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Gene Expression and Levels of Tgf-Β in Pbmc Is Associated With Severity of Symptoms in Chronic Heart Failure



Saadati S1 ; Eskandari V2 ; Rahmani F3, 4 ; Mahmoudi MJ5 ; Rahnemoon Z6 ; Rahmati Z1 ; Gorzin F1 ; Hedayat M7, 8 ; Amirzargar AA1 ; Rezaei N3, 8
Authors
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Authors Affiliations
  1. 1. Department of Immunology, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Cellular and Molecular Research Center, Faculty of Medicine, Guilan University of Medical Sciences, Rasht, Iran
  3. 3. Research Center for Immunodeficiencies, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. NeuroImaging Network (NIN), Universal Scientific Education and Research Network (USERN), Tehran, Iran
  5. 5. Department of Cardiology, Amir Alam Hospital, Tehran University of Medical Sciences, Tehran, Iran
  6. 6. Cardiac Heart Center, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  7. 7. Division of Immunology, Boston Children's Hospital, Harvard Medical School, Boston, MA, United States
  8. 8. Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Boston, MA, United States

Source: Avicenna Journal of Medical Biotechnology Published:2020

Abstract

Background: TGF-β1 is known to promote cardiac remodeling and fibrosis during Congestive Heart Failure (CHF). In this study, an attempt was made to investigate expression of Transforming Growth Factor beta1 (TGF-β1) and relative expansion or contraction of regulatory T-cell (Tregs) population in peripheral blood of patients with Chronic Heart Failure (CHF). Methods: Real-time PCR assay was used to investigate expression and post-stimulation levels of TGF-β1 in cell culture supernatant of Peripheral Blood Mononuclear Cells (PBMC) of 42 patients with CHF and 42 controls. Flow cytometry was used to identify relative counts of CD4+ CD25+ FoxP3+ Tregs. Results: PBMCs in patients with CHF expressed higher levels of TGF-β1 compared to controls. Post-stimulation levels of TGF-β1 expression were significantly higher in New York Heart Association (NYHA) functional class IV patients compared to stage I patients. Tregs were significantly expanded in PBMC in CHF, while the CD4+ helper T-cells were unchanged. Treg expansion was more significant in NYHA functional class I patients compared to class IV patients. Conclusion: Expansion of Treg population in CHF provides an extrinsic source for TGF-β1 production to induce reactive fibrosis and cardiac remodeling. Relative decrease in Treg population at advanced stages of CHF is indicative of a loss of regulatory characteristics in these cells and unopposed proinflammatory milieu. © 2020, Avicenna Journal of Medical Biotechnology.
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Experts (# of related papers)
Nima Rezaei (1)
Ali Akbar Amirzargar (1)