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

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 Class III-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 therapeutic impact of CD treatment in symptomatic ACHF includes negative regulation of the NF-kB signaling in monocytes and the improvement of the SHP-1 activity.

Suppression of PTPN6 exacerbates aluminum oxide nanoparticle-induced COPD-like lesions in mice through activation of STAT pathway

“…Taking advantage of contemporary bioinformatics approaches, we previously showed that PTPN6 plays a vital role in cellular responses to Al 2 O 3 NPs exposure [ 14 ]. With respect to the up-stream regulator of PTPN6, activation of pro-inflammatory pathway as well as oxidative stress have been reported to suppress the expression of PTPN6 [ 41 , 42 ]. Suppression of PTPN6 recruits neutrophil to the injury site and increases neutrophil adhesion in vivo ; however, overwhelming accumulation of neutrophils in the tissue may also cause damage [ 43 ].…”