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Original Research Communications |
1 From the Differentiation Control Section, Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, National Institutes of Health, Bethesda, MD; and ROW Sciences, Inc, Gaithersburg, MD.
Background: Retinoic acid is necessary for the growth and differentiation of organisms and exerts its molecular actions by binding to specific nuclear receptors that belong to the thyroid-steroid hormone receptor superfamily. Steroids and retinoids control the differentiation of the female reproductive epithelia: estrogen maintains the squamous differentiation of vaginal and ectocervical epithelia, whereas retinoic acid maintains the simple columnar endocervical and uterine epithelia. These lining epithelia transform into a squamous metaplastic phenotype in vitamin A–deficient animals. Furthermore, mortality due to vitamin A deficiency is usually attributed to infection resulting in part from dysfunction of the protective epithelia.
Objective: Our objective was to test the hypothesis that estrogen depletion might change the squamous metaplastic response to vitamin A deficiency and affect animal survival.
Design: We used female SENCAR mice maintained on a purified vitamin A–deficient diet containing either 0 or 3 µg retinoic acid/g diet. Mice were either ovariectomized or intact. Squamous cells arising in the normally simple columnar epithelium of the endocervix and uterine cavity were monitored by keratin 5 expression with immunohistochemistry.
Results: Ovariectomy did not change the time to onset of vitamin A deficiency. It increased the number of squamous metaplastic cells and prolonged survival in mice consuming a vitamin A–deficient diet by as much as 40%.
Conclusions: Factors other than epithelial differentiation per se control survival outcome of vitamin A–deficient mice. The results also show a significant increase in longevity of vitamin A– deficient mice when ovariectomized.
Key Words: Retinoic acid • estrogen • female reproductive epithelium • ovariectomy • survival • vitamin A deficiency • differentiation • mice
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