Abstract
Transmembrane protein 184A (TMEM184A) was recently identified as the heparin receptor in vascular cells. Heparin binds specifically to TMEM184A and induces anti-proliferative signaling in vitro. Though it is highly conserved, the physiological function of TMEM184A remains unknown. The objective of this study was to investigate the expression and effects on vascular regeneration of TMEM184A using the adult zebrafish regenerating caudal fin as an in vivo model. Here, we show that Tmem184a is expressed in vascular endothelial cells (ECs) of mature and regenerating zebrafish fins. Transient morpholino (MO)-mediated knockdown of Tmem184a using two validated MOs results in tangled regenerating vessels that do not grow outward and limit normal overall fin regeneration. A significant increase in EC proliferation is observed. Consistent with in vitro work with tissue culture vascular cells, heparin has the opposite effect and decreases EC proliferation which also hinders overall fin regeneration. Collectively, our study suggests that Tmem184a is a novel regulator of angiogenesis.
Highlights
Heparan sulfates (HS) are long chains of polysaccharides covalently attached to a class of proteins called proteoglycans (HSPGs)
We have recently reported the in vitro expression and function of TMEM184A in vascular cells
We generated an antibody against the zebrafish Tmem184a protein
Summary
Heparan sulfates (HS) are long chains of polysaccharides covalently attached to a class of proteins called proteoglycans (HSPGs). Though HSPGs are expressed ubiquitously, their functions are tissue specific and depend on certain properties of the glycosaminoglycan chains (i.e., number of chains, length, charge) and the core protein. These chains have binding sites for several different types of proteins, and these interactions are a critical part of the regulation of many biological processes. Several members of the fibroblast growth factor family and their receptors interact with HSPGs and other cofactors, such as integrins as part of the pro-angiogenic process (Chiodelli et al, 2015)
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