Search bioRxiv⌕ Search

Biology subjects

Price, A. S.

Publications and source records attributed to Price, A. S..

2 recordsLinked to original sources

Primary Human Macrophages Exhibit Functional CYP3A4 Activity with Marked Expression-Function Discordance and Cocaine-Induced Catalytic Activation

CYP3A4 is a phase I drug-metabolizing enzyme responsible for transformation of ~50% of clinically relevant drugs. While extensively characterized in hepatocytes, its role in immune cells remains poorly understood. Here, using primary human monocyte-derived macrophages, we identify an understudied extrahepatic site of CYP3A4-mediated drug metabolism. Macrophages from 100 independent donors expressed CYP3A4 and its transcriptional regulators, Pregnane X Receptor (PXR) and Constitutive Androstane Receptor (CAR), with substantial interindividual variability. Importantly, CYP3A4 protein expression was accompanied by measurable catalytic activity in intact macrophages, yet CYP3A4 mRNA, protein abundance, and activity lacked concordance, demonstrating that expression alone may not predict function. In vivo, CYP3A4 was expressed in rhesus macaque Kupffer cells, further supporting macrophages as a potential pharmacologic entity. We next evaluated cocaine as a potential modulator of CYP3A4, due to its role in xenobiotic clearance. Cocaine had a dichotomous effect on expression, increasing CYP3A4 in some donors while producing no change or decreases in others, a phenotype associated with PXR, CAR, and the sigma-1 cocaine receptor. Strikingly, despite these divergent expression responses, cocaine increased CYP3A4 catalytic activity in all donors, reaching or exceeding levels induced by rifampicin, a clinically relevant CYP3A4 inducer. In rhesus macaques, cocaine also decreased antiretroviral therapy tissue concentrations, coincident with increased CYP3A4 and PXR. Together, these findings establish macrophages as a functionally active extrahepatic site of CYP3A4 metabolism and reveal a critical disconnect between CYP3A4 expression and catalytic function. Moreover, our findings identify interindividual variability and expression-activity discordance as important considerations for personalized medicine and understanding clinically relevant drug-drug interactions in the context of substance use.

pharmacology and toxicology↗

Roadmap for Canonical and Extended Endocannabinoid System Receptors in Peripheral Organs of Preclinical Animal Models

The endocannabinoid system is widely expressed throughout the body and is comprised of receptors, ligands, and enzymes that maintain metabolic, immune, and reproductive homeostasis. Increasing interest in the endocannabinoid system has arisen due to these physiologic roles, policy changes leading to more widespread recreational use, and the therapeutic potential of Cannabis and phytocannabinoids. Rodents have been the primary preclinical model of focus due to their relative low cost, short gestational period, genetic manipulation strategies, and gold-standard behavioral tests. However, the potential for lack of clinical translation to non-human primates and humans is high as cross-species comparisons of the endocannabinoid system has not been evaluated. To bridge this gap in knowledge, we evaluate the relative gene expression of 14 canonical and extended endocannabinoid receptors in seven peripheral organs of C57/BL6 mice, Sprague-Dawley rats, and non-human primate rhesus macaques. Notably, we identify species- and organ-specific heterogeneity in endocannabinoid receptor distribution where there is surprisingly limited overlap among the preclinical models. Importantly, we determined there were only five receptors (CB2, GPR18, GPR55, TRPV2, and FAAH) that had identical expression patterns in mice, rats, and rhesus macaques. Our findings demonstrate a critical, yet previously unappreciated, contributor to challenges of rigor and reproducibility in the cannabinoid field, which has profound implications in hampering progress in understanding the complexity of the endocannabinoid system and development of cannabinoid-based therapies.

molecular biology↗