What the attendees said....
I really valued the experience of the ISH New Investigator Symposium in San Francisco as it gave me a forum in which to present my research and be critically evaluated by experts in the hypertension field.
What the attendees said…………
5th ISH New Investigator Symposium on Hypertension and Cardiovascular Disease
8th September 2014, San Francisco, CA, USA
HANA A. ITANI
My scientific goal is to elucidate mechanisms of hypertension and its attendant end-organ damage. To accomplish this goal, I completed a Ph.D. in the Molecular and Cellular Biology Program at the University of Iowa, under the supervision of Dr. Curt Sigmund. The University of Iowa and Dr. Sigmund’s laboratory are renowned for research in hypertension and the biology of renin. During my Ph.D. Training, I identified two new molecular mechanisms involved in regulation of renin (REN) gene expression. I was awarded the pre-doctoral Caroline tum sudden award by the American Physiological society for this work. Following completion of my Ph.D., I accepted an Academic Faculty position in Lebanon, and was active in training young scientist throughout teaching, mentorship, and supervision of graduate students projects. In recent years, it has become apparent that inflammation and immunity contribute to hypertension. I therefore decided to pursue a postdoctoral Research fellowship in College of Medicine, Divisions of Clinical Pharmacology and Vascular Biology in Dr. Harrison’s laboratory at Vanderbilt University. Dr. Harrison has performed seminal studies defining the role of adaptive immunity in hypertension and Inflammation. As a Post-Doctoral Research Fellow under the mentorship of Dr. Harrison, I am most interested in the role of memory CD8+ T cells in sustained or recurrent hypertension. I have developed a research project in which I have discovered that memory CD4+ cells and CD8+ T cells accumulate in the kidney during sustained hypertension and are major sources of the inflammatory cytokines IL-17A and IFN-γ. These memory cells seem to accumulate over time with repeated hypertensive challenges. This is important because memory cells are very long lived and sensitize individuals to repeated hypertensive stimuli thus contributing to renal damage. I was awarded the NIH F32 Individual Postdoctoral Fellowship to complete these studies, and First Place Excellence in Renal Research Award by the American Physiological Society. My ultimate goal is to mature as an independent investigator and to establish my own laboratory.
It is a great honor to receive the New Investigator Presentation Award at the International Society of Hypertension (ISH) and present my project at the ISH symposium in San Francisco. I value the excellent scientific discussions and feedback received from ISH New Investigator Committee and peers. As a Trainee, attending ISH is a great opportunity to meet pioneers in the field of hypertension, to develop collaborations among peers and networking skills, and to learn more about novel discoveries in hypertension. Dr. Gabriel Navar’s keynote lecture has provided valuable insights on how to develop a scientific career, grant writing skills, and how to transition from a mentee to a mentor, which is a critical process to gain independence as research scientist. I encourage Colleagues and Trainees to join ISH and attend scientific symposium in the future to benefit from this great learning experience.
Previous studies in our lab has shown that the development of hypertension is dependent on Cytochrome P 450 1 B1 (CYP1B1) activity. My study addressed the role of CYP1B1 in Ang II-induced abdominal aortic aneurysm in ApoE KO mice. Results indicated a role for CYP1B1 in the development of AAA in ApoE KO mice which was prevented by CYP1B1 gene disruption or by inhibition of the enzyme activity chemically using 2,3,4,5 Tetramethoxystilbene (TMS). These CYP1B1 mediated pathological changes were found to occur via increased oxidative stress and platelet aggregation. Thus, CYP1B1 inhibition could be a putative therapeutic target for Ang II induced AAA.
I really enjoyed attending the ISH meeting in San Francisco. The smaller scale of the meeting ensured that it was easier to interact with people in a relaxed mode while also getting an overview of the cutting edge research being undertaken in hypertension and cardiovascular diseases. I particularly thank the organizers for taking extra steps to provide a platform for early career investigators to share their work to a larger audience.
Our laboratory has made the novel observations that the damage-associated molecular pattern (DAMP), mitochondrial DNA, is elevated in the circulation of spontaneously hypertensive rats (SHR) and the enzymes responsible for its degradation, deoxyribonuclease I and II, had decreased serum and tissue activity, respectively. Therefore, we sought to inhibit the contribution of mtDNA on innate immune system activation, via inhibition of Toll-like receptor (TLR)9, in young and old SHR with Chloroquine (CQ). We observed that CQ improved vascular relaxation to acetylcholine in young and old SHR through cyclooxygenase and ERK1/2-dependent mechanisms. Interestingly however, only young SHR had diminished expression of representative TLR signaling molecules (MyD88 and TRAF6) after treatment CQ. Overall, this study supports the targeting of innate immune system in the treatment of hypertension and its associated hallmarks (e.g., impaired vascular reactivity), possibly during the pre-hypertensive phase.
I really valued the experience of the ISH New Investigator Symposium in San Francisco as it gave me a forum in which to present my research and be critically evaluated by experts in the hypertension field. All the research presented was novel and significant and this stimulated the interaction between the young investigators and leaders in the field of hypertension, which I especially appreciated. A special mention must be extended to Dr. Gabriel Navar (Tulane University) for his inspiring keynote address, as well as Helen Horsfield (ISH Secretariat) for her excellent organization of the event. I look forward to participating in this event more in the future.
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