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多种激酶在毒蕈碱M3受体介导的大鼠结肠纵肌收缩中的作用

Role of various kinases in muscarinic M3 receptor-mediated contraction of longitudinal muscle of rat colon.

作者信息

Anderson Charles D, Kendig Derek M, Al-Qudah Mohammad, Mahavadi Sunila, Murthy Karnam S, Grider John R

机构信息

Department of Physiology and Biophysics, VCU Program in Enteric Neuromuscular Sciences, Virginia Commonwealth University, USA.

出版信息

J Smooth Muscle Res. 2014;50:103-19. doi: 10.1540/jsmr.50.103.

Abstract

The longitudinal muscle layer in gut is the functional opponent to the circular muscle layer during peristalsis. Differences in innervation of the layers allow for the contraction of one layer concurrently with the relaxation of the other, enabling the passage of gut contents in a controlled fashion. Differences in development have given the cells of the two layers differences in receptor populations, membrane lipid handling, and calcium handling profiles/behaviors. The contractile activity of the longitudinal muscle is largely mediated by cholinergic neural input from myenteric plexus. Activation of muscarinic receptors leads to rapid activation of several kinases including MLC kinase, ERK1/2, CaMKII and Rho kinase. Phosphorylation of myosin light chain (MLC20) by MLC kinase (MLCK) is a prerequisite for contraction in both circular and longitudinal muscle cells. In rat colonic longitudinal muscle strips, we measured muscarinic receptor-mediated contraction following incubation with kinase inhibitors. Basal tension was differentially regulated by Rho kinase, ERK1/2, CaMKII and CaMKK. Selective inhibitors of Rho kinase, ERK1/2, CaMKK/AMPK, and CaMKII each reduced carbachol-induced contraction in the innervated muscle strips. These inhibitors had no direct effect on MLCK activity. Thus unlike previously reported for isolated muscle cells where CaMKII and ERK1/2 are not involved in contraction, we conclude that the regulation of carbachol-induced contraction in innervated longitudinal muscle strips involves the interplay of Rho kinase, ERK1/2, CaMKK/AMPK, and CAMKII.

摘要

肠道中的纵行肌层在蠕动过程中是环形肌层的功能拮抗者。两层神经支配的差异使得一层收缩的同时另一层舒张,从而使肠道内容物以可控的方式通过。发育上的差异使得两层细胞在受体群体、膜脂质处理以及钙处理特征/行为方面存在差异。纵行肌的收缩活动很大程度上由肌间神经丛的胆碱能神经输入介导。毒蕈碱受体的激活导致包括肌球蛋白轻链激酶(MLC激酶)、细胞外信号调节激酶1/2(ERK1/2)、钙/钙调蛋白依赖性蛋白激酶II(CaMKII)和 Rho 激酶在内的几种激酶迅速激活。MLC激酶(MLCK)使肌球蛋白轻链(MLC20)磷酸化是环形肌细胞和纵行肌细胞收缩的先决条件。在大鼠结肠纵行肌条中,我们在与激酶抑制剂孵育后测量了毒蕈碱受体介导的收缩。基础张力受 Rho 激酶、ERK1/2、CaMKII 和 CaMKK 的不同调节。Rho 激酶、ERK1/2、CaMKK/AMPK 和 CaMKII 的选择性抑制剂均降低了神经支配的肌条中卡巴胆碱诱导的收缩。这些抑制剂对 MLCK 活性没有直接影响。因此,与之前报道的分离肌细胞中 CaMKII 和 ERK1/2 不参与收缩不同,我们得出结论,神经支配的纵行肌条中卡巴胆碱诱导的收缩调节涉及 Rho 激酶、ERK1/2、CaMKK/AMPK 和 CAMKII 的相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f585/5137316/6b092083a0fa/jsmr-50-103-g001.jpg

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