Jisu Oh, of Washington University in St. Louis, and colleagues analyzed data from macrophages from obese diabetics with hypertension and vitamin D deficiency and four other control groups varying in these factors. Macrophages were cultured in media that contained 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) or that was vitamin D deficient, and then exposed to LDL cholesterol.
The researchers found that, in diabetic patients, 1,25(OH)2D3 -- the active form of vitamin D -- suppressed foam cell formation. Deleting the vitamin D receptor in macrophages from patients with diabetes sped up modified LDL-induced foam cell formation.
"In this study, we demonstrate that activation of vitamin D receptor signaling prevents foam cell formation by reducing modified LDL cholesterol uptake in macrophages from diabetic patients. Through suppression of endoplasmic reticulum stress and c-Jun N-terminal kinase activation, 1,25(OH)2D3 downregulates two critical scavenger receptors involved in macrophage cholesterol deposition. Impairment of vitamin D receptor signaling confirmed acceleration of foam cell formation in diabetics. Taken together, these results suggest that modulation of vitamin D signaling is a potential therapeutic target to prevent vascular disease progression," the authors write.
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