The hypoxia-induced membrane depolarization and subsequent constriction of small resistance pulmonary arteries occurs, in part, via inhibition of oxygen sensitive potassium channels open at the resting membrane potent...The hypoxia-induced membrane depolarization and subsequent constriction of small resistance pulmonary arteries occurs, in part, via inhibition of oxygen sensitive potassium channels open at the resting membrane potential in pulmonary arteries smooth muscle cells (PASMCs), so the oxygen sensitive potassium channels in PASMCS play a vital role in the occurrence and development of hypoxic pulmonary vasoconstriction (HPV). Inhibition the function of channels by specific antagons, Antibody-based dissection of the pulmonary arterial smooth muscle cell K+ current, the O2 sensitivity of cloned K+ channels expressed in heterologous expression systems and gene targeting to knockout specific K+ channels have all been examined to identify the molecular components of the pulmonary arterial O2-sensitive K+ channels. Although the mechanism of K+ channel inhibition by hypoxia is unknown, it appears that K+ α -subunits do not sense O2 directly. Rather, they are most likely inhibited through interaction with an unidentified O2 sensor and/or α-subunit. This review summarizes the role of K+ channels in hypoxic pulmonary vasoconstriction, the recent progress toward the identification of K+ channel subunits involved in this response, and the possible mechanisms of K+ channel regulation by hypoxia. [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The hypoxia-induced membrane depolarization and subsequent constriction of small resistance pulmonary arteries occurs, in part, via inhibition of oxygen sensitive potassium channels open at the resting membrane potential in pulmonary arteries smooth muscle cells (PASMCs), so the oxygen sensitive potassium channels in PASMCS play a vital role in the occurrence and development of hypoxic pulmonary vasoconstriction (HPV). Inhibition the function of channels by specific antagons, Antibody-based dissection of the pulmonary arterial smooth muscle cell K+ current, the O2 sensitivity of cloned K+ channels expressed in heterologous expression systems and gene targeting to knockout specific K+ channels have all been examined to identify the molecular components of the pulmonary arterial O2-sensitive K+ channels. Although the mechanism of K+ channel inhibition by hypoxia is unknown, it appears that K+ α -subunits do not sense O2 directly. Rather, they are most likely inhibited through interaction with an unidentified O2 sensor and/or α-subunit. This review summarizes the role of K+ channels in hypoxic pulmonary vasoconstriction, the recent progress toward the identification of K+ channel subunits involved in this response, and the possible mechanisms of K+ channel regulation by hypoxia. [
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。
