Partha Dutta, DVM, Ph.D.

Professor and Director, Center for Cardiovascular Inflammation, The role of the immune system on cardiovascular disease

Possible Rotation Projects:

  • The importance of brain regions in controlling inflammation and cardiac remodeling after myocardial infarction.
  • Cellular metabolism in macrophages in cardiovascular disease
  • Epigenetic alterations of macrophages in modulating inflammation

Training Technologies Used:

  • Flow cytometry
  • Cytek Aurora
  • ChipCytometry
  • scRNA seq
  • scATAC seq
  • spatial transcriptomics
  • machine learning
  •  intravital microscopy
Education & Training
  • DVM, West Bengal University of Animal and Fishery Sciences, India, 2003
  • MS, Wichita State University, KS, 2006
  • PhD, University of Wisconsin-Madison, WI, 2010
Recent Publications

Vasamsetti SB, Sadaf S, Uddin MA, Shen J, Johny E, Mondal A, Florentin J, Lei L, Mannan A, Rao KS, Sembrat J, Rojas M, Sipula I, Kastroll J, Jurczak MJ, Shiva S, O’Doherty RM, Yechoor V, Dutta P. Tissue-resident macrophage survival in chronic inflammation depends on mitochondrial function regulated by SerpinB2. Nature Communications. 2026. PMCID: PMC12902017

 

Ohayon-Steckel L, Zhang X, Haque S, Uddin MA, Dasari A, Kurian DG, Coppin E, Natarajan N, Johny E, Dutta A, Ouyang Y, Espinosa-Diez C, Stiekema L, Stroes ES, Sadovsky Y, Wang B, Dutta p. miR-499 in platelet-derived extracellular vesicles augments inflammatory cell generation and cardiac remodeling after myocardial infarction. Circulation. 2025. PMCID: PMC12743312

 

Natarajan N, Florentin J, Johny E, Xia H, O’Neill S P, Lei L, Shen J, Ohayon L, Johnson A R, Rao K, Li X, Zhao Y, Zhang Y, Tavakoli S, Shiva S, Das J, Dutta P. Aberrant mitochondrial DNA synthesis in macrophages exacerbates inflammation and atherosclerosis. Nature Communications. 2024. PMCID: PMC11347661.

 

Coppin E, Zhang X, Ohayon L, Johny E, Dasari A, Zheng KH, Stiekema L, Cifuentes-Pagano E, Pagano PJ, Chaparala S, Stroes ES, Dutta P. Peripheral ischemia imprints epigenetic changes in hematopoietic stem cells to propagate inflammation and atherosclerosis. Atheroscler Thromb Vasc Biol. 2023. PMCID: PMC10213134.This article was chosen as “Editor’s Pick” in the June 2023 issue: PMID: 37051930.

 

Florentin J, Zhao J, Tai Y-Y, O’Neil SP, Kumar R, Arunkumar A, Watson A, Sembrat J, Bullock GC, Sanders L, Kassa B, Rojas M, Graham BB, Chan SY, Dutta P. Interleukin-6 mediates neutrophil mobilization from bone marrow in pulmonary hypertension. Cell and Mol Immunol. 2021. 18(2). PMCID: PMC8027442.

 

Vasamsetti SB, Coppin E, Zhang X, Florentin J, Koul S, Gotberg M, Clugston AS, Thoma F, Sembrat J, Bullock GC, Kostka D, St. Croix CM, Chattopadhyay A, Rojas M, Mulukutla S, Dutta P. Apoptosis of hematopoietic progenitor-derived adipose tissue resident macrophages contributes to insulin resistance after myocardial infarction. Sci Trans Med. 2020. 12(553). PMCID: PMC7813555

 

Zhao J, Florentin J, Tai Y, Torrino S, Ohayon L, Brzoska T, Tang T, Negi V, Woodcock CC, Risbano M, Nouraje SM, Sundd P, Bertero T*, Dutta P*, Chan SY*. Long range endocrine delivery of circulating miR-210 to endothelium promotes pulmonary hypertension. Circ Res. 2020. PMCID: PMC7429300. *Co-senior authors.

 

Vasamsetti SB, Florentin J, Coppin E, Stiekema L, Zheng KH, Nisar MU, Levinthal D, Rojas M, Stroes ES, Kim K, Dutta P. Sympathetic neuronal activation triggers myeloid progenitor proliferation and differentiation. Immunity. 2018. 49(1):93-106. PMCID: PMC6051926.

 

Dutta P#, Hoyer FF, Grigoryeva LS, Sager HB, Leuschner F, Courties G, Borodovsky A, Novobrantseva Y, Ruda VM, Fitzgerald K, Iwamoto Y, Wojtkiewicz G, Sun Y, Da Silva N, Libby P, Anderson DG, Swirski FK,  Weissleder R, and Nahrendorf M. Macrophages retain hematopoietic stem cells in the spleen via VCAM-1 in atherosclerosis. J Exp Med 2015 Apr 6;212(4): 497-512. PMCID: PMC4387283. #Corresponding author

 

Dutta P, Courties G, Wei Y, Leuschner F, Gorbatov R, Robbins CS, Iwamoto Y, Thompson B, Carlson AL, Heidt T, Majmudar MD, Lasitschka F, Etzrodt M, Waterman P, Waring MT, Chicoine AT, van der Laan AM, Niessen HW, Piek JJ, Rubin BB, Butany J, Stone JR, Katus HA, Murphy SA, Morrow DA, Sabatine MS, Vinegoni C, Moskowitz MA, Pittet MJ, Libby P, Lin CP, Swirski FK, Weissleder R, and Nahrendorf M. Myocardial infarction accelerates atherosclerosis. Nature 2012. Jul 19;487(7407):325-329. PMCID: PMC3401326

 

Full List of Publications

 

Research Interests

Cardiovascular disease is the leading cause of death in developed countries. Inflammation aggravates outcome of cardiovascular disease including atherosclerosis and infarct healing after myocardial infarction (MI) (Nature Biotechnology, 2011). During progression of atherosclerosis, myeloid cells destabilize lipid-rich plaques in the arterial wall and cause their rupture, thus triggering myocardial infarction and stroke. Survivors of acute coronary syndromes have a high risk of recurrent events for unknown reasons. We showed that the systemic response to ischemic injury aggravates chronic atherosclerosis (Nature, 2012). After myocardial infarction or stroke, ApoE-/- mice developed larger atherosclerotic lesions with a more advanced morphology and inflammation. This disease acceleration persisted over many weeks and was associated with markedly increased monocyte recruitment.

One of our current research interests focuses on immunology of cardiovascular disease. Our published studies have demonstrated the merit of myeloid cells in disease pathogenesis (Immunity, 2018; Science Translational Medicine, 2020, Nature Communications, 2024; Circulation, 2026; and Nature Communications, 2026) We are investigating how myeloid cells, such as monocytes and macrophages, induce inflammation in metabolic disease such as type II diabetes and cardiovascular disease such as myocardial infarction. The ultimate goal of the lab is to develop potential therapeutic avenues to check generation of myeloid cells in the bone marrow and spleen, and recruitment of myeloid cells to sites of inflammation such as adipose tissue and the myocardium. We are also keenly interested to investigate differential functions of tissue resident and monocyte-derived macrophages in steady state and disease.