# NIH grant: TRPV1-Mediated Vascular and Neuronal Dysregulation by Natural vs. Synthetic Cannabinoids (1K99DA064783-01A1) — retained record

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NIH grant 1K99DA064783-01A1: TRPV1-Mediated Vascular and Neuronal Dysregulation by Natural vs. Synthetic Cannabinoids
Institute: {'code': 'DA', 'abbreviation': 'NIDA', 'name': 'National Institute on Drug Abuse', 'admin_org_id': '12500072', 'admin_funding_url': ''}. PI: Nerea  Jimenez Tellez. Award: $160840.
Start: 2026-08-01T00:00:00.
Project Summary
The widespread use of natural (NCs) and synthetic cannabinoids (SCs) raises significant public health
concerns due to their potential impact on vascular and neuronal health. While NCs like cannabidiol (CBD)
and delta-9-tetrahydrocannabinol (Δ9-THC) have been studied extensively, SCs such as cannabinol (CBN)
and hexahydrocannabinol (HHC) are increasingly used despite limited understanding of their safety and
mechanisms. This K99/R00 project will investigate the differential impact of these compounds on vascular
and neuronal function, with a focus on TRPV1, a key regulator of endothelial and neuronal processes. Using
in vitro and in vivo models, alongside human data, this study aims to elucidate the mechanisms underlying
cannabinoid toxicity, thereby informing regulatory policies and therapeutic applications. During the K99
phase, I will examine TRPV1-mediated endothelial dysfunction and neurovascular crosstalk using a
genetically diverse iPSC-derived “cell village” model of 20 healthy donors. iPSC-derived endothelial cells
(iPSC-ECs) and cortical neurons (iPSC-CNs) will be utilized to evaluate cannabinoid-induced alterations in
endothelial barrier integrity, inflammation, and neuronal function. Specific Aim 1 investigates TRPV1-
mediated endothelial dysfunction, while Specific Aim 2 examines its impact on neuronal function through
direct exposure or endothelial-conditioned media. Specific Aim 3 extends these findings to adolescent rats,
evaluating vascular function, neuroinflammation, and cognition, and integrates human data to complement
the findings. This project is guided by an expert mentoring team, including primary mentor Dr. Joseph Wu
(iPSC modeling and cardiovascular biology) and co-mentor Dr. Erin Gibson (neuroinflammation). My advisory
committee, comprising Dr. Matt Springer (vascular biology in rodents and humans), Dr. Marlene Rabinovitch
(vascular science), Dr. Judith Hellman (cannabinoids and inflammation), and Dr. Ivan Soltesz
(electrophysiology), will provide diverse expertise to support my training. During the K99 phase, I will develop
expertise in vascular biology, neuroinflammation, and electrophysiology, which will enable my transition to
the independent R00 phase. In the R00 phase, I will expand this work to in vivo models and integration of
human data, identifying conserved mechanisms of cannabinoid-induced toxicity and informing strategies to
mitigate public health risks. Ultimately, this project will bridge the fields of vascular and neuronal biology to
address critical public health challenges. By integrating preclinical and translational studies, this research will
advance understanding of cannabinoid toxicity, inform regulatory policies, and explore therapeutic
opportunities. My long-term goal is to establish an independent research group that leverages iPSC-based
models and multi-omics approaches to study neurovascular health, thereby contributing to safer therapeutic
strategies and improved public health outcomes.
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