Dataset Information

Compensatory Upregulation of LPA₂ and Activation of the PI3K-Akt Pathway Prevent LPA₅-Dependent Loss of Intestinal Epithelial Cells in Intestinal Organoids.

ABSTRACT: Renewal of the intestinal epithelium is orchestrated by regenerative epithelial proliferation within crypts. Recent studies have shown that lysophosphatidic acid (LPA) can maintain intestinal epithelial renewal in vitro and conditional deletion of Lpar5 (Lpar5^iKO) in mice ablates the intestinal epithelium and increases morbidity. In contrast, constitutive Lpar5 deletion (Lpar5^cKO) does not cause a defect in intestinal crypt regeneration. In this study, we investigated whether another LPA receptor (LPAR) compensates for constitutive loss of LPA₅ function to allow regeneration of intestinal epithelium. In Lpar5^cKO intestinal epithelial cells (IECs), Lpar2 was upregulated and blocking LPA₂ functio

SUBMITTER: Liang Z

PROVIDER: S-EPMC9324510 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature

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Dataset Information

Compensatory Upregulation of LPA₂ and Activation of the PI3K-Akt Pathway Prevent LPA₅-Dependent Loss of Intestinal Epithelial Cells in Intestinal Organoids.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Dataset Information

Compensatory Upregulation of LPA2 and Activation of the PI3K-Akt Pathway Prevent LPA5-Dependent Loss of Intestinal Epithelial Cells in Intestinal Organoids.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Compensatory Upregulation of LPA₂ and Activation of the PI3K-Akt Pathway Prevent LPA₅-Dependent Loss of Intestinal Epithelial Cells in Intestinal Organoids.