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Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

1 Jan 2017Article

The NF-kB regulates the SHP-1 expression in monocytes in congestive heart failure

Mirko Pesce 1, Sara Franceschelli 2,*, Alessio Ferrone 2, Antonia Patruno 2, Alfredo Grilli 1, Maria Anna De Lutiis 1, Francesca R. Pluchinotta 3, Sonia Bergante 3, Guido Tettamanti 2,3, Graziano Riccioni 4, Mario Felaco 2, Lorenza Speranza 2
Affiliations
Article Info

1 Department of Psychological, Health and Territorial Sciences, University “G. D’Annunzio”, Chieti, Italy

2 Department of Medicine and Science of Aging, University “G. D’Annunzio”, Chieti, Italy

3 IRCCS “S. Donato” Hospital, San Donato Milanese, Piazza Edmondo Malan, 20097 Milan, Italy

4 Intensive Cardiology Care Unit, San Camillo de Lellis Hospital, San Severo (FG) 71016, Italy

Abstract

It has been shown that functional recovery of patients with acute congestive heart failure (ACHF) after treatment with conventional drugs (CD) is mediated by suppression of inflammation in peripheral blood mononuclear cells. Here, we analyzed gene expression profiles of monocytes from symptomatic ACHF patients (NYHA ClassIII-IV) before and after pharmacological treatment with CD. The treatment was associated with selective down-regulation of “TNFR signaling” and pro-inflammatory mediators CCL5, MIP-1α receptor, CD14, ITGAM, and significant up-regulation of “TNFR signaling” as evidenced by increase in anti-inflammatory factors including NF-kBIA, TNFAIP3 and SHP-1. In monocyte TNF-alpha-stimulated there is a down-regulation of the phosphatase SHP-1 which induces a significant activation of TAK-1/IKK/NF-kB signaling. These findings suggest that the therapeuticimpact of CD treatment in symptomatic ACHF includes negative regulation of the NF-kB signaling in monocytes and the improvement of the SHP-1 activity.

Keywords

  • ACHF
  • Pharmacological Treatment
  • Monocytes
  • Inflammation
  • NF-kB
  • SHP-1
  • TAK-1

References