What is it about?
As a global epidemic, the prevalence of obesity has increased at an alarming rate over the past several decades. Besides enhancing caloric intake and reducing exercise are predominant factors that drive the development of obesity, both generating new adipocytes and increasing lipid content of adipocytes are major contributors that lead to obesity. Therefore, a tight control of adipogenesis is critical in regulating whole-body energy homeostasis, and the identification of the molecular mechanisms involved in regulating adipogenic differentiation is essential to research new targets and providing precious information for treating or control of obesity. Long noncoding RNAs (lncRNAs) have recently been defined as pivotal regulators in adipogenesis. Here, we identified a novel lncRNA, Plnc1, that was mainly expressed in adipose tissue. Obese mice have higher Plnc1 expression in epididymal, inguinal and perirenal fat than non-obese mice. Plnc1 was induced in established adipogenic lines and bone marrow stromal cells. Plnc1 knockdown decreased adipocyte differentiation, and conversely, overexpression of Plnc1 promoted adipogenesis. Moreover, it is well known that PPARγ2 is a master regulator in adipogenic differentiation, and we found Plnc1 could improve the activation and demethylation of PPARγ2 promoter during adipogenic differentiation. Taken together, The current study indicates that Plnc1 induces adipocyte differentiation from progenitor cells and this function may depend upon its upregulation of the transcriptional activity and demethylation of PPARγ2 promoter during adipogenic differentiation. Plnc1 may serve as a possible therapeutic target in metabolic disorders caused by adipogenic dysregulation like obesity.
Featured Image
Read the Original
This page is a summary of: Long noncoding RNA
Plnc1
controls adipocyte differentiation by regulating peroxisome proliferator‐activated receptor γ, The FASEB Journal, October 2018, Wiley,
DOI: 10.1096/fj.201800739rrr.
You can read the full text:
Contributors
The following have contributed to this page







