GSE161334
Transcriptome analysis upon Hmg20a knockdown in astrocytes
We recently demonstrated that the 'Metabesity' factor HMG20A is essential for beta cell functional maturity and adaptation to physiological stress. As this chromatin remodeling factor also dictates CNS development, we sought to determine whether HMG20A is expressed in astrocytes and whether it potentiates astrocyte function in response to environmental cues. To investigate the function and regulatory mechanism of HMG20A, RNA-seq was performed on astrocytes treated or not with a siHMG20A. HMG20A silencing in astrocytes resulted in repression of pro-inflammatory, cholesterol homeostasis and epithelial-to-mesenchymal transition pathways. This results indicate that HMG20A coordinates the astrocyte polarization state. Under physiological pressure such as obesity and insulin resistance that induces low grade inflammation, HMG20A expression is increased to induce astrogliosis in an attempt to preserve the neuronal network and glucose homeostasis. onetheless, a chronic metabesity state or functional mutations will result in lower levels of HMG20A, failure to promote astrogliosis and increase susceptibility of neurons to stress-mediated apoptosis. Overall design: mRNA profiles of murine astrocytes treated with siControl or siHmg20a were generated by deep sequencing, in duplicates, using Illumina Nexseq.