In a study appearing in the January 4, 2006 issue of the Journal of Clinical Investigation, Gary Owens and colleagues from the University of Virginia determine what causes smooth muscle cells (SMCs) to turn on or turn off the expression of certain SMC genes during healthy and disease states.
Smooth muscle cells are present in many parts of the body, including blood vessel walls, stomach, intestine, lungs, and bladder, and they play a key role in stroke, high blood pressure, heart attack, gastric reflux, asthma, and incontinence.
These cells can change shape and size in response to environmental triggers such as injury, and can stop or start making cell proteins that will benefit the healing process. It was previously known that serum response factor (SRF) controls SMC gene transcription by binding to structures known as CArG box DNA sequences found within the genes specifically expressed by SMCs.
However, the mechanisms controlling this interaction had not been well determined. Owens and colleagues now show that it is the methylation of histones in the DNA that regulates SRF binding to CArG box chromatin of SMC genes. This suggests a novel mechanism of regulation of SMC gene expression that can influence the differentiation of SMCs during both normal development and disease states such as vascular injury.
TITLE: Control of SRF binding to CArG box chromatin regulates smooth muscle gene expression in vivo
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Brooke Grindlinger
press_releasesthe-jci
Journal of Clinical Investigation
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