Regulation of Paracellular Fluxes of Amino Acids by Claudin-8 in Normal Mouse Intestinal MCE301 Cells

Ema Okamoto, Shunsuke Matsuda, Yuta Yoshino, Yoshifumi Morikawa, Koichi Suenami, Yoshiaki Tabuchi, Toshiyuki Matsunaga, Akira Ikari*

*この論文の責任著者

研究成果: ジャーナルへの寄稿学術論文査読

4 被引用数 (Scopus)

抄録

The ingested proteins are catabolized to di/tri-peptides and amino acids (AAs), which are absorbed through various transporters in the small intestinal and colonic epithelial cells. Tight junctions (TJs) are formed between neighboring cells and restrict paracellular fluxes to mineral ions and aqueous molecules. However, it is unknown whether the TJs are implicated in the control of paracellular fluxes to AAs. The paracellular permeability is controlled by claudins (CLDNs), which comprise a family of over 20 members. Here, we found that CLDN8 expression is decreased by AAs deprivation in normal mouse colon-derived MCE301 cells. The reporter activity of CLDN8 was not significantly changed by AAs deprivation, whereas the stability of CLDN8 protein was decreased. MicroRNA analysis showed that AAs deprivation increases the expression of miR-153-5p which targets CLDN8. The AAs deprivation-induced decline of CLDN8 expression was reversed by a miR-153-5p inhibitor. The CLDN8 silencing enhanced the paracellular fluxes to AAs, especially middle molecular size AAs. The expression levels of colonic CLDN8 and miR-153-5p in aged mice were lower and higher than those in young mice, respectively. We suggest that AAs deprivation downregulates CLDN8-dependent barrier function, mediated by the elevation of miR-153-5p expression in the colon, in order to enhance the AAs absorption.

本文言語英語
論文番号1346
ジャーナルNutrients
15
6
DOI
出版ステータス出版済み - 2023/03

ASJC Scopus 主題領域

  • 食品科学
  • 栄養および糖尿病

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