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收缩激动剂对肺动脉平滑肌中丝切蛋白磷酸化状态的不同影响。

Distinct effects of contraction agonists on the phosphorylation state of cofilin in pulmonary artery smooth muscle.

作者信息

Dai Yan-Ping, Bongalon Shaner, Mutafova-Yambolieva Violeta N, Yamboliev Ilia A

机构信息

Department of Pharmacology, Center of Biomedical Research Excellence, University of Nevada School of Medicine, Reno, NV 89557, USA.

出版信息

Adv Pharmacol Sci. 2008;2008:362741. doi: 10.1155/2008/362741. Epub 2007 Nov 6.

DOI:10.1155/2008/362741
PMID:21188136
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3005805/
Abstract

We hypothesized that agonist-induced contraction correlates with the phospho-cofilin/cofilin (P-CF/CF) ratio in pulmonary artery (PA) rings and cultured smooth muscle cells (PASMCs). PA rings were used for isometric contractions and along with PASMCs for assay of P-CF/CF by isoelectric focusing and immunoblotting. The P-CF/CF measured 22.5% in PA and differentiated PASMCs, but only 14.8% in undifferentiated PASMCs. With comparable contraction responses in PA, endothelin-1 (100 nM) and norepinephrine (1 μM) induced a 2-fold increase of P-CF/CF, while angiotensin II (1 μM) induced none. All agonists activated Rho-kinase and LIMK2, and activation was eliminated by inhibition of Rho-kinase. Microcystin LF (20 nM) potentiated the angiotensin II, but not the 5-hydroxytryptamine (1 μM)-mediated increase of P-CF/CF. In conclusion, all tested agonists activate the Rho-kinase-LIMK pathway and increase P-CF/CF. Angiotensin II activates PP2A and counteracts the LIMK-mediated CF phosphorylation. CF phosphorylation stabilizes peripheral actin structures and may contribute to the maximal contraction of PA.

摘要

我们推测激动剂诱导的收缩与肺动脉（PA）环和培养的平滑肌细胞（PASMCs）中的磷酸化丝切蛋白/丝切蛋白（P-CF/CF）比值相关。PA环用于等长收缩实验，并与PASMCs一起通过等电聚焦和免疫印迹法检测P-CF/CF。在PA和分化的PASMCs中，P-CF/CF为22.5%，而在未分化的PASMCs中仅为14.8%。在PA中具有相当的收缩反应时，内皮素-1（100 nM）和去甲肾上腺素（1 μM）可使P-CF/CF增加2倍，而血管紧张素II（1 μM）则无此作用。所有激动剂均激活Rho激酶和LIMK2，且抑制Rho激酶可消除这种激活。微囊藻毒素LF（20 nM）增强血管紧张素II介导的P-CF/CF增加，但不增强5-羟色胺（1 μM）介导的P-CF/CF增加。总之，所有测试的激动剂均激活Rho激酶-LIMK途径并增加P-CF/CF。血管紧张素II激活PP2A并抵消LIMK介导的丝切蛋白磷酸化。丝切蛋白磷酸化稳定外周肌动蛋白结构，并可能有助于PA的最大收缩。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/231d/3005805/811b34b10019/APS2008-362741.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/231d/3005805/db0caaf03f47/APS2008-362741.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/231d/3005805/fd4a12d911b0/APS2008-362741.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/231d/3005805/db44433abe2b/APS2008-362741.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/231d/3005805/2a991f30afc1/APS2008-362741.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/231d/3005805/811b34b10019/APS2008-362741.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/231d/3005805/db0caaf03f47/APS2008-362741.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/231d/3005805/fd4a12d911b0/APS2008-362741.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/231d/3005805/db44433abe2b/APS2008-362741.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/231d/3005805/2a991f30afc1/APS2008-362741.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/231d/3005805/811b34b10019/APS2008-362741.005.jpg

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