氧糖剥夺/复糖复氧模型组(OGD/R组)、Gas6治疗组(Gas6...目的研究重组人生长停滞特异性蛋白6(Gas6)对大鼠肾上腺嗜铬细胞瘤PC12细胞氧糖剥夺/复糖复氧是否有保护作用及可能机制。方法体外培养PC12细胞,随机分为3组:正常对照组(Control组)、氧糖剥夺/复糖复氧模型组(OGD/R组)、Gas6治疗组(Gas6组)。应用MTT法测定细胞活力,比色法测定乳酸脱氢酶(LDH)释放量,分光光度法检测半胱氨酸蛋白酶(Caspase-3)活性变化,流式细胞仪检测细胞凋亡率。结果OGD/R组与Control组比较细胞活力降低,LDH释放量、Caspase-3活性和凋亡率增加(<0.01)。而Gas6组与OGD/R组比较,细胞活力增加,LDH释放量、Caspase-3活性和凋亡率均减低(<0.01)。结论 Gas 6对PC12细胞氧糖剥夺/复糖复氧的保护作用可能与抑制Caspase-3活化抗细胞凋亡相关。展开更多
文摘Epidemiological studies have shown a high prevalence of low serum testosterone levels in men with cardiovascular disease. Moreover, the tyrosine kinase receptor Axl, the ligand of which is growth arrest-specific protein 6 （GAS6）, is expressed in the vasculature, and serum GAS6 levels are associated with endothelial dysfunction and cardiovascular events. Testosterone regulates GAS6 gene transcription directly, which inhibits calcification of vascular smooth muscle cells and provides a mechanistic insight into the cardioprotective action of androgens. This study was designed to determine the correlation between serum GAS6 and testosterone levels in male patients with coronary heart disease （CHD）. We recruited 225 patients with CHD and 102 apparently healthy controls, Serum concentrations of GAS6 and soluble Axl were quantified by an enzyme-linked immunosorbent assay. Levels of high-sensitivity C-reactive protein, testosterone, estradiol, and other routine biochemical markers were also measured. Testosterone decreased from 432.69 ± 14.40 to 300.76± 6.23 ng d1-1 （P 〈 0.001） and GAS6 decreased from 16.20± 0.31 to 12.51 ± 0.19 ng ml-1 （P 〈 0.001） in patients with CHD, compared with control subjects. Multiple linear regression analysis showed that serum testosterone and GAS6 levels were positively associated in male patients with CHD. Alterations in GAS6 levels may influence the development of CHD. Downregulation of GAS6/Axl signaling in the presence of low sex hormone levels during disease progression is a potential mechanism by which GAS6 affects CHD. This study provides novel results regarding the influence of sex hormones on serum GAS6 levels in patients with CHD.
文摘目的探讨生长停滞特异性蛋白6(growth arrest-specifi c protein 6,Gas6)调控巨噬细胞极化在创面修复中的作用。方法采用清洁级雄性B6小鼠随机(随机数字法)分为正常组、皮肤缺损组、皮肤缺损组+生理盐水组、皮肤缺损+Gas6(1μg)组、皮肤缺损+Gas6(5μg)组和皮肤缺损+Gas6(10μg)组,每组16只,其中10只用来观察各组小鼠皮肤创面愈合情况,剩余6只于造模后第5天分离创面组织巨噬细胞,酶联免疫吸附法(ELISA)检测IL-6,IL-10水平,RTPCR检测精氨酸酶-1(Arg-1)、诱导性一氧化氮合酶(iNOS)的mRNA表达水平,流式细胞术检测巨噬细胞M1型标记物CD197和M2型标记物CD163、F4/80的表达,HE染色检测皮肤创面病理改变,Masson染色分析创面肉芽组织及胶原沉积情况。结果皮肤缺损造模后第3天伤口表面开始结痂。Gas6治疗组伤口面积小于PBS组,伤口愈合情况优于PBS组。与正常组相比,皮肤缺损组小鼠第5天巨噬细胞CD197的比例升高明显(P=0.0049)、CD163和F4/80双阳性的比例明显降低(P=0.0086)、IL-6水平明显升高(P=0.0013)、IL-10水平明显升高(P=0.0014)、iNOS mRNA水平明显升高(P=0.008)、Arg-1 mRNA水平明显降低(P=0.0121)、组织炎症浸润加重。与PBS对照组相比,Gas6治疗组CD197的比例明显下降(P=0.000)、CD163和F4/80双阳性比例明显升高(P=0.000)、IL-6水平明显降低(P=0.000)、IL-10水平明显升高(P=0.0003)、iNOS mRNA水平明显降低(P=0.0018)、Arg-1 mRNA水平明显升高(P=0.001)、组织炎性细胞减少,胶原纤维增多。结论Gas6可促使皮肤缺损小鼠巨噬细胞由M1向M2转化,加快缺损皮肤创面愈合。
文摘目的:探讨血浆CA125、纤维蛋白原(fibrinogen,FIB)、D-二聚体(D-dimer,D-D)及血清生长停滞特异性蛋白6(growth arrest-specific protein 6,Gas6)检测在子痫前期并发胎盘早剥患者中的临床意义。方法:本文为回顾性研究,将2017年12月-2019年12月在笔者所在医院妇产科门诊或住院治疗的76例子痫前期并发胎盘早剥患者设为并发胎盘早剥组,将2017年12月-2019年12月在笔者所在医院妇产科门诊或住院治疗的104例子痫前期未并发胎盘早剥患者设为未并发胎盘早剥组。另选取正常妊娠且孕周满37周的30例孕妇作为对照组。比较三组血浆CA125、FIB、D-D水平、血清Gas6水平,分析子痫前期患者血浆CA125、FIB、D-D水平、血清Gas6水平异常与并发胎盘早剥情况;依据子痫前期严重程度将患者分为轻度组(n=68)和重度组(n=112),比较两组CA125、FIB、D-D、Gas6水平及并发胎盘早剥情况,采用Pearson相关性分析CA125、FIB、D-D、Gas6与子痫前期并发胎盘早剥的相关性。结果:三组血浆CA125、FIB、D-D及血清Gas6水平比较,差异均有统计学意义(P<0.001);并发胎盘早剥组和未并发胎盘早剥组血浆CA125、FIB、D-D水平均明显高于对照组,血清Gas6水平明显低于对照组(P<0.001),且并发胎盘早剥组血浆CA125、FIB、D-D水平均明显高于未并发胎盘早剥组,血清Gas6水平明显低于未并发胎盘早剥组,差异有统计学意义(P<0.001)。三项指标同时异常者,胎盘早剥发生率高达87.50%,上述4项指标同时异常者胎盘早剥发生率高达90.91%,而单一指标异常者胎盘早剥发生率较低。重度组血浆CA125、FIB、D-D水平均明显高于轻度组,血清Gas6水平明显低于轻度组,差异有统计学意义(P<0.05)。重度组血浆CA125、D-D水平及血清Gas6水平异常率及胎盘早剥发生率均高于轻度组,差异有统计学意义(P<0.01)。Pearson相关性分析显示,血浆CA125、FIB、D-D水平与子痫前期并发胎盘早剥呈正相关,�
文摘目的研究重组人生长停滞特异性蛋白6(Gas6)对大鼠肾上腺嗜铬细胞瘤PC12细胞氧糖剥夺/复糖复氧是否有保护作用及可能机制。方法体外培养PC12细胞,随机分为3组:正常对照组(Control组)、氧糖剥夺/复糖复氧模型组(OGD/R组)、Gas6治疗组(Gas6组)。应用MTT法测定细胞活力,比色法测定乳酸脱氢酶(LDH)释放量,分光光度法检测半胱氨酸蛋白酶(Caspase-3)活性变化,流式细胞仪检测细胞凋亡率。结果OGD/R组与Control组比较细胞活力降低,LDH释放量、Caspase-3活性和凋亡率增加(<0.01)。而Gas6组与OGD/R组比较,细胞活力增加,LDH释放量、Caspase-3活性和凋亡率均减低(<0.01)。结论 Gas 6对PC12细胞氧糖剥夺/复糖复氧的保护作用可能与抑制Caspase-3活化抗细胞凋亡相关。
