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Dewan S.A. Majid, MBBS, PhD
Dewan S.A. Majid, MBBS, PhD

Education

  • MBBS (Bachelor of Medicine, Bachelor of Surgery): The Chittagong University (Sylhet Medical College), Bangladesh, 1978.
  • PhD: University of Leeds, England, United Kingdom, 1989.
  • Postdoctoral Training: Tulane University, Department of Physiology, 1990-1991.

Biography

Dr. Dewan Majid received his MBBS degree from Sylhet Medical College under Chittagong University, Bangladesh in 1976, where he continued his professional service in different positions as Assistant Surgeon, Assistant Registrar and then Registrar, in the Department of Surgery.  In 1981, he moved to Libya to work as a Casualty Medical Officer in Al-Fatah Hospital at Al-Marj, Libya. In 1984, he moved to England, UK to continue his post-graduation studies in Leeds University from where he received his PhD degree in ‘Cardiovascular & Renal Physiology’ in 1989.  He joined the Department of Physiology at Tulane University School of Medicine in 1990 as Post-doctoral Fellow in the Renal Physiology laboratory under the direction of Dr. L.G. Navar.  He then continued his service as the Faculty in the same Department since 1992. Through succession of different ranks, he rose to the rank of the Professor of Physiology at Tulane in 2007.  He is also an active member of the ‘Tulane Hypertension & Renal Center of Excellence (THRCE)’ and currently serving as a Director of Mouse Phenotyping Core of THRCE. Dr. Majid’s research has focused on the importance of the regulation of kidney function by various vasoactive factors and their interactive roles in the development of hypertension. His research works has been funded primarily by grants from the NHLBI, NIGMS, LA Board of Regents and American Society of Hypertension etc. He received many awards and recognitions for his scientific contributions including ‘Harry Goldblatt Award’ for Cardiovascular Research from AHA (American Heart Association), ‘Hoechst Marion Roussel Young Scholar Award’ from ASH (American Society of Hypertension), ‘Prof. S.C. Mahalanobish Memorial Oration Award’ from PSI (Physiological Society of India) and ‘Academic Excellence Award’ from BMANA (Bangladesh Medical Association in North America).  Dr. Majid is an active member and fellow of many scientific societies including APS, AHA, ASN, ASH etc.  He has served on various grant study sections (AHA, VA etc.) and on Editorial Boards for various national (AJP, Hypertension, ASH etc.) and international (CEPP, Antioxidants, AAJMS, BUJHC etc) journals.

Research

The overall research interests in Dr. Majid’s laboratory are mainly focused on the elucidation of the intrarenal mechanisms regulating renal hemodynamics and renal function by various vasoactive factors including nitric oxide, superoxide, angiotensin II as well as various pro-and anti-inflammatory molecules. These research activities are concentrated to investigate the renal mechanism for the development of hypertension. The experimental efforts are currently directed to obtain an improved understanding of how inflammatory cytokines, particularly tumor necrosis factor-alpha (TNF-α) could be involved in the patho-physiology of salt-sensitive hypertension (SSH). TNF-α induced responses are mediated by two receptors, TNF-α receptor type 1 (TNFR1) and type 2 (TNFR2) which are differentially expressed and regulated in the kidney. Current experiments in the laboratory are investigating the hypothesis that ‘Chronic high salt intake induces a differential activation of TNFR1 and TNFR2 at the condition of oxidative stress, which reciprocally regulates angiotensinogen (AGT) formation in the kidney leading to salt retention and thus, to the development of hypertension.’ This hypothesis suggesting a dysfunctional ‘TNFα-TNFR-AGT axis’ in the pathophysiology of SSH is supported by the recent findings in Dr. Majid’s laboratory. Future studies in this laboratory will be conducted in both in-vivo studies (acute and chronic studies in rats and mice) and in-vitro cultured cells preparations (HK-2, M-1 and RAW cells). High salt induced responses will be assessed in conditions of oxidative stress induced by inhibition of nitric oxide or by angiotensin II treatment in these studies. Using this integrated approach, it is anticipated that these experiments will be able to identify more definitive roles for TNF-α in the pathophysiology of SSH and associated renal injury which would help to develop an effective treatment strategy in this clinical condition targeting the specific TNF-α receptors.  

Laboratory Members:   

Alexander Castillo – Laboratory Research Technician

 

Publications

  1. Majid DSA (2011). Tumor necrosis factor- alpha and kidney function: Experimental findings in mice. Adv Exp Med Biol. 2011;691:471-480
  2. Castillo A, Islam MT, Prieto MC, Majid DSA (2012) Tumor necrosis factor-alpha receptor type 1, not the type 2, mediates its acute responses in the kidney. Am J Physiol Renal Physiol. 15;302:F1650-7
  3. Singh P, Bahrami L, Castillo A, Majid DSA (2013). TNF-α type 2 receptor mediates renal inflammatory response to chronic angiotensin II administration with high salt intake in mice. Am J Physiol Renal Physiol. 2013; 304: F991-9.
  4. Whiting C, Castillo A, Haque MZ, Majid DSA (2013). Protective role of the endothelial isoform of nitric oxide synthase in ANG II-induced inflammatory responses in the kidney. Am J Physiol Renal Physiol.; 305:F1031-41
  5. Singh P, Castillo A, Majid DSA (2014): Decrease in IL-10 and increase in TNF-α levels in renal tissues during systemic inhibition of nitric oxide in anesthetized mice. Physiological Reports, 2: e00228
  6. Majid DSA, Prieto MC, Navar LG (2015). Salt-Sensitive Hypertension: Perspectives on Intrarenal Mechanisms, Curr Hypertens Rev. 2015;11(1):38-483.
  7. Maiti AK, Islam MT, Satou R, Majid DS (2016). Enhancement in cellular Na+K+ATPase activity by low doses of peroxynitrite in mouse renal tissue and in cultured HK2 cells. Physiological Reports, 4: e12766.
  8. Majid DS, Navar LG (2016). The hot button issue of salt-sensitive hypertension. BLDE Univ J Health Sci 2016;1:65
  9. Mehaffey E, Majid DSA (2017). Tumor necrosis factor-alpha, kidney function and hypertension. Am J Physiol Renal Physiol. 535 [Epub ahead of print]
  10. Singh P, Castillo A, Islam, MT, Majid DSA (2017). Evidence for pro-hypertensive, pro-inflammatory effect of interleukin-10 during chronic high salt intake in the condition of elevated angiotensin II level. Hypertension. (in press)

 

PubMed listing of Dewan S.A. Majid, MBBS, Ph.D

Areas of Expertise

Research

The overall research interests in Dr. Majid’s laboratory are mainly focused on the elucidation of the intrarenal mechanisms regulating renal hemodynamics and renal function by various vasoactive factors including nitric oxide, superoxide, angiotensin II as well as various pro-and anti-inflammatory molecules. These research activities are concentrated to investigate the renal mechanism for the development of hypertension. The experimental efforts are currently directed to obtain an improved understanding of how inflammatory cytokines, particularly tumor necrosis factor-alpha (TNF-α) could be involved in the patho-physiology of salt-sensitive hypertension (SSH). TNF-α induced responses are mediated by two receptors, TNF-α receptor type 1 (TNFR1) and type 2 (TNFR2) which are differentially expressed and regulated in the kidney. Current experiments in the laboratory are investigating the hypothesis that ‘Chronic high salt intake induces a differential activation of TNFR1 and TNFR2 at the condition of oxidative stress, which reciprocally regulates angiotensinogen (AGT) formation in the kidney leading to salt retention and thus, to the development of hypertension.’ This hypothesis suggesting a dysfunctional ‘TNFα-TNFR-AGT axis’ in the pathophysiology of SSH is supported by the recent findings in Dr. Majid’s laboratory. Future studies in this laboratory will be conducted in both in-vivo studies (acute and chronic studies in rats and mice) and in-vitro cultured cells preparations (HK-2, M-1 and RAW cells). High salt induced responses will be assessed in conditions of oxidative stress induced by inhibition of nitric oxide or by angiotensin II treatment in these studies. Using this integrated approach, it is anticipated that these experiments will be able to identify more definitive roles for TNF-α in the pathophysiology of SSH and associated renal injury which would help to develop an effective treatment strategy in this clinical condition targeting the specific TNF-α receptors.  

Laboratory Members:   

Alexander Castillo – Laboratory Research Technician