Beneficial Effects of Angiotensin-(1–7) on CD34+ Cells From Patients With Heart Failure. Issue 3 (March 2018)

• Record Type: Journal Article
• Authors: Cole-Jeffrey, Colleen T.; Pepine, Carl J.; Katovich, Michael J.; Grant, Maria B.; Raizada, Mohan K.; Hazra, Sugata
• Is Part Of: Journal of cardiovascular pharmacology. Volume 71:Issue 3(2018)
• Publication Date: 2018-03
• Subjects: CD34+ cells -- renin–angiotensin system -- angiotensin-(1–7) -- heart failure; Cardiovascular Diseases -- drug therapy -- Periodicals; Cardiovascular System -- drug effects -- Periodicals; Cardiovascular pharmacology -- Periodicals; Cardiovascular agents -- Periodicals; Cardiovascular agents; Cardiovascular pharmacology; Periodicals; 615.7105
• DOI: 10.1097/FJC.0000000000000556
• Languages: English
• ISSNs: 0160-2446

Abstract

Abstract : Abstract: The dysfunctional nature of CD34 + cells from patients with heart failure (HF) may make them unsuitable for autologous stem-cell therapy. In view of evidence that the vasoprotective axis of the renin–angiotensin system (RAS) improves CD34 + cell functions, we hypothesized that CD34 + cells from patients with HF will be dysfunctional and that angiotensin-(1–7) [Ang-(1–7)] would improve their function. Peripheral blood was collected from New York Heart Association class II-IV patients with HF (n = 31) and reference subjects (n = 16). CD34 + cell numbers from patients with HF were reduced by 47% ( P < 0.05) and also displayed 76% reduction in migratory capacity and 56% ( P < 0.05) lower production of nitric oxide. These alterations were associated with increases in RAS genes angiotensin-converting enzyme and AT2R (595%, P < 0.05) mRNA levels and 80% and 85% decreases in angiotensin-converting enzyme 2 and Mas mRNA levels, respectively. Treatment with Ang-(1–7) enhanced CD34 + cell function through increased migratory potential and nitric oxide production, and reduced reactive oxygen species generation. These data show that HF CD34 + cells are dysfunctional, and Ang-(1–7) improves their functions. This suggests that activation of the vasoprotective axis of the RAS may hold therapeutic potential for autologous stem-cell therapy in patients with HF.