Assistant Professor
Department of Obstetrics and Gynecology

Scott & White Hospital Building # 1, Room # 352, 2401 S 31st Street
Temple, Texas 76508
Phone: 254-724-3624
Fax: 254-724-1046

Education and Post-Graduate Training

  • B.Sc. (Hons) and M.Sc. in Biochemistry and Molecular Biology, University of Dhaka, Bangladesh (1988 & 1990)
  • Ph.D: Gifu University, Gifu, Japan (2000)
  • Postdoctoral Fellow: Japan Society for Promotion of Science, Gifu University, Japan (2003-2005)
  • Postdoctoral Research Associate, Assistant Research Scientist: Texas A& M Health Science Center College of Medicine and Scott & White Healthcare, Temple, Texas, USA (2006-2010).


  • Assistant Professor, Department of Obstetrics and Gynecology, Texas A&M University College of Medicine/Scott & White Healthcare, Temple, Texas, USA (2011 to present)
  • Staff Research Scientist, Scott & White Memorial Healthcare, Temple, Texas, USA (2011 to present)
  • Research Faculty, Obstetrics and Gynecology Residency and Female Pelvic Medicine and Reconstructive Surgery Fellowship Programs, Scott & White Healthcare, Temple, Texas, USA (2011 to present)
  • Graduate Faculty Member, Texas A&M Health Science Center School of Graduate Studies, Temple, Texas, USA (2012 to present)
  • Adjunct Faculty, Texas Bioscience Institute, Temple, Texas, USA (2012 to present)
  • Assistant Research Scientist, Texas A&M Health Science Center, Temple, TX (2010-2011)
  • Lecturer, Assistant Professor and Associate Professor,  Department of Biochemistry and Molecular Biology, University of Dhaka, Bangladesh (1991-2006)

Research Interests

Preeclampsia (preE) is a systemic and hypertensive pregnancy disorder, which occurs in 3 to 10% of all gestations—accounting for approximately 60,000 maternal deaths per year worldwide. PreE is characterized by the de novo onset of hypertension and proteinuria in pregnancy. The triggers of this condition remain elusive, and pathogenic mechanisms remain ambiguous, resulting in a failure to develop specific screening, preventive, and treatment strategies.

Dr. Uddin’s lab focuses on translational research in maternal fetal medicine especially hypertension during pregnancy. The long-term goal of his lab is to determine the pathogenesis and molecular signaling in hypertension during pregnancy (preE). The potential significance of his research is that successful completion may identify molecular therapeutic targets may be identified to effectively treat preE. He is using animal models (rodents and small monkey species), several human cell lines, and patients for his research.

Research Topics 

Studies on the (pro) renin and its Receptor Associated Novel Renin-Angiotensin System and Placental Perfusion in Preeclampsia: preE affects the placenta which releases substances into the circulation that affect the mother's kidney, liver, and brain. It often results in premature delivery of the baby. Dr. Uddin is looking at the renin-angiotensin system (RAS) in preE, specifically, (pro)renin and its receptor, in the dysregulation of circulation through the uterine-placental circulation during the preE process. In evaluating the function of RAS, (pro)renin, and (pro)renin receptor in a rat model of preE, Dr. Uddin found that the utero-placental RAS was activated and the maternal circulatory RAS was suppressed. However, both the utero-placental receptor and circulatory levels of (pro)renin are increased in these rats. He proposes the hypothesis that (pro)renin receptor-mediated activation of RAS leads to an alteration placental circulation reducing the exchange of oxygen and nutrients in the placenta. His overall goal is to understand the involvement of (pro)renin and its receptor in the cause of the altered extent and timing for regulation of perfusion (the passage of fluids)  through the maternal-fetal unit in the pathogenesis of preE. These studies are intended to provide new evidence that (pro)renin and its receptor play key roles in dysregulation of perfusion and point to promising new therapeutic targets.

Preeclampsia in the Owl Monkey Model to Understand the Pathogenesis: A class of endogenous cardiotonic hormones that can trigger preE in rodents and is increased in patients with preE. In order to test the safety of agents that may block the effects of these agents without harming mother or developing fetus, a species with more similarity to humans than rats must be tested first. One type of monkey species, the owl monkey, a small neotropical monkey from South America, is sensitive to agents and mechanisms that produce increased blood pressure. There are good breeding populations of the monkey in research facilities in central Texas. Previous work by Dr. Uddin and others supports the novel hypothesis that cardiotonic hormones might also produce preE in nonhuman primates using a specific molecular pathway that can be blocked in cultured cells by inhibitors. These studies will examine whether these agents and this mechanism for preE pathogenesis can be demonstrated for the first time in a primate species and whether such treatments are safe to use in pregnancy. 

Evaluate potential linkage between the risk of developing preeclampsia and the presence of diabetes in pregnant patients or the development of gestational diabetes: The concept is that poor glucose regulator control may stimulate one of more mechanisms of cells involved in the vascular remodeling during implantation and placental development, so that pathways leading to vascular compromise are stimulated. The focus of the studies used to develop these risk factor assessments was pooling results from a meta-analysis of many studies of patients with and without preE symptoms.  Based on some preliminary work in our lab, we suspect that elevated glucose levels in pregnancy may stimulate a cascade of vascular development that will predispose to development of placental vascular compromise. Under such conditions, vascular responses can trigger preE pathways. Therefore, we propose to obtain epidemiologic information from a large patient population with subsets of patients who become pregnant who also have pre-existing diabetes and patients who develop gestational diabetes in ethnic groups with high frequencies of both diabetes and preE in pregnancy.

Dr. Uddin’s translational research group consists of basic and physician scientists including medical students, residents, fellows and research associates. Prospective postgraduate and medical students are encouraged to contact Dr. Uddin if interested in this area of research.

Selected Publications

    • Uddin MN, Allen S, Jones R, Glaser SS, Zawieja DC, Kuehl TJ. Pathogenesis of preeclampsia: translational aspects: marinobufagenin and angiogenic imbalance as biomarkers of the syndrome. Transl Res. 2012; 160: 99-113.
    • Afroze SH, Uddin MN, Cao X, Asea A, Gizachew D. Internalization of exogenous ADP-ribosylation factor 6 (Arf6) proteins into cells. Mol Cell Biochem. 2011 Apr 27.
    • Munshi MK, Uddin MN, Glaser SS. The role of the renin-angiotensin system in liver fibrosis. Exp Biol Med (Maywood). 2011; 236: 557-66.
    • Agunanne E, Horvat D, Harrison R, Uddin MN, Jones R, Kuehl TJ, Abi Ghanem D, Berghman LC, Romo D, Lai X,  Puschett JB. Marinobufagenin levels in preeclamptic patients: a preliminary report. Am J Perinatol. 2011 Mar 4.
    • Abi-Ghanem D, Lai X, Berghman LR, Horvat D, Li J, Romo D, Uddin MN, Kamano Y, Nogawa T, Xu JP, Pettit GR, Puschett JB. A chemifluorescent immunoassay for the determination of marinobufagenin in body fluids. J Immunoassay and Immunochemistry. 2011; 32: 31- 46.
    • Uddin MN, Horvat D, DeMorrow S, Agunanne E, Puschett J. Marinobufagenin is an upstream modulator of Gadd45a stress signaling in preeclampsia. Biochim Biophys Acta. 2010 Sep 17.
    • Uddin MN, Agunanne E, Horvat D, Puschett JB. Resibufogenin Administration Prevents Oxidative Stress in a Rat Model of Human Preeclampsia. Hypertens Pregnancy. 2010 Dec 21.
    • Agunanne E, Uddin MN, Horvat D, Puschett JB. An analysis of the role of angiogenic factors in a rat model of preeclampsia. Am J Nephrol. 2010; 32: 332-9.
    • Puschett JB, Agunanne E, Uddin MN. Emerging role of the bufodienolides in cardiovascular and renal disease. Am J Kidney Diseases. 2010 Apr 21.
    • Puschett JB, Agunanne E, Uddin MN. Marinobufagenin, resibufagenin and preeclampsia. Biochim Biophys Acta. 2010 Feb 16.
    • Nurun Nabi AHM, Biswas KB, Arai Y, Uddin MN, Nakagawa T, Ebihara A, Ichihara A, Inagami T, Suzuki F. Functional characterization of the decoy peptide, R10pIFLKRMPSI. Front Biosci (Elite Ed). 2010; 2: 1211-1217.
    • Uddin MN, Agunanne E, Horvat D, Puschett JB. Alterations in the Renin-Angiotensin System in a Rat Model of Human Preeclampsia. Am J Nephrol. 2010; 31: 171-177.
    • Agunanne E, Horvat D, Uddin MN, Puschett JB. The treatment of preeclampsia in a rat model employing Digibind®. Am J Perinatol. 2010; 27: 299-305.
  • Uddin MN, Childs EW, Horvat D, Puschett JB. Marinobufagenin enhances endothelial permeability via activation of apoptotic signaling. Am J Physiol Regul Integr Comp Physiol. 2009; 296: R1726-R1734.
  • Uddin MN, McLean LB, Hunter FA, Horvat D, Severson J, Tharakan B,  Childs EW,  Puschett  JB. Vascular Leak in a Rat Model of Preeclampsia. Am J Nephrol. 2009; 30: 26-33.
  • Horvat D, Uddin MN, Severson S, Puschett JB. Resibufogenin prevents the manifestations of preeclampsia in an animal model of the syndrome. Hypertension in Pregnancy. 2009; 18: 1-9.
  • Uddin MN, Horvat D, Glaser S, Mitchell BM, Puschett JB. Examination of the cellular mechanism by which marinobufagenin inhibits cytotrophoblast function. J Biol Chem.  2008; 283: 17946-17953.
  • Uddin MN,  Horvat D, Glaser S, Danchuk S, Mitchell BM, Sullivan DE, Morris CA,  Puschett JB. Marinobufagenin inhibits proliferation and migration of cytotrophoblast and CHO cells. Placenta 2008; 29: 266-273.
  • Uddin MN, Nurun Nabi AHM, Nakagawa T, Ichihara A, Inagami T, Suzuki F. Non-proteolytic activation of prorenin: activation by (pro)renin receptor and its inhibition by a prorenin prosegment, decoy peptide. Frontiers in Bioscience. 2008; 13: 745-753.
  • Danchuk S, Sukhanov S, Horvat D, Uddin MN, Puschett JB. Effects of Resibufogenin in experimental hypertension. Amer J Nephrol. 2008; 28: 8-13.
  • Sultana A, Nurun Nabi AHM, Uddin MN, Maruyama H, Suzuki KM, Mishima S, Suzuki F. A dipeptide YY derived from royal jelly proteins inhibit renin activity. International J Mol. Med. 2008; 21: 677-682.
  • Nurun Nabi AHM, Uddin MN, Nakagawa T, Iwata H, Ichihara A, Park EY, Inagami T, Suzuki F. Biochemical and enzymatic properties of prorenin: role of the “handle” peptide of the prosegment sequence in the binding and activation of prorenin molecule in receptor associated prorenin system. Frontiers in Bioscience. 2007; 12: 4810-4817.
  • Kaneshiro Y, Ichihara A, Takemitsu T, Sakoda M, Nurun Nabi AHM, Uddin MN, Nakagawa T, Nishiyama A, Suzuki F, Inagami T, Itoh H. Slowly Progressive, Angiotensin II- Independent Glomerulosclerosis in Human-(Pro) renin-Receptor-Transgenic Rats. J Am Soc Nephrol. 2007; 18: 1789-1795.
  • Hayashi T, Urayama O, Hori M, Sakamoto S, Uddin MN, Iwanaga S, Hayashi K, Suzuki F, Kawai K, Murakami K. Laughter modulates prorenin receptor gene expression in patients with type 2 diabetes. J Psychosom Res. 2007; 62: 703-706.
  • Nurun Nabi AHM, Kageshima A, Uddin MN, Nakagawa T, Park EY, Suzuki F. Binding properties of rat prorenin and renin to the recombinant rat renin/prorenin receptor prepared by a baculovirus expression system. International J Mol Med. 2006; 18: 483- 488.
  • Uddin MN, Iwanaga S, Nurun Nabi AHM, Urayama O, Hayashi K, Hayashi T, Kawai K, Sultana A, Murakami K, Suzuki F. Laughter therapy modulates the parameters of renin-angiotensin system in patients with type 2 diabetes. International J Mol Med. 2005; 16: 1077- 1081.
  • Nurun Nabi AHM, Uddin MN, Nakagawa T, Orihashi T, Ebihara A, Nakamura Y, Suzuki F. Roles of His9 (P2 subsite) and His13 (P3’ subsite) in angiotensinogen for catalytic reaction of renin. International J Mol. Med. 2005; 16: 103 - 7.
  • Ichihara A, Hayashi M, Kaneshiro Y, Suzuki F, Nakagawa T, Tada Y, Koura Y, Nishiyama A, Okada H, Uddin MN, Nurun Nabi AHM, Ishida Y, Inagami T, Saruta T. Inhibition of diabetic nephropathy by a decoy peptide corresponding to the handle region for non-proteolytic activation of prorenin. J Clin Invest. 2004; 114: 1128-1135.
  • Suzuki F, Hayakawa M, Nakagawa T, Uddin MN, Ebihara A, Iwasawa A, Ishida Y, Nakamura Y, Murakami K. Human prorenin has the regions of gate and handle for its non-proteolytic activation. J Biol Chem. 2003; 278: 22217-22222.
  • Rahman SM, Huda MN, Uddin MN, Akhtaruzzaman S. Short-term administration of Conjugated Linoleic acid reduces liver triglyceride concentration and phosphatidate phosphohydrolase activity in OLETF rats. Journal of Biochemistry and Molecular Biology. 2002; 35: 494-497.
  • Ebihara A, Uddin MN, Yoshida S, Kondou T, Nakagawa T, Fukamizu A, Suzuki F, Nakamura Y, Murakami K. Sialic acid residue of ovine angiotensinogen does not affect the reactivity to Human renin. Biomed Res. 2000; 21: 105-109.
  • Ebihara A, Kondou T, Mizuno S, Nakagawa T, Uddin MN, Inui Y, Fukamizu A, Suzuki F, Nakamura Y, Murakami K. Molecular properties of recombinant ovine angiotensinogen. Biomed Res. 2000; 21: 247-254.
  • Suzuki F, Hatano Y, Nakagawa T, Terazawa K, Gotoh A, Uddin MN, Ishida Y, Yakamura Y. Non-proteolytic Activation of Human Prorenin by Anti-prorenin Prosegment (pf # 1 : 15P) Antiserum. Biosci Biotech Biochem. 1999; 63: 550-554.
  • Uddin MN, Suzuki F, Nagai T, Nakagawa T, Nakamura Y. Tyrosine-83 of Human Renin Contributes to Biphasic pH Dependence of the Renin-angiotensinogen Reaction. Biosci Biotech Biochem. 1999; 63, 1143-114.
  • Uddin MN, Takahashi K, Nagai T, Nakagawa T, Suzuki F, Nakamura Y. Two peaks in pH Dependence of Renin-angiotensinogen Reaction. Biosci Biotech Biochem. 1998; 62: 338-340.