Literature DB >> 20428474

Sm22α transcription occurs at the early onset of the cardiovascular system and the intron 1 is dispensable for its transcription in smooth muscle cells during mouse development.

Maozhou Yang, Hong Jiang, Li Li.   

Abstract

SM22α, also known as SM22, has been widely used as a smooth muscle cell (SMC) marker and is known to be expressed in the embryonic heart. The intron 1 of Sm22 contains multiple important and evolutionarily conserved regulatory elements. To determine the role of the intron 1 in Sm22 transcriptional regulation and the function of SM22 during development, we generated a Sm22 knockout mouse by replacing the intron 1 and the translation initiation with a nuclear localized LacZ (nLacZ) reporter. The resulting Sm22 knockout mice (Sm22(-)/(-)) were viable and fertile without any apparent developmental defects. Using X-gal staining assay, we found that Sm22 transcription was detectable in the chorion formation region and in the heart field before formation of the heart tube at E7.5, namely much earlier than the looped heart stage where it had been previously reported. The expression of lacZ progressively expanded throughout the heart tube by E8.5. LacZ was transiently expressed in the heart and somites and then became restricted to the vascular and visceral SMC organs. These results indicate that SM22 is not required for mouse basal homeostatic function and that the intron 1 is dispensable for Sm22 transcription during development. Given the importance of vasculature in organogenesis and in diseases, this mouse line may be a valuable tool to trace the development and pathology of the cardiovascular system.

Entities:  

Keywords:  SM22α; Transgelin; cardiac crescent; intron 1; knockout mouse; smooth muscle cells

Year:  2009        PMID: 20428474      PMCID: PMC2860299     

Source DB:  PubMed          Journal:  Int J Physiol Pathophysiol Pharmacol        ISSN: 1944-8171


  35 in total

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  11 in total

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4.  Disruption of SM22 promotes inflammation after artery injury via nuclear factor kappaB activation.

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5.  An essential requirement for β1 integrin in the assembly of extracellular matrix proteins within the vascular wall.

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6.  α5 and αv integrins cooperate to regulate vascular smooth muscle and neural crest functions in vivo.

Authors:  Christopher J Turner; Kwabena Badu-Nkansah; Denise Crowley; Arjan van der Flier; Richard O Hynes
Journal:  Development       Date:  2015-02-15       Impact factor: 6.868

7.  Deletion of SM22α disrupts the structure and function of caveolae and T-tubules in cardiomyocytes, contributing to heart failure.

Authors:  Jun Wu; Wei Wang; Yaomeng Huang; Haochen Wu; Jiabin Wang; Mei Han
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10.  SM22α suppresses cytokine-induced inflammation and the transcription of NF-κB inducing kinase (Nik) by modulating SRF transcriptional activity in vascular smooth muscle cells.

Authors:  Xiaohua Dai; Devi Thiagarajan; Jingye Fang; Jianbin Shen; Neeraja Priyanka Annam; Zhao Yang; Hong Jiang; Donghong Ju; Youming Xie; Kezhong Zhang; Yan Yuan Tseng; Zhe Yang; Arun K Rishi; Hui J Li; Maozhou Yang; Li Li
Journal:  PLoS One       Date:  2017-12-28       Impact factor: 3.240

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