Selenium-induced cell migration and proliferation: relevance to angiogenesis and microangiopathy.
Selenium, as selenomethionine, selenocystine, or selenious acid, activated both capillary and aortal endothelial cells of bovine origin. To low concentrations of selenium (10(-7) M) retinal capillary cells (BRCE) responded by a fivefold increase in migration rate whereas the migration rate of aortal cells was not markedly altered. In contrast, the proliferation rate of aortal cells was increased up to 300% or more by selenium addition whereas the proliferation rate of capillary derived cells was almost unaffected. Selenomethionine was strongly angiogenic by the corneal pocket or chorioallantoic membrane assays. These findings bear on the establishment of criteria for defining angiogenic factors and may also relate to selenium deficiency-linked vascular disease.
D000818:Animals; D001011:Aorta / Q000166:cytology / Q000187:drug effects; D001808:Blood Vessels / Q000166:cytology / Q000187:drug effects*; D002196:Capillaries / Q000166:cytology / Q000187:drug effects; D002417:Cattle; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D002465:Cell Movement / Q000187:drug effects; D004727:Endothelium / Q000166:cytology / Q000187:drug effects; D009389:Neovascularization, Pathologic; D012643:Selenium / Q000172:deficiency / Q000494:pharmacology*; D012645:Selenomethionine / Q000494:pharmacology; D014652:Vascular Diseases / Q000209:etiology*
D012645:Selenomethionine; D012643:Selenium