Regulation of Prostacyclin in Pulmonary Hypertension

Ohio State University, Columbus OH

Investigators

Linked publications & trials

Abstract

DESCRIPTION (provided by applicant): Candidate: The candidate, Patrick Nana-Sinkam, M.D., is an Instructor in the Division of Pulmonary Sciences and Critical Care Medicine at the University of Colorado Health Sciences Center. He is currently supported by an NIH minority supplement grant to the parent grant NIH E PATHO. PROJ IV 5P01 HL066254-03S1, "Prostacyclin Synthase and Prostacyclin Receptor in Severe Pulmonary Hypertension." Dr. Nana-Sinkam has previously worked on transgenic murine models of disease and has developed a particular interest in the eicosanoid pathway and its role in disease susceptibility as well as identifying products with clinical application. His short-term goal is to continue to develop both the professional and research skills to eventually become an independent investigator. Long term, Dr. Nana-Sinkam hopes to develop a successful, independently funded laboratory in eicosanoid biology. This proposed Mentored Clinical Scientist Award would provide him with the support to develop these skills. Career Development: Dr. Nana-Sinkam's career development will include: 1) developing new research skills such as the development of transgenic animal models, research design and professional skills necessary in an academic center, 2) formal educational activities including courses in molecular biology techniques and grant writing, and 3) involvement in administrative activities essential to developing professional skills such as serving on the School of Medicine's Admission and Scholarship Committees and Ethnic Minority Affairs Committee. Environment: Dr. Nana-Sinkam is currently in an environment that is conducive to excellent research. His sponsor, Dr. Mark Geraci, and co-sponsors, Drs. Norbert Voelkel and Raphael Nemenoff, are outstanding, extramurally funded, independent investigators with established records in research. Research: Dr. Nana-Sinkam's general goals will be to attempt to elucidate the mechanisms by which prostacyclin prevent vascular remodeling and are regulated in pulmonary hypertension. The hypotheses will be that 1) the development of a conditional transgenic murine model for overexpression of prostacyclin synthase can assist in defining the temporal relationship between gene expression and remodeling, 2) key regulators of gene transcription involved in suppression of prostacyclin in pulmonary hypertension can be identified by a model for gene transcriptional regulation, and 3) prostacyclin synthease gene polymorphisms exist in defined human populations and have a potential impact on gene function and subsequent susceptibility to disease.