لمحة حول المتجر

Dr. Naik begin his scientific career earning a Master’s degree in Exercise Physiology from the University of Wisconsin - Milwaukee. This work focused on determining the cellular mechanisms mediating functional hyperemia in skeletal muscle. He continued to pursue his interest in cardiovascular physiology at the University of New Mexico School of Medicine, earning a PhD in Biomedical Sciences where he investigated the signaling pathway mediating vasodilation in response to heme oxygenase-derived carbon monoxide. Dr. Naik completed his postdoctoral training at the University of Mississippi School of Medicine where his research investigated the vascular dysfunction associated with obesity and metabolic syndrome. Dr. Naik joined the UNM SOM Department of Cell Biology and Physiology as a senior research scientist in 2011 and was promoted to the rank of assistant professor in 2017.

بيان الشخصية

Dr Naik’s focuses on understanding the cellular mechanisms by which endothelial and vascular smooth muscle cells communicate in order to regulated blood flow to meet the metabolic demands of body organs. His most recent work has focused on the role of endothelial-derived gaseous signaling molecules, carbon monoxide and hydrogen sulfide in endothelial-dependent dilation as well as the role of calcium microdomains in ion channel activation. His work was the first to demonstrate that H2S-induced vasodilation involves TRPV4 channels through the formation of Ca2+-sparklets and strengthens our previous observation that a novel endothelial Ca2+-activated large conductance calcium activated K+ channels participate in vasodilation in small mesenteric arteries.

مجالات التخصص

Cardiopulmonary physiology Vascular biology Endothelial biology Vascular smooth muscle biology ion channels

إنجازات وجوائز

Dynamic Breath Gas Sensor (DBGS) for the Detection of Pulmonary Edema (NIH: collaborator), 3/1/2020 - 2/28/2021 Vascular Smooth Muscle Function in Pulmonary Hypertension (NIH: Collaborator), 02/01/2013-04/30/2023 Endothelial Cell Membrane cholesterol and TRPV4 channel function in Hypertension (CVMD: PI), 7/1/2019 - 6/30/2020 Detection of Ca2+ signaling microdomains in the intact endothelium (CVMD: PI), 7/1/2017 - 6/30/2018 Role of Ca2+-Sparks in the Pulmonary Vasculature (CVMD: PI), 7/1/2011 - 6/30/2012

اللغات

  • الانجليزية

أبحاث

يركز بحث الدكتور نايك على فهم الآليات الخلوية التي تتواصل من خلالها خلايا العضلات الملساء البطانية والأوعية الدموية من أجل تنظيم تدفق الدم لتلبية متطلبات التمثيل الغذائي لأعضاء الجسم. ركز أحدث أعماله على دور جزيئات الإشارات الغازية المشتقة من البطانة ، وأول أكسيد الكربون وكبريتيد الهيدروجين في التمدد المعتمد على البطانة وكذلك دور النطاقات الدقيقة للكالسيوم في تنشيط قناة الأيونات. كان عمله أول من أظهر أن H.2يتضمن توسع الأوعية المستحث بـ S قنوات TRPV4 من خلال تكوين Ca2+-البقع ويقوي ملاحظتنا السابقة أن رواية غشائية Ca2+- ينشط الموصلية الكبيرة للكالسيوم المنشط ك+ تشارك القنوات في توسع الأوعية في الشرايين المساريقية الصغيرة.

تدريس المقررات

Pulmonary physiology phase 1 medical curriculum BIOM 510 - Physiology BIOM 657 - Advanced Cellular and Systems Physiology BIOM 659 - Seminar: Cardiovascular Biology

البحث والمنح الدراسية

Morales-Loredo H, Barrera A, Garcia JM, Pace CE, Naik JS, Gonzalez Bosc LV, Kanagy NL. Hydrogen sulfide regulation of renal and mesenteric blood flow. Am J Physiol Heart Circ Physiol. 2019 Nov 1;317(5):H1157-H1165. doi: 10.1152/ajpheart.00303.2019. Epub 2019 Oct 18. PMID: 31625777; PMCID: PMC6879921. Naik JS, Walker BR. Endothelial-dependent dilation following chronic hypoxia involves TRPV4-mediated activation of endothelial BK channels. Pflugers Arch. 2018 Apr;470(4):633-648. doi: 10.1007/s00424-018-2112-5. Epub 2018 Jan 29. PMID: 29380056; PMCID: PMC5854740. Naik JS, Osmond JM, Walker BR, Kanagy NL. Hydrogen sulfide-induced vasodilation mediated by endothelial TRPV4 channels. Am J Physiol Heart Circ Physiol. 2016 Dec 1;311(6):H1437-H1444. doi: 10.1152/ajpheart.00465.2016. Epub 2016 Oct 7. PMID: 27765747; PMCID: PMC5206343. Jackson-Weaver O, Osmond JM, Naik JS, Gonzalez Bosc LV, Walker BR, Kanagy NL. Intermittent hypoxia in rats reduces activation of Ca2+ sparks in mesenteric arteries. Am J Physiol Heart Circ Physiol. 2015 Dec 1;309(11):H1915-22. doi: 10.1152/ajpheart.00179.2015. Epub 2015 Sep 25. PMID: 26408536; PMCID: PMC4698382. Jackson-Weaver O, Osmond JM, Riddle MA, Naik JS, Gonzalez Bosc LV, Walker BR, Kanagy NL. Hydrogen sulfide dilates rat mesenteric arteries by activating endothelial large-conductance Ca²?-activated K? channels and smooth muscle Ca²? sparks. Am J Physiol Heart Circ Physiol. 2013 Jun 1;304(11):H1446-54. doi: 10.1152/ajpheart.00506.2012. Epub 2013 Mar 22. PMID: 23525712; PMCID: PMC4073893.