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Mechanical forces generated by adhesive attachment of endothelial cells influence the nuclear envelope and, therefore gene transcription. Alternation in EC mechanical forces may result in aberrant gene transcription leading to lethal vascular diseases such as acute lung injury. We found that missing EC-FAK increases intracellular tension, which in turn promotes nuclear envelop protein emerin and DNA methyltransferase 3a. Methylation of transcription factor KLF2 promoter by DNMT3a reduced KLF2 synthesis and transcription of the essential barrier-maintaining gene, S1PR1. With FAK-deficient or WT-damaged endothelium, pulmonary artery ostasis in lungs was reversed by vascularisation in lungs by restoring KLF2 or S1PR1 expression, impairing emerin, or DNMT3a activity.
Source link: https://www.ncbi.nlm.nih.gov/bioproject/857070
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