The Role of Vitamin A-Storing Cells (Stellate Cells) in Inflammation and Tumorigenesis

Abstract

Characteristic localization and distribution of vitamin A-storing cells (stel-late cells) were demonstrated as hepatic stellate cells in the hepatic lobule and as subepithelial myofibroblasts in the colonic crypt. The stem cell-stem cell niche is maintained by stellate cells in the periportal area and crypt base. Periportal vitamin A-rich stellate cells decrease in patients with chronic hepatitis C who are habitual smokers. Mice fed a vitamin A-supplemented diet show reduced severity of dextran sulfate sodium (DSS)-induced colitis and development of subsequent colonic neoplasia in a model of the ulcerative colitis-dysplasia-carcinoma sequence, compared with mice fed a vitamin A-deficient diet. Decreased colonic subepithelial myofibroblasts and IgA/IgG-positive cells, and increased CD11c-positive dendritic cells in the colonic mucosa, in the vitamin A-deficient state suggest dysfunction of the stem cell niche at the colonic crypt base and colonic immunity. Accordingly, vitamin A deficiency may worsen inflammation and subsequent tumor development, indicating the possibility that vitamin A supplementation might be effective against chronic inflammation and cancer development.