Sema3A and neuropilin-1 expression and distribution in rat white adipose tissue

Abstract

Semaphorins are cell surface and/or soluble signals that exert an inhibitory control on axon guidance. Sema3A, the vertebrate-secreted semaphorin, binds to neuropilin-1, which together with plexins constitutes the functional receptor. To verify whether Sema3A is produced by white adipocytes and, in that case, to detect its targets in white adipose tissue, we studied the cell production and tissue distribution of Sema3A and neuropilin-1 in rat retroperitoneal and epididymal adipose depots. Sema3A and neuropilin-1 were detected in these depots by Western blotting. The immunohistochemical results showed that Sema3A is produced in, and possibly secreted by, smooth muscle cells of arteries and white adipocytes. Accordingly, neuropilin-1 was found on perivascular and parenchymal nerves. Such a pattern of distribution is in line with a role for secreted Sema3A in the growth and plasticity of white adipose tissue nerves. Indeed, after fasting, when white adipocytes are believed to be overstimulated by noradrenaline and rearrangement of the parenchymal nerve supply may occur, adipocytic expression of Sema3A is reduced. Finally, the presence of neuropilin-1 in some white adipocytes raises the interesting possibility that Sema3A also exerts an autocrine-paracrine role on these cells.

Regional-dependent Increase of Sympathetic Innervation in Rat White Adipose Tissue during Prolonged Fasting

“…Nonetheless, it should be noted that white adipocytes have recently been shown to produce and secrete nerve growth factor (Peeraully et al 2004). Furthermore, expression of Sema3A, a neurorepellent factor, is reduced in smooth muscle cells of WAT arteries and white adipocytes of fasted rats (Giordano et al 2003), suggesting that a rearrangement of vascular and parenchymal nerves occurs in this condition. Double staining of slimmed WAT sections with TH and the pan-nerve marker PGP 9.5 evidenced very few non-noradrenergic nerves at the vascular and the parenchymal levels.…”

The Changing Balance Between Osteoblastogenesis and Adipogenesis in Aging and its Impact on Hematopoiesis

“…Addition of anti-NP1 antibody into these co-cultures abrogated this effect. NP1 is one of the receptors for vascular endothelial growth factor, is known to be expressed in WAT and bone marrow (BM) APs, and is known to suppress granulopoiesis [5, 60, 61]. …”

“…Concomitant with these changes, there is also a decline in hematopoiesis with aging affecting both myeloid and lymphoid lineage cells accompanied by a gradual replacement of bone marrow stromal cells with adipose tissue [3, 4]. As osteoblasts (OBs) and adipocytes (APs) share a common mesenchymal ancestor [5] and are in intimate contact with hematopoietic cells within the bone marrow, understanding how aging affects the development and interactions between these cell lineages may ultimately help older individuals combat bone loss diseases and hematopoietic disorders.…”

Semaphorin 3C is a novel adipokine linked to extracellular matrix composition

“…Very little is known regarding the role of SEMA3 members in WAT. Only one publication has studied the expression of Sema3a in rat WAT [10]. SEMA3s signal through cognate receptors and coreceptors termed plexins (PLXNs) and neuropilins (NRPs), respectively, but the intracellular pathways are poorly characterised [11].…”