Thermogelling PLGA-PEG-PLGA from PolySciTech used in testing of cardiovascular healing post stenosis

Heart disease remains the most common cause of death world-wide. Although emplacement of cardiovascular stent can reduce damage from heart attack by maintaining blood flow there is the potential for restenosis as the tissue can in-grow into the stent structure and reclose the vessel. Recently, researchers at University of Virginia, University of Wisconsin, and Ohio State University used PLGA-PEG-PLGA (AK012) from PolySciTech (www.polyscitech.com) to create thermogels that provide for controlled delivery of a PLK4 inhibitor (centrinone-B) to enable study into the post-stent healing process. This research holds promise to improve outcomes from cardiovascular repair operations. Read more: Li, Jing, Go Urabe, Yitao Huang, Mengxue Zhang, Bowen Wang, Lynn Marcho, Hongtao Shen, K. Craig Kent, and Lian-Wang Guo. "A role for polo-like kinase 4 in vascular fibroblast cell-type transition." Basic to Translational Science 6, no. 3 (2021): 257-283. https://www.jacc.org/doi/abs/10.1016/j.jacbts.2020.12.015

“Highlights:  PLK4, previously known as a centriole-associated factor, regulates the transcription factor activity of serum response factor. PLK4 inhibition blocks the profibrogenic cell state transition of vascular fibroblasts. PLK4’s activation and gene expression are regulated by PDGF receptor and epigenetic reader BRD4, respectively. Summary: Periadventitial administration of a PLK4 inhibitor mitigates vascular fibrosis. Polo-like kinase 4 (PLK4) is canonically known for its cytoplasmic function in centriole duplication. Here we show a noncanonical PLK4 function of regulating the transcription factor SRF’s nuclear activity and associated myofibroblast-like cell-type transition. In this context, we have further found that PLK4’s phosphorylation and transcription are respectively regulated by PDGF receptor and epigenetic factor BRD4. Furthermore, in vivo experiments suggest PLK4 inhibition as a potential approach to mitigating vascular fibrosis.”