Effect of depletion of LEMD3 on gene expression of A7r5 vascular smooth muscle cells [RNA-seq]

The contractile phenotype of vascular smooth muscle cells is essential for maintaining vascular homeostasis.In this study, we found that LEMD3, a nuclear membrane protein, may be involved in maintaining the contractile phenotype of vascular smooth muscle cells through a genome-scale CRISPR screen. Mechanistically, we combined RNA-seq with ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) to find out differentially expressed genes and altered chromatin accessibility. By overlapping down-regulated genes and genes located in less accessible chromatin regions, we identified 143 genes including VSMCs contractile genes such as Acta2, Cnn1, Tagln, and key transcription factor Srf, suggesting that LEMD3 maintains VSMCs contractile phenotype by regulating chromatin accessibility. A7r5 cells were transfected with scrambled siRNA or siRNA targeting Lemd3.