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The miR-181 family regulates colonic inflammation through its activity in the intestinal epithelium

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The miR-181 family regulates colonic inflammation through its activity in the intestinal epithelium. / Jimenez, Monica T; Clark, Megan L; Wright, Jasmine M; Michieletto, Michaël F; Liu, Suying; Erickson, Isabel; Dohnalova, Lenka; Uhr, Giulia T; Tello-Cajiao, John; Joannas, Leonel; Williams, Adam; Gagliani, Nicola; Bewtra, Meenakshi; Tomov, Vesselin T; Thaiss, Christoph A; Henao-Mejia, Jorge.

In: J EXP MED, Vol. 219, No. 12, e20212278, 05.12.2022.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Jimenez, MT, Clark, ML, Wright, JM, Michieletto, MF, Liu, S, Erickson, I, Dohnalova, L, Uhr, GT, Tello-Cajiao, J, Joannas, L, Williams, A, Gagliani, N, Bewtra, M, Tomov, VT, Thaiss, CA & Henao-Mejia, J 2022, 'The miR-181 family regulates colonic inflammation through its activity in the intestinal epithelium', J EXP MED, vol. 219, no. 12, e20212278. https://doi.org/10.1084/jem.20212278

APA

Jimenez, M. T., Clark, M. L., Wright, J. M., Michieletto, M. F., Liu, S., Erickson, I., Dohnalova, L., Uhr, G. T., Tello-Cajiao, J., Joannas, L., Williams, A., Gagliani, N., Bewtra, M., Tomov, V. T., Thaiss, C. A., & Henao-Mejia, J. (2022). The miR-181 family regulates colonic inflammation through its activity in the intestinal epithelium. J EXP MED, 219(12), [e20212278]. https://doi.org/10.1084/jem.20212278

Vancouver

Jimenez MT, Clark ML, Wright JM, Michieletto MF, Liu S, Erickson I et al. The miR-181 family regulates colonic inflammation through its activity in the intestinal epithelium. J EXP MED. 2022 Dec 5;219(12). e20212278. https://doi.org/10.1084/jem.20212278

Bibtex

@article{ee554e809cbc43b5a2103dc14e2d99ee,
title = "The miR-181 family regulates colonic inflammation through its activity in the intestinal epithelium",
abstract = "The intestinal epithelium is a key physical interface that integrates dietary and microbial signals to regulate nutrient uptake and mucosal immune cell function. The transcriptional programs that regulate intestinal epithelial cell (IEC) quiescence, proliferation, and differentiation have been well characterized. However, how gene expression networks critical for IECs are posttranscriptionally regulated during homeostasis or inflammatory disease remains poorly understood. Herein, we show that a conserved family of microRNAs, miR-181, is significantly downregulated in IECs from patients with inflammatory bowel disease and mice with chemical-induced colitis. Strikingly, we showed that miR-181 expression within IECs, but not the hematopoietic system, is required for protection against severe colonic inflammation in response to epithelial injury in mice. Mechanistically, we showed that miR-181 expression increases the proliferative capacity of IECs, likely through the regulation of Wnt signaling, independently of the gut microbiota composition. As epithelial reconstitution is crucial to restore intestinal homeostasis after injury, the miR-181 family represents a potential therapeutic target against severe intestinal inflammation.",
keywords = "Animals, Colitis/chemically induced, Epithelial Cells/metabolism, Inflammation/genetics, Intestinal Mucosa, Mice, MicroRNAs/genetics",
author = "Jimenez, {Monica T} and Clark, {Megan L} and Wright, {Jasmine M} and Michieletto, {Micha{\"e}l F} and Suying Liu and Isabel Erickson and Lenka Dohnalova and Uhr, {Giulia T} and John Tello-Cajiao and Leonel Joannas and Adam Williams and Nicola Gagliani and Meenakshi Bewtra and Tomov, {Vesselin T} and Thaiss, {Christoph A} and Jorge Henao-Mejia",
note = "{\textcopyright} 2022 Jimenez et al.",
year = "2022",
month = dec,
day = "5",
doi = "10.1084/jem.20212278",
language = "English",
volume = "219",
journal = "J EXP MED",
issn = "0022-1007",
publisher = "Rockefeller University Press",
number = "12",

}

RIS

TY - JOUR

T1 - The miR-181 family regulates colonic inflammation through its activity in the intestinal epithelium

AU - Jimenez, Monica T

AU - Clark, Megan L

AU - Wright, Jasmine M

AU - Michieletto, Michaël F

AU - Liu, Suying

AU - Erickson, Isabel

AU - Dohnalova, Lenka

AU - Uhr, Giulia T

AU - Tello-Cajiao, John

AU - Joannas, Leonel

AU - Williams, Adam

AU - Gagliani, Nicola

AU - Bewtra, Meenakshi

AU - Tomov, Vesselin T

AU - Thaiss, Christoph A

AU - Henao-Mejia, Jorge

N1 - © 2022 Jimenez et al.

PY - 2022/12/5

Y1 - 2022/12/5

N2 - The intestinal epithelium is a key physical interface that integrates dietary and microbial signals to regulate nutrient uptake and mucosal immune cell function. The transcriptional programs that regulate intestinal epithelial cell (IEC) quiescence, proliferation, and differentiation have been well characterized. However, how gene expression networks critical for IECs are posttranscriptionally regulated during homeostasis or inflammatory disease remains poorly understood. Herein, we show that a conserved family of microRNAs, miR-181, is significantly downregulated in IECs from patients with inflammatory bowel disease and mice with chemical-induced colitis. Strikingly, we showed that miR-181 expression within IECs, but not the hematopoietic system, is required for protection against severe colonic inflammation in response to epithelial injury in mice. Mechanistically, we showed that miR-181 expression increases the proliferative capacity of IECs, likely through the regulation of Wnt signaling, independently of the gut microbiota composition. As epithelial reconstitution is crucial to restore intestinal homeostasis after injury, the miR-181 family represents a potential therapeutic target against severe intestinal inflammation.

AB - The intestinal epithelium is a key physical interface that integrates dietary and microbial signals to regulate nutrient uptake and mucosal immune cell function. The transcriptional programs that regulate intestinal epithelial cell (IEC) quiescence, proliferation, and differentiation have been well characterized. However, how gene expression networks critical for IECs are posttranscriptionally regulated during homeostasis or inflammatory disease remains poorly understood. Herein, we show that a conserved family of microRNAs, miR-181, is significantly downregulated in IECs from patients with inflammatory bowel disease and mice with chemical-induced colitis. Strikingly, we showed that miR-181 expression within IECs, but not the hematopoietic system, is required for protection against severe colonic inflammation in response to epithelial injury in mice. Mechanistically, we showed that miR-181 expression increases the proliferative capacity of IECs, likely through the regulation of Wnt signaling, independently of the gut microbiota composition. As epithelial reconstitution is crucial to restore intestinal homeostasis after injury, the miR-181 family represents a potential therapeutic target against severe intestinal inflammation.

KW - Animals

KW - Colitis/chemically induced

KW - Epithelial Cells/metabolism

KW - Inflammation/genetics

KW - Intestinal Mucosa

KW - Mice

KW - MicroRNAs/genetics

U2 - 10.1084/jem.20212278

DO - 10.1084/jem.20212278

M3 - SCORING: Journal article

C2 - 36074090

VL - 219

JO - J EXP MED

JF - J EXP MED

SN - 0022-1007

IS - 12

M1 - e20212278

ER -