Year: 2011
Type: article
Abstract: Smooth muscle cells (SMCs) express a unique set of microRNAs (miRNAs) which regulate and maintain the differentiation state of SMCs. The goal of this study was to investigate the role of miRNAs during the development of gastrointestinal (GI) SMCs in a transgenic animal model. We generated SMC-specific Dicer null animals that express the reporter, green fluorescence protein, in a SMC-specific manner. SMC-specific knockout of Dicer prevented SMC miRNA biogenesis, causing dramatic changes in phenotype, function, and global gene expression in SMCs: the mutant mice developed severe dilation of the intestinal tract associated with the thinning and destruction of the smooth muscle (SM) layers; contractile motility in the mutant intestine was dramatically decreased; and SM contractile genes and transcriptional regulators were extensively down-regulated in the mutant SMCs. Profiling and bioinformatic analyses showed that SMC phenotype is regulated by a complex network of positive and negative feedback by SMC miRNAs, serum response factor (SRF), and other transcriptional factors. Taken together, our data suggest that SMC miRNAs are required for the development and survival of SMCs in the GI tract.
Source: PLoS ONE
Institutions: University of Nevada, Reno, Wonkwang University
Language: English
Subfield: Cancer Research
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $2,382
Awards: G1029519325, G1499456869, Zeiss LSM 510 Laser Scanning Confocal Microscope, G2909819244, G3110762171, Smooth Muscle Plasticity: A COBRE, G429603982, G4450675560, G4643788992, G5677807595, G6721281873, G7232274118, KLHL 10-mediated uniquitination during spermiogenesis, G9000059918, G9000333481
OpenAlex ID: W1997524334