Endocrine Abstracts

Vitamin D (VitD) was shown to affect biology of vascular wall by regulating cell proliferation. However, its effects on vascular extracellular matrix (ECM) remain largely unaddressed. We investigated effects of VitD (calcitriol) on composition of ECM deposed by cultured endothelial cells (HAEC) and smooth muscle cells (HASMC) isolated from human aorta, and compared them to effects of ascorbate (VitC). Cellular monolayers were treated with or without vitamins for 72 h, then ECM were exposed by differential cell removal and ECM contents for collagen types I (CoI-I) and IV (Col-IV), elastin, heparan sulfate (HS), chondroitin sulfate (ChS) and hyaluronic acid (HA) were assessed immunoenzymatically. HASMC and HAEC demonstrated a significant difference in composition of ECM deposed under standard cultured conditions. HAEC deposed by one order more of Col-IV as compared to HASMC, whereas deposition of Col-I did not differ. HS deposition by HAEC was two-fold higher, whereas deposition of ChS was by two orders lower than by HASMC. Deposition of both elastin and HA were 30% higher in HAEC cultures. Treatment with 100 μM VitC increased Col-I, Col-IV, HS and HA content in HASMC-ECM by 8, 6, 2.3 and 1.5 folds, respectively. VitD had dose-dependent stimulatory effects on Col-I deposition by HASMC (increase by 42.5% at 1 μM), which were additive to the effects of VitC. In contrast, Col-IV and HS contents in HASMC-ECM were decreased by VitD by 25% each, counteracting stimulatory effects of VitC. HA content in HASMC-ECM was not affected by VitD. Neither vitamin had any effects on elastin nor ChS content in HASMC-ECM. Content of all tested compounds in ECM produced by HAEC was independent of either vitamin treatment. In conclusion, VitD was shown capable to affect composition of vascular ECM. Significance of these effects is a subject for discussion.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details unavailable.