Establishment and maintenance of proper immunity requires a precise balance between cellular adhesion and proliferation. A disruption in either event culminates in a variety of pathologies encompassing immunosuppression, auto immunity, and cancer. Retinoids, profoundly affect immune function by mediating cellular adhesion and proliferation in certain leukocytes. Retinoids, by binding to retinoid receptors (RARs or RXRs), modify the expression of a variety of signaling proteins involved in immune cell proliferation and adhesion including, integrins. Integrins are a family of transmembrane heterodimeric receptors consisting of non-covalently linked alpha and beta subunits that are considered to be the principle receptors involved in attachment to the extracellular matrix and provide adhesive interactions that control cellular proliferation. Currently, the contributions by RARs and RXRs in immune cell adhesion and proliferation have not been examined. In this study, the effect of all-trans-retinoic acid agonists on K562 cellular proliferation was examined. Interestingly, K562 cellular proliferation levels were decreased in a time- and concentration-dependent manner when cells were treated with the RARgamma agonist. In the presence of the RARalpha or RARbeta agonists, K562 cellular proliferation was comparable to the vehicle control. Our study is the first to demonstrate that specific retinoid agonists alter cellular proliferation in K562 cells.

Effect of retinoid receptor agonists on K562 cellular proliferation

2019 Spring National Meeting

The official archive and repository for all ACS Meetings & Expositions abstracts and select posters or presentations.