CD36 maintains the gastric mucosa and associates with gastric disease

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F21%3A00549772" target="_blank" >RIV/67985823:_____/21:00549772 - isvavai.cz</a>

Výsledek na webu

<a href="https://doi.org/10.1038/s42003-021-02765-z" target="_blank" >https://doi.org/10.1038/s42003-021-02765-z</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1038/s42003-021-02765-z" target="_blank" >10.1038/s42003-021-02765-z</a>

Jazyk výsledku

angličtina

Název v původním jazyce

CD36 maintains the gastric mucosa and associates with gastric disease

Popis výsledku v původním jazyce

The gastric epithelium is often exposed to injurious elements and failure of appropriate healing predisposes to ulcers, hemorrhage, and ultimately cancer. We examined the gastric function of CD36, a protein linked to disease and homeostasis. We used the tamoxifen model of gastric injury in mice null for Cd36 (Cd36(-/-)), with Cd36 deletion in parietal cells (PC-Cd36(-/-)) or in endothelial cells (EC-Cd36(-/-)). CD36 expresses on corpus ECs, on PC basolateral membranes, and in gastrin and ghrelin cells. Stomachs of Cd36(-/-) mice have altered gland organization and secretion, more fibronectin, and inflammation. Tissue respiration and mitochondrial efficiency are reduced. Phospholipids increased and triglycerides decreased. Mucosal repair after injury is impaired in Cd36(-/-) and EC-Cd36(-/-), not in PC-Cd36(-/-) mice, and is due to defect of progenitor differentiation to PCs, not of progenitor proliferation or mature PC dysfunction. Relevance to humans is explored in the Vanderbilt BioVu using PrediXcan that links genetically-determined gene expression to clinical phenotypes, which associates low CD36 mRNA with gastritis, gastric ulcer, and gastro-intestinal hemorrhage. A CD36 variant predicted to disrupt an enhancer site associates (p < 10(-17)) to death from gastro-intestinal hemorrhage in the UK Biobank. The findings support role of CD36 in gastric tissue repair, and its deletion associated with chronic diseases that can predispose to malignancy.

Název v anglickém jazyce

CD36 maintains the gastric mucosa and associates with gastric disease

Popis výsledku anglicky

The gastric epithelium is often exposed to injurious elements and failure of appropriate healing predisposes to ulcers, hemorrhage, and ultimately cancer. We examined the gastric function of CD36, a protein linked to disease and homeostasis. We used the tamoxifen model of gastric injury in mice null for Cd36 (Cd36(-/-)), with Cd36 deletion in parietal cells (PC-Cd36(-/-)) or in endothelial cells (EC-Cd36(-/-)). CD36 expresses on corpus ECs, on PC basolateral membranes, and in gastrin and ghrelin cells. Stomachs of Cd36(-/-) mice have altered gland organization and secretion, more fibronectin, and inflammation. Tissue respiration and mitochondrial efficiency are reduced. Phospholipids increased and triglycerides decreased. Mucosal repair after injury is impaired in Cd36(-/-) and EC-Cd36(-/-), not in PC-Cd36(-/-) mice, and is due to defect of progenitor differentiation to PCs, not of progenitor proliferation or mature PC dysfunction. Relevance to humans is explored in the Vanderbilt BioVu using PrediXcan that links genetically-determined gene expression to clinical phenotypes, which associates low CD36 mRNA with gastritis, gastric ulcer, and gastro-intestinal hemorrhage. A CD36 variant predicted to disrupt an enhancer site associates (p < 10(-17)) to death from gastro-intestinal hemorrhage in the UK Biobank. The findings support role of CD36 in gastric tissue repair, and its deletion associated with chronic diseases that can predispose to malignancy.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30105 - Physiology (including cytology)

Projekt

<a href="/cs/project/LTAUSA18104" target="_blank" >LTAUSA18104: Role antioxidační obrany v syntéze antidiabetických lipokinů</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2021

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Communications Biology

ISSN

2399-3642

e-ISSN

2399-3642

Svazek periodika

4

Číslo periodika v rámci svazku

1

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

15

Strana od-do

1247

Kód UT WoS článku

000714075700003

EID výsledku v databázi Scopus

2-s2.0-85118426796