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毒蕈碱型乙酰胆碱受体和G(α)q信号传导对快肌纤维中慢肌球蛋白重链2基因表达的抑制作用

Repression of slow myosin heavy chain 2 gene expression in fast skeletal muscle fibers by muscarinic acetylcholine receptor and G(alpha)q signaling.

作者信息

Jordan Theresa, Li Jinyuan, Jiang Hongbin, DiMario Joseph X

机构信息

Department of Cell Biology and Anatomy, Chicago Medical School, North Chicago, IL 60064, USA.

出版信息

J Cell Biol. 2003 Sep 1;162(5):843-50. doi: 10.1083/jcb.200303164.

DOI:10.1083/jcb.200303164
PMID:12952937
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2172810/
Abstract

Gene expression in skeletal muscle fibers is regulated by innervation and intrinsic fiber properties. To determine the mechanism of repression of slow MyHC2 expression in innervated fast pectoralis major (PM) fibers, we investigated the function of the muscarinic acetylcholine receptor (mAchR) and G(alpha)q. Both mAchR and G(alpha)q are abundant in medial adductor (MA) and PM fibers, and mAchR and G(alpha)q interact in these fibers. Whereas innervation of PM fibers was insufficient to induce slow MyHC2 expression, inhibition of mAchR activity with atropine in innervated PM fibers induced slow MyHC2 expression. Increased G(alpha)q activity repressed slow MyHC2 expression to nondetectable levels in innervated MA fibers. Reduced mAchR activity decreased PKC activity in PM fibers, and increased G(alpha)q activity increased PKC activity in PM and MA fibers. Decreased PKC activity in atropine-treated innervated PM fibers correlated with slow MyHC2 expression. These data suggest that slow MyHC2 repression in innervated fast PM fibers is mediated by cell signaling involving mAchRs, G(alpha)q, and PKC.

摘要

骨骼肌纤维中的基因表达受神经支配和内在纤维特性的调节。为了确定在受神经支配的快肌胸大肌（PM）纤维中慢肌球蛋白重链2（MyHC2）表达受抑制的机制，我们研究了毒蕈碱型乙酰胆碱受体（mAchR）和Gαq的功能。mAchR和Gαq在大内收肌（MA）和PM纤维中均大量存在，且在这些纤维中相互作用。虽然PM纤维的神经支配不足以诱导慢MyHC2表达，但在受神经支配的PM纤维中用阿托品抑制mAchR活性可诱导慢MyHC2表达。Gαq活性增加会将慢MyHC2表达抑制到受神经支配的MA纤维中无法检测到的水平。mAchR活性降低会降低PM纤维中的蛋白激酶C（PKC）活性，而Gαq活性增加会增加PM和MA纤维中的PKC活性。阿托品处理的受神经支配的PM纤维中PKC活性降低与慢MyHC2表达相关。这些数据表明，受神经支配的快PM纤维中慢MyHC2的抑制是由涉及mAchR、Gαq和PKC的细胞信号传导介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0741/2172810/38e514fb52ac/200303164f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0741/2172810/c46a8b71806a/200303164f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0741/2172810/0f919813b076/200303164f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0741/2172810/4cf5532114f0/200303164f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0741/2172810/5c65842c9c10/200303164f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0741/2172810/066d4d31313b/200303164f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0741/2172810/38e514fb52ac/200303164f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0741/2172810/c46a8b71806a/200303164f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0741/2172810/0f919813b076/200303164f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0741/2172810/4cf5532114f0/200303164f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0741/2172810/5c65842c9c10/200303164f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0741/2172810/066d4d31313b/200303164f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0741/2172810/38e514fb52ac/200303164f6.jpg

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