Targetting interleukins and chemokine mediated signalling pathway in DCM caused by LMNA 289A>G

Lamins are type V intermediate filament proteins underlying the inner nuclear membrane which provide structural rigidity to the nucleus, tether the chromosomes and maintain nuclear homeostasis. Studies have identified developmentally regulated regions of the genome that are dynamically associated with the nuclear lamina. A large number of mutations in LMNA gene encoding lamin A/C results in a wide array of human diseases, collectively termed as laminopathies. Dilated Cardiomyopathy (DCM) is one such cardiovascular disease which is associated with systolic dysfunction of left or both ventricles leading to cardiac arrhythmia culminating into myocardial infarction. In this work, we have unravelled the gene expression by RNA Sequencing analysis in mouse myoblast cell line in the context of the missense mutation LMNA 289A>G (Lys97Glu) that is found in DCM afflicted patients with severe symptoms. Overall design: Comparative gene expression profiling analysis of RNA-seq data of wild type lamin A and K97E lamin A (DCM mutant) transfected C2C12- mouse myoblast cells. All the samples were studied in duplicates.