**Abstract**

Characteristic localization and distribution of vitamin A-storing cells (stellate cells) were demonstrated as hepatic stellate cells in the hepatic lobule and as subepithelial myofbroblasts in the colonic crypt. Te 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-defcient diet. Decreased colonic subepithelial myofbroblasts and IgA/IgG-positive cells, and increased CD11c-positive dendritic cells in the colonic mucosa, in the vitamin A-defcient state suggest dysfunction of the stem cell niche at the colonic crypt base and colonic immunity. Accordingly, vitamin A defciency may worsen infammation and subsequent tumor development, indicating the possibility that vitamin A supplementation might be efective against chronic infammation and cancer development.

**Keywords:** vitamin A-storing cells, stellate cells, subepithelial myofbroblasts, stem cell niche, chronic hepatitis, DSS colitis, ulcerative colitis, colonic tumorigenesis

## **1. Introduction**

In mammals, vitamin A is mostly stored in the liver, particularly in perisinusoidal stellate cells. It is also detectable in the lung, kidney, and intestine. Storage of total retinol is increased considerably in the lungs, kidneys, and intestines of rats fed a vitamin A-rich diet [1]. Vitamin A-rich lipids can be identifed in the cells using electron microscopy [2]. Vitamin A-storing cells (stellate cells) correspond to subepithelial myofbroblasts in the lung and intestine [3]. Stellate cells are necessary for the diferentiation of epithelial cells, known as the stem cell niche [4–7].

It is thought that defciency of vitamin A worsens infammation and accelerates tumorigenesis, possibly due to local immunity and stem cell niche dysfunction [3, 8–11]. Data presented and discussed in this chapter show (1) the distribution, localization, and function of stellate cells in the liver and intestine, and (2) the role of stellate cells in infammation and tumorigenesis.
