A novel designer natriuretic peptide CD-NP suppresses TGF-beta 1 induced collagen Type I production in human cardiac fibroblasts

Abstract

Background TGF-beta 1 (TGF), is one of the potent profibrotic factors which plays a fundamental role in myocardial remodeling. Cardiac fibrosis results from excessive deposition of extracellular matrix including collagen type I (Col I) which is mainly produced by cardiac fibroblasts. CD-NP is a novel engineered designer natriuretic peptide (NP) which consists of the ring structure of human C-type NP (CNP) and the C-terminal tail of Dendroaspis NP (DNP). This unique chimeric represents the first dual particulate gaunylyl cyclase receptor activator known to co-activate both natriuretic peptide receptor (NPR)-A and NPR-B. Previously we reported that CD-NP stimulates the production of the NPR-A/B and the second messenger cyclic guanosine monophosphate (cGMP) in human cardiac fibroblasts (CFs). Here we hypothesized that CD-NP would suppress Col I expression stimulated by TGF in CFs.