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首页> 外文期刊>American Journal of Physiology >Developmental changes in Ca2+ homeostasis and contractility in gallbladder smooth muscle.
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Developmental changes in Ca2+ homeostasis and contractility in gallbladder smooth muscle.

机译：胆囊平滑肌中Ca2 +稳态和收缩力的发育变化。

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摘要

Relatively little is known about the contribution of Ca(2+)-dependent and -independent mechanisms in the contractility of neonatal gastrointestinal smooth muscle. We therefore studied Ca(2+) homeostasis and Ca(2+) sensitization mechanisms in 10-day-old and adult guinea pig gallbladder smooth muscle to elucidate developmental changes in these processes. Gallbladder contractility was evaluated by isometrical tension recordings from strips, intracellular Ca(2+) concentration was estimated by epifluorescence microscopy of fura-2-loaded isolated cells, and protein expression and phosphorylation were assessed by Western blot analysis. The neonatal gallbladder contracted significantly less to CCK than adult tissue, but this correlated with an increased Ca(2+) mobilization, suggesting immaturity of Ca(2+) sensitization mechanisms. The enhanced Ca(2+) release in the newborn gallbladder was the result of the increase in the size of the releasable Ca(2+) pool. Moreover, in neonatal smooth muscle cells, neither the plasma membrane Ca(2+) pump nor the Na(+)/Ca(2+) exchanger collaborate in the extrusion of Ca(2+). In contrast, in these cells, there is an increase in phospholamban phosphorylation, which could drive to an overactivity of the sarco(endo)plasmic reticulum Ca(2+)-ATPase pump. The reduced Ca(2+) sensitivity in neonatal tissues was demonstrated by the lack of effect to Y-27362, an inhibitor of Rho kinase (ROCK), and GF-109203X, an inhibitor of PKC, on agonist-induced contraction. In addition, the neonatal gallbladder showed lower levels of RhoA, ROCK, PKC, and two effectors [C-kinase-dependent inhibitor of 17 kDa (CPI-17) and myosin phosphatase targetting 1 (MYPT1)] as well as an absence of CPI-17 and MYPT1 phosphorylation in response to agonists. In conclusion, our results indicate that the main mechanisms involved in smooth muscle contractility are under developmental regulation.
机译：关于Ca（2+）依赖性和非依赖性机制在新生儿胃肠道平滑肌收缩性中的作用知之甚少。因此，我们在10天和成年豚鼠胆囊平滑肌中研究Ca（2+）稳态和Ca（2+）致敏机制，以阐明这些过程中的发育变化。胆囊收缩力是通过等轴测拉伸条来评估的，细胞内Ca（2+）的浓度是通过呋喃2加载的分离细胞的落射荧光显微镜来评估的，蛋白质表达和磷酸化是通过蛋白质印迹分析来评估的。新生儿胆囊收缩到CCK明显少于成人组织，但这与增加的Ca（2+）动员相关，表明Ca（2+）致敏机制不成熟。新生胆囊中增强的Ca（2+）释放是可释放Ca（2+）库大小增加的结果。此外，在新生儿平滑​​肌细胞中，质膜Ca（2+）泵和Na（+）/ Ca（2+）交换剂都没有参与Ca（2+）的挤出。相反，在这些细胞中，phosphorlamban磷酸化增加，这可能会导致肌浆网（内质网）Ca（2 +）-ATPase泵的过度活跃。缺乏对Rho激酶（ROCK）抑制剂Y-27362和PKC抑制剂GF-109203X对激动剂诱导的收缩的影响，证明了新生儿组织中Ca（2+）敏感性的降低。此外，新生儿胆囊显示出较低的RhoA，ROCK，PKC和两种效应子[17kDa的C激酶依赖性抑制剂（CPI-17）和靶向肌球蛋白的磷酸酶1（MYPT1）]以及不存在CPI -17和MYPT1磷酸化对激动剂的反应。总之，我们的结果表明，涉及平滑肌收缩力的主要机制处于发育调节之下。

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