Prostacyclin Receptor Regulation --- from Transcription to Trafficking

Title: Prostacyclin Receptor Regulation --- from Transcription to Trafficking

Volume: 11 Issue: 7

Author(s): C. Midgett, J. Stitham, K.A. Martin and J. Hwa

Affiliation:

Keywords: Prostacyclin receptor, activation, desensitization, dimerization, internalization, transcriptional regulation, homeostasis, hemostasis, atherothrombosis, atherosclerosis, inflammatory disease, coronary syndrome, stroke, platelets, restenotic lesions

Abstract: The prostacyclin receptor (IP - International Union of Pharmacology nomenclature) is a member of the seven transmembrane G-protein coupled receptor (GPCR) superfamily. Recent concerns with selective and non-selective COX-1/COX-2 inhibition have exposed an important cardioprotective role for IP in preventing atherothrombosis. Receptor dysfunction (genetic variants) or reduced signaling (COX-2 inhibition) in high cardiovascular risk patients leads to increased cardiovascular events. These clinical observations have also been confirmed genetically by mouse knockout studies. Thus, receptor regulation is paramount in ensuring correct function in the prevention of atherothrombosis. This review summarizes recent literature on how this important receptor is regulated, from transcription to transport (to and from the membrane surface). These regulatory processes are critical in ensuring that IP receptors are adequately expressed and functional on the cell surface.

Cite this article as:

Midgett C., Stitham J., Martin K.A. and Hwa J., Prostacyclin Receptor Regulation --- from Transcription to Trafficking, Current Molecular Medicine 2011; 11 (7) . https://dx.doi.org/10.2174/156652411800615144