Consumption of 1-Kestose Upregulates MicroRNA-200 and-192/215 Families in Lamina Propria Leukocytes of the Murine Large Intestine

1Citations
Citations of this article
1Readers
Mendeley users who have this article in their library.

Abstract

By comparing germ-free mice and specific pathogen-free mice, we recently demonstrated that the presence of gut commensals upregulates microRNA-200 family members in lamina propria leukocytes (LPL) of the murine large intestine. The present study tested whether the consumption of 1-kestose (KES), an indigestible oligosaccharide that alters gut microbiota composition, influences the microRNA expression in the LPL. Supplementation of KES (4%) in drinking water for 2 wk increased the levels of miR-182-5p,-205-5p,-290a-5p, miR-200 family members (miR-141-3p,-200a-3p,-200b-3p,-200c-3p, and-429-3p) as well as miR-192/215 family members (miR-192-5p,-194-5p, and-215-5p) as determined by microarray analysis in large intestinal LPL of C57BL/6 mice. Quantitative reverse transcription-PCR further confirmed the increase in miR-192-5p,-194-5p,-200a-3p,-200b-3p,-200c-3p,-205-5p, and 215-5p. KES consumption significantly increased Bifidobacterium pseudolongum in the cecal contents. In a separate experi-ment, intragastric administration of B. pseudolongum (109 CFU/d) for 7 d increased the levels of miR-182-5p,-194-5p, and-200a-3p and tended to increase the levels of miR-200b-3p,-215-5p, and-429-3p. These results suggest that dietary KES influences miRNA expression in the large intestinal LPL, which may be associated with the increased population of B. pseudolongum.

Cite

CITATION STYLE

APA

Ohsaka, F., Honma, D., Kadota, Y., Tochio, T., & Sonoyama, K. (2023). Consumption of 1-Kestose Upregulates MicroRNA-200 and-192/215 Families in Lamina Propria Leukocytes of the Murine Large Intestine. Journal of Nutritional Science and Vitaminology, 69(2), 150–154. https://doi.org/10.3177/jnsv.69.150

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free