Lamin-B1 contributes to the proper timing of epicardial cell migration and function during embryonic heart development.

ABSTRACT: Lamin proteins form a meshwork beneath the nuclear envelope and contribute to many different cellular processes. Mutations in lamins cause defective organogenesis in mouse models and human diseases that affect adipose tissue, brain, skeletal muscle, and the heart. In vitro cell culture studies have shown that lamins help maintain nuclear shape and facilitate cell migration. However, whether these defects contribute to improper tissue building in vivo requires further clarification. By studying the heart epicardium during embryogenesis, we show that Lb1-null epicardial cells exhibit in vivo and in vitro migratory delay. Transcriptome analyses of these cells suggest that Lb1 influences the expression of cell adhesion genes, which could affect cell migration during epicardium development. The

SUBMITTER: Tran JR 

PROVIDER: S-EPMC5156536 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature