目的探索FKBP12.6基因敲除对葡聚糖硫酸钠诱导小鼠急性结肠炎模型结肠动力的影响及其初步机制。方法分别提取FKBP12.6基因敲除(knock-out,KO)组小鼠及野生小鼠(wild-type,WT)组结肠平滑肌m RNA,并利用反转录、RTPCR检测,证明FKBP12.6在...目的探索FKBP12.6基因敲除对葡聚糖硫酸钠诱导小鼠急性结肠炎模型结肠动力的影响及其初步机制。方法分别提取FKBP12.6基因敲除(knock-out,KO)组小鼠及野生小鼠(wild-type,WT)组结肠平滑肌m RNA,并利用反转录、RTPCR检测,证明FKBP12.6在野生型小鼠结肠平滑肌中表达。选择8~12周龄、雌雄比4∶9的野生型小鼠及与其年龄、性别相匹配同窝对照FKBP12.6基因敲除小鼠各26只,分别将其随机分为对照组及结肠炎组,即野生型对照组、野生型结肠炎组、基因敲除对照组、基因敲除结肠炎组,每组各13只。两结肠炎组小鼠均通过饮用3%葡聚糖硫酸钠(DSS)溶液7 d诱导急性结肠炎模型。对比两结肠炎组小鼠临床表现、体质量减轻程度、结肠长度。测定4组小鼠离体结肠环形肌条静息状态下收缩情况。利用蛋白印迹方法检测结肠平滑肌钙通路相关蛋白(三磷酸肌醇受体1、受磷蛋白、大电导钙激活钾通道)表达。结果 KO对照组与WT对照组相比,结肠长度无差异。WT结肠炎组及KO结肠炎组临床表现、体质量减轻程度、结肠长度无差异。静息状态下,WT对照组及KO对照组结肠收缩频率无差异;WT结肠炎组较KO结肠炎组结肠自发收缩频率明显加快[(15.22±2.90)次/5 min vs(2.10±0.38)次/5 min,n=9,P<0.01];WT结肠炎组较WT对照组结肠自发收缩频率加快[(15.22±2.90)次/5 min vs(3.78±1.64)次/5 min,n=9,P<0.01];而KO结肠炎组较KO对照组结肠收缩频率无明显变化。蛋白印迹结果表明WT对照组与KO对照组IP3R1、PLB、BKCa无差异。在两结肠炎组中,KO组较WT组IP3R1表达减少(0.56±0.14 vs 0.84±0.09,P<0.05),BKCa表达上调(0.97±0.14 vs 0.53±0.13,P<0.05),PLB表达无统计学差异。结论 FKBP12.6敲除对DSS诱导小鼠结肠炎模型临床表现、体质量及结肠长度变化程度无影响。FKBP12.6敲除后DSS诱导小鼠结肠炎模型结肠平滑肌收缩频率接近野生对照组小鼠。展开更多
Male mice deficient in FKBP12.6 display cardiac hypertrophy, but the underlying mechanism is still unclear. Here we report that the cardiac hypertrophy is a physiological response
Ca2+ release through ryanodine receptors (RyRs) plays an important role in excitation-contraction coupling in heart and smooth muscle. FKBP12.6 proteins
FK506 binding protein 12.6 (FKBP12.6) is the protein in the ryanodine receptor complex, but its function is controversial in different reported work. Some conclude that FKBP12.
文摘目的探索FKBP12.6基因敲除对葡聚糖硫酸钠诱导小鼠急性结肠炎模型结肠动力的影响及其初步机制。方法分别提取FKBP12.6基因敲除(knock-out,KO)组小鼠及野生小鼠(wild-type,WT)组结肠平滑肌m RNA,并利用反转录、RTPCR检测,证明FKBP12.6在野生型小鼠结肠平滑肌中表达。选择8~12周龄、雌雄比4∶9的野生型小鼠及与其年龄、性别相匹配同窝对照FKBP12.6基因敲除小鼠各26只,分别将其随机分为对照组及结肠炎组,即野生型对照组、野生型结肠炎组、基因敲除对照组、基因敲除结肠炎组,每组各13只。两结肠炎组小鼠均通过饮用3%葡聚糖硫酸钠(DSS)溶液7 d诱导急性结肠炎模型。对比两结肠炎组小鼠临床表现、体质量减轻程度、结肠长度。测定4组小鼠离体结肠环形肌条静息状态下收缩情况。利用蛋白印迹方法检测结肠平滑肌钙通路相关蛋白(三磷酸肌醇受体1、受磷蛋白、大电导钙激活钾通道)表达。结果 KO对照组与WT对照组相比,结肠长度无差异。WT结肠炎组及KO结肠炎组临床表现、体质量减轻程度、结肠长度无差异。静息状态下,WT对照组及KO对照组结肠收缩频率无差异;WT结肠炎组较KO结肠炎组结肠自发收缩频率明显加快[(15.22±2.90)次/5 min vs(2.10±0.38)次/5 min,n=9,P<0.01];WT结肠炎组较WT对照组结肠自发收缩频率加快[(15.22±2.90)次/5 min vs(3.78±1.64)次/5 min,n=9,P<0.01];而KO结肠炎组较KO对照组结肠收缩频率无明显变化。蛋白印迹结果表明WT对照组与KO对照组IP3R1、PLB、BKCa无差异。在两结肠炎组中,KO组较WT组IP3R1表达减少(0.56±0.14 vs 0.84±0.09,P<0.05),BKCa表达上调(0.97±0.14 vs 0.53±0.13,P<0.05),PLB表达无统计学差异。结论 FKBP12.6敲除对DSS诱导小鼠结肠炎模型临床表现、体质量及结肠长度变化程度无影响。FKBP12.6敲除后DSS诱导小鼠结肠炎模型结肠平滑肌收缩频率接近野生对照组小鼠。
文摘Male mice deficient in FKBP12.6 display cardiac hypertrophy, but the underlying mechanism is still unclear. Here we report that the cardiac hypertrophy is a physiological response
文摘Ca2+ release through ryanodine receptors (RyRs) plays an important role in excitation-contraction coupling in heart and smooth muscle. FKBP12.6 proteins
文摘FK506 binding protein 12.6 (FKBP12.6) is the protein in the ryanodine receptor complex, but its function is controversial in different reported work. Some conclude that FKBP12.
