Bryant Lab

Dr. Bryant and another scientist conducting an experiment

About Dr. Bryant


Andrew J. Bryant, MD
Assistant Professor of Medicine

Research interests

Our laboratory focuses on the unique role that bone-marrow derived cells play in creating an immunotolerant microenvironment within the lung, contributing to pulmonary vascular remodeling and eventual development of high blood pressure in the lungs (pulmonary hypertension).  Specifically, we examine the role of the following related pathways in understanding the mechanisms of lung vasculopathy:

  1. Arginine metabolism: Myeloid-derived suppressor cells (MDSC) inhibit the adaptive immune response in a variety of pulmonary-related diseases including cancer, tuberculosis and obstructive sleep apnea.  Recently our group has demonstrated that these cells are necessary for the development of pulmonary hypertension, as well.  One of the mechanisms they do so is through release of proteins that influence the cellular utilization of the amino acid arginine.  Broadly, we study how arginine metabolism by these cells contributes to vessel fibrosis and narrowing, leading to pulmonary hypertension.
  2. Chemokine receptor expression and activation:  Myeloid-derived cells traffic to the lungs based upon activation of cell surface receptors that coordinate the complex anti-inflammatory response to resolving pulmonary injury.  Our lab examines how proteolytic cell-specific activation of these receptors, through canonical ligand interactions, leads to accumulation of leukocytes within the lung, leading to muscularization of pulmonary vessels and elevated pressures within the lung. 
  3. Circadian core clock signaling: In our most recent set of studies we are exploring the fundamental role of circadian influence on leukocyte activation, and involvement in pulmonary hypertension secondary to fibrosis or emphysema.

Lab Faculty and Staff

Laboratory Technician

Matthew Alves


Assistant Professor of Medicine

Andrew Bryant


Biological Scientist

Chunhua Fu


Laboratory Technician

Laylo Mukhsinova


Post-Doctoral Fellow

Aline Oliveira


Graduate Assistant

Ann Pham


Research Support


  • PH Accelerated Bayer (PHAB) Bryant (PI) 07/01/2020 – 06/30/2022 – Bayer Foundation “Myeloid cell senescence in the development of pulmonary hypertension”
  • R01HL142776 Bryant (PI) 08/01/2019 – 07/31/2024 NIH R01 – NHLBI “Role of CXCR2-mediated cell trafficking in pulmonary vascular remodeling”
  • KHL144085A Bryant (PI) 07/01/2018 – 06/30/2023 NIH K08 – NHLBI “Role of myeloid-derived suppressor cells in pulmonary hypertension associated with pulmonary fibrosis”


  • University of Florida Clinical and Translational Science Institute,“Vascular Hypoxic Signaling Regulation of Pulmonary Hypertension,” Pearson (P1), 01/16/2016-12/01/2017.
    Gilead Sciences Research Scholars Program in Pulmonary Hypertension“Role of myeloid-derived suppressor cell trafficking in development of pulmonary hypertension,” Bryant (PI), 01/17/2017-12/31/2018.
  • American Lung Association — Biomedical Research Grant, “Role of CXCR2-mediated cell trafficking in pulmonary hypertension,” Bryant (PI), 07/01/2017-06/30/2018.
    Institutional Start-Up Funds. University of Florida College of Medicine, Gatorade Fund, Bryant (PI), 07/01/2014- 06/30/2018.
  • Margaret Q. Landenberger Research Program, Bryant (PI) 01/31/2017-01/31/2019.
  • University of Florida Institute on Aging, UF OAIC Pilot Award, Leeuwenburgh (PI), 08/01/2015-03/31/2016.
  • NIH/NHLBI, “Clinical and Translational Research Training Program in Pulmonary Medicine,” Bernard (PI), 041/01/2007-06/30/2014.
  • American Thoracic Society $50,000, “Hypoxia Inducible Factor Regulation of Secondary Pulmonary Hypertension,” Bryant (PI), 01/15/13-01/14/14.

Publication Highlights

  • Bryant AJ, Shenoy V, Fu C, Marek G, Lorentsen KJ, Herzog EL, Brantly ML, Avram D, Scott EW.  Myeloid-derived suppressor cells are necessary for the development of pulmonary hypertension.  Am J Respir Cell Mol Biol. 2018 Feb;58(2):170-180.
  • Pi L, Fu C, Lu Y, Zhou J, Shenoy V, Lipson KE, Scott EW, Bryant AJ. Vascular endothelial cell-specific connective tissue growth factor (CTGF) is necessary for development of chronic hypoxia-induced pulmonary hypertension.  Front Physiol. 2018 Feb 27;9:138.
  • Rathinasabapathy A, Bryant AJ, Suzuki T, Moore C, Shay S, Gladson S, West JD, Carrier EJ. rhACE2 therapy modifies bleomycin-induced pulmonary hypertension via rescue of vascular remodeling. Front Physiol. 2018 Apr 9;9:271.
  • Bryant AJ, Mehrad B, Brusko TM, West JD, Moldawer LL.  Myeloid-derived suppressor cells and pulmonary hypertension.  Int J Mol Sci. 2018 Aug 3;19(8). pii: E2277.
  • Smith LC, Moreno S, Robertson L, Robinson S, Gant K, Bryant AJ, Sabo-Attwood T. Transforming growth factor beta1 targets estrogen receptor signaling in bronchial epithelial cells. Respir Res. 2018 Aug 30;19(1):160.
  • Bryant AJ, Fu C, Lu Y, Brantly ML, Mehrad B, Moldawer LL, Brusko TM, Brittain EL, West JD, Austin ED, Hamid R.  A checkpoint on innate myeloid cells in pulmonary arterial hypertension.  Pulm Circ. 2019 Jan-Mar;9(1):2045894018823528.
  • Oliviera AC, Fu C, Lu Y, Williams MA, Pi L, Brantly ML, Ventetuolo CE, Machuca TN, Raizada MK, Scott EW, Bryant AJ.  Chemokine signaling axis between endothelial and myeloid cells regulates development of pulmonary hypertension associated with pulmonary fibrosis and hypoxia.  Am J Physiol Lung Cell Mol Physiol. 2019 Jul 31. doi: 10.1152/ajplung.00156.2019.
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