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Brett Mitchell, PhD, FAHA

Brett Mitchell
Brett Mitchell, PhD, FAHA

Professor

Director, Summer Undergraduate Research Program

Director, Medical Sciences MS Degree Program

Contact

Medical Physiology
8447 Riverside Pkwy
2412 Medical Research and Education Building 2
Bryan, TX 77807
brettmitchell@tamu.edu
Phone: 979.436.0751

Biography

Brett Mitchell is a Professor of Medical Physiology located in Bryan, Texas. He received his BA in Health Fitness/Biology from Gustavus Adolphus College in 1995, and his MS in Human Physiology from the University of Wisconsin-La Crosse in 1996. He received his PhD in Physiology from the Medical College of Georgia in 2003, where he worked with Dr. Clinton Webb studying endothelial dysfunction and hypertension. His postdoctoral work was performed at Universities Space Research Association, located at NASA's Johnson Space Center in Houston. Brett then joined the faculty of Baylor College of Medicine in the Department of Molecular Physiology and Biophysics, where he began studying the role of immunophilins in endothelial function and blood pressure regulation. Brett joined the faculty at the Texas A&M University Health Science Center in July 2007 as an Assistant Professor and in 2012 received tenure and was promoted to Associate Professor. In 2020 he was promoted to Professor.

Education and Training

  • Gustavus Adolphus School, BA, Health Fitness/Biology, 1995
  • University of Wisconsin-LaCrosse, MS, Human Physiology, 1996
  • Medical School of Georgia, PhD, Physiology, 2003

Research Interests

  • Immunity, Inflammation, and Hypertension
  • Our research focuses on understanding the molecular mechanisms involved in the development of endothelial dysfunction and hypertension caused by various immune system activators such as salt, angiotensin II, viruses, and bacteria. Alterations in both the innate and adaptive immune system can elicit persistent, pro-inflammatory effects on major blood pressure-regulating organs such as the kidney and blood vessels. Our goal is to develop therapies that target certain immune cells and the immune system-cardiovascular system interaction in an effort to reduce the incidence and severity of hypertension. Our research focuses on the following:
  • Renal lymphatic vessels and immune cell trafficking in hypertension
  • Immunosuppressive drugs and how they cause hypertension
  • Hypertension and organ damage during pregnancy (Preeclampsia)

Representative Publications

Google Scholar Profile

NCBI Bibliography

ResearchGate Profile

  • Balasubbramanian D, Baranwal G, Clark MCC, Goodlett B, Mitchell BM*, Rutkowski JM*. Kidney-specific lymphangiogenesis increases sodium excretion and lowers blood pressure in mice. J Hypertens 2020;38:874-885. PMC7754173 doi: 10.1097/HJH.0000000000002349. (*BMM and JMR are Co-Corresponding Authors)
  • Lopez Gelston CA, Balasubbramanian D, Abouelkheir GR, Lopez AH, Hudson KR, Johnson ER, Muthuchamy M, Mitchell BM*, Rutkowski JM*. Enhancing renal lymphatic expansion prevents hypertension in mice. Circ Res 2018;122:1094-1101. (*BMM and JMR are Co-Corresponding Authors) (Cover image of renal lymphatics was selected by the Editors)
  • Chatterjee P, Chiasson VL, Seerangan G, De Guzman E, Milad M, Bounds KR, Gasheva O, Tobin RP, Hatahet M, Kopriva S, Jones KA, Newell-Rogers MK, Mitchell BM. Depletion of MHC class II invariant chain peptide or gamma-delta T-cells ameliorates experimental preeclampsia. Clin Sci (Lond) 2017;131:2047-2058. (Project was selected as 1 of 64 from universities around the country for 2018 STAT MADNESS competition, reached the Final Four)
  • Chiasson VL, Pakanati AR, Hernandez M, Young KJ, Bounds KR, Mitchell BM. Regulatory T cell augmentation or interleukin-17 inhibition prevents calcineurin inhibitor-induced hypertension in mice. Hypertension 2017;70:183-191. (1 of 3 papers from the entire issue chosen for a Clinical Implications foreword) PMC5501301
  • Chatterjee P*, Chiasson VL*, Pinzur L, Raveh S, Abraham E, Jones KA, Bounds KR, Ofir R, Flaishon L, Chajut A, Mitchell BM. Human placenta-derived stromal cells decrease inflammation, placental injury, and blood pressure in hypertensive pregnant mice. Clin Sci (Lond) 2016;130:513-523.
  • Nguyen H, Chiasson VL, Young KJ, Chatterjee P, Mitchell BM. Interleukin-17 causes rho-kinase-mediated endothelial dysfunction and hypertension. Cardiovasc Res 2013;97:696-704. PMC3583258
  • Chiasson VL, Jones KA, Kopriva SE, Mahajan A, Young KJ, Mitchell BM. Endothelial cell transforming growth factor-* receptor activation causes tacrolimus-induced renal arteriolar hyalinosis. Kidney Int 2012;82:857-866. PMC3396764 **Editorial Commentary: Morrissey JJ. Direct or indirect endothelial cell transforming growth factor-* receptor activation initiates arteriolar hyalinosis. Kidney Int 2012;82:838-839.
  • Chatterjee P*, Weaver LE*, Doersch KM*, Kopriva SE, Chiasson VL, Allen SJ, Narayanan AM, Young KJ, Jones KA, Kuehl TJ, Mitchell BM. Placental Toll-like receptor 3 and Toll-like receptor 7/8 activation contributes to preeclampsia in humans and mice. PLoS ONE 2012;7:e41884. PMC3407075
  • Chiasson VL, Talreja D, Young KJ, Chatterjee P, Banes-Berceli A, Mitchell BM. FK506 binding protein 12 deficiency in endothelial and hematopoietic cells decreases regulatory T cells and causes Th17 cell-mediated hypertension. Hypertension 2011;57:1167-1175. PMC3108179 **Editorial Commentary: Didion SP. Tacrolimus-induced hypertension: What's endothelial and hematopoietic FKBP12 got to do with it? Hypertension 2011;57:1058-1060.
  • Long C, Cook LG, Wu GY, Mitchell BM. Removal of FK506 Binding Protein 12/12.6 from endothelial ryanodine receptors leads to an intracellular calcium leak and endothelial dysfunction. Arterioscler Thromb Vasc Biol 2007;27:1580-1586.

Recent Publications