Activin A increases arterial pressure in the hypothalamic paraventricular nucleus in rats by angiotension II

Abstract

Activin A, a member of the transforming growth factor β superfamily, plays an important role in the central nervous system as a neurotrophic and neuroprotective factor. The hypothalamic paraventricular nucleus (PVN) in the central nervous system is characterized as an important integrative site to regulate arterial pressure (AP). However, whether activin A in the PVN is involved in the regulation of AP is not well characterized. This study aimed to determine the effect of activin A on AP in the PVN in rats. The results showed that activin βA, activin type IIA and IIB receptors (ActRIIA and ActRIIB), and Smad2 and Smad3 mRNA expressions were detectable in the PVN of WKY rats by reverse-transcription PCR, and the expression of ActRIIA protein in the PVN was further confirmed by immunohistochemical staining. A microinjection of angiotensin II (AngII) (0.1 nmol/100 nl) or activin A (2 ng/100 nl) into the PVN increased AP significantly in WKY rats (P<0.05). Moreover, activin A (5 ng/ml) promoted AngII release from the primary cultured PVN neurons that can increase AP and upregulated the expressions of ActRIIA and Smad3 mRNA in the primary cultured PVN neurons (P<0.05). These data suggest that activin A can regulate AP in the PVN in an autocrine or a paracrine manner, which is related to AngII release and the ActRIIA-Smad3 signal pathway.

Activin A induces apoptosis of mouse myeloma cells via the mitochondrial pathway

“…It was initially isolated from porcine follicular fluid and is also known as follicle-stimulating hormone (FSH) releasing protein, due to its capacity to induce the release of FSH from the pituitary gland (1). Subsequent research has demonstrated that activin A is involved in pleiotropic functions including inflammation, arterial pressure regulation, embryonic development and tumourigenesis (2)(3)(4)(5). As with other TGF-β superfamily members, activin A functions through the serine/threonine kinase pathway.…”