#4000 ROLE OF ENDOTHELIAL CELLS IN VASCULAR CALCIFICATION

Abstract Background and Aims Vascular calcification (VC) represents a common pathological feature of cardiovascular disease VC caused by hyperphosphatemia is one the hallmarks chronic kidney (CKD). Therefore, elucidating pathogenesis may have significant clinical benefits for CKD patients. smooth muscle cells challenged with high-phosphate (Pi) actively participate to trans-differentiating into simil-osteoblastic that acquire capability deposit hydroxyapatite crystals in extracellular matrix tunica media arteries. The role endothelial (ECs) high-Pi has been poorly investigated until now. Nonetheless, following particular stimuli ECs can lose their characteristics several different phenotypes transdifferentiating process known as endothelial-to-mesenchymal transition (EndMT). Given central patients wellbeing we decided investigate whether process. Method We set up an vitro model human aortic (HAECs) 2, 2.5, 3, 3.5 mM 7 days. Calcium deposition, cell viability trans-differentiation were evaluated. Results In our observed deposition calcium phosphate induced resulted from 3 Pi (Ctr 0.43 ± 0.01; 6.72 1.15; 17.31 1.88; micromol Ca++/mg protein; P < .01; Fig 1A-B). found mediated Pi-influx, demonstrated inhibition Phosphonoformic acid (PFA), inhibitor Na/Pi cotransporter Pit-1 (3.5 15.52 1.97; 1 PFA 0.6 0.05; .0001; 1A, C). addition, did not show any toxic effect at every concentration tested compared control cells. Pi-treated clear change cell-morphology cobblestone spindle shaped, recognized sign EndMT. Moreover, composition more similar osteoblastic matrix. facts, treated Alcian Blue positive, staining binds glycosaminoglycans contained bone matrix, blue granules calcium-phosphate cytoplasm Starting day 5 was confirmed up-regulation SNAIL N-cadherin mRNA expressions, master genes markers EndMT process, respectively. A modification phenotype also supported progressive decrease protein expression Von Willebrand factor VE-Cadherin 9 (−53.7% −32.6% respectively). till some differentiation signs such increase RUNX2 BMP2 protective MGP levels. Conclusion Our data demonstrate HAECs are able calcify. High-Pi induces loss through More studies needed better elucidate Figure 1:(A) Representative images PFA, stained Alizarin Red. (B–C) measured de-staining normalized content expressed #x03BC;mol Ca++/protein.