Factors affecting placental vasculogenesis

Key factors: Endothelial colony forming cells

1) ECFCs in umbilical cord blood serum exhibit inhibition to vascular tubule formation and migration.

2) Low or minimal binding of VDRE to VEGF promoter sites may be associated with diminished VEGF production, leading to preeclampsia.

1) Exogenous (1, 25 (OH) 2D (3) reverses adverse effects of ECFCs, with improved tubule formation and migration.

2) The active form, 1, 25 (OH) 2D (3), has functional synergism to stimulate VEGF expression of rat VSMC when VDRE binds to both of the VEGF promoter sites.

Factors affecting placental Loss of immune tolerance

Key factors: ANG-II and AT1-AA.

1) An immunological loss of self-tolerance during placental ischemia results in B cell secretion of AT1-AA, affecting the RAAS system. This results in vasoconstriction and intravascular fluid distribution.

1) Vitamin D down regulates B cell proliferation, plasma cell differentiation and IgG antibodies secretion.

2) AT1-AA associated with preeclampsia were reduced with Vitamin D supplementation in the RUPP rat model of PE.

3) Short-term severe Vitamin D deficiency in rats had higher mean systolic BP and upregulated Ang-II and its counter-regulatory breakdown product. This aggravated hypertension and target-organ damage.

4) 8-week of cholecalciferol therapy in hypertensive patients with hypovitaminosis D significant showed circulating renin-angiotensin-aldosterone levels and vascular function improved.