Gene Expression and Levels of TGF-B in PBMC Is Associated with Severity of Symptoms in Chronic Heart Failure

Samaneh Saadati; Vajiheh Eskandari; Farzaneh Rahmani; Mohammad Jafar Mahmoudi; Zahra Rahnemoon; Zahra Rahmati; Fatemeh Gorzin; Mona Hedayat; Ali Akbar Amirzargar; Nima Rezaei

Gene Expression and Levels of TGF-B in PBMC Is Associated with Severity of Symptoms in Chronic Heart Failure

Avicenna J Med Biotechnol. 2020 Apr-Jun;12(2):132-134.

Authors

Affiliations

¹ Department of Immunology, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
² Cellular and Molecular Research Center, Faculty of Medicine, Guilan University of Medical Sciences, Rasht, Iran.
³ Research Center for Immunodeficiencies, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran.
⁴ NeuroImaging Network (NIN), Universal Scientific Education and Research Network (USERN), Tehran, Iran.
⁵ Department of Cardiology, Amir Alam Hospital, Tehran University of Medical Sciences, Tehran, Iran.
⁶ Cardiac Heart Center, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
⁷ Division of Immunology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
⁸ Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Boston, MA, USA.

PMID: 32431798
PMCID: PMC7229453

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.

Keywords: Cell culture techniques; Chronic heart failure; T-lymphocytes; Transforming growth factor beta1.