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CD36 maintains the gastric mucosa and associates with gastric disease

M. Jacome-Sosa, ZF. Miao, VS. Peche, EF. Morris, R. Narendran, KM. Pietka, D. Samovski, HG. Lo, T. Pietka, A. Varro, L. Love-Gregory, JR. Goldenring, O. Kuda, ER. Gamazon, JC. Mills, NA. Abumrad

. 2021 ; 4 (1) : 1247. [pub] 20211102

Language English Country Great Britain

Document type Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't

Persistent link   https://www.medvik.cz/link/bmc22003246

Grant support
R01 DK048370 NIDDK NIH HHS - United States
R01 DK060022 NIDDK NIH HHS - United States
R01 HG011138 NHGRI NIH HHS - United States
R01 DK101332 NIDDK NIH HHS - United States
S10 RR027552 NCRR NIH HHS - United States
P30 DK056341 NIDDK NIH HHS - United States
P30 DK056338 NIDDK NIH HHS - United States
P30 DK052574 NIDDK NIH HHS - United States
R56 AG068026 NIA NIH HHS - United States
R01 DK105129 NIDDK NIH HHS - United States
R01 CA239645 NCI NIH HHS - United States
R01 DK094989 NIDDK NIH HHS - United States

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.

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$a The gastric epithelium is often exposed to injurious elements and failure of appropriate healing predisposes to ulcers, hemorrhage, and ultimately cancer. We examined the gastric function of CD36, a protein linked to disease and homeostasis. We used the tamoxifen model of gastric injury in mice null for Cd36 (Cd36-/-), with Cd36 deletion in parietal cells (PC-Cd36-/-) or in endothelial cells (EC-Cd36-/-). CD36 expresses on corpus ECs, on PC basolateral membranes, and in gastrin and ghrelin cells. Stomachs of Cd36-/- mice have altered gland organization and secretion, more fibronectin, and inflammation. Tissue respiration and mitochondrial efficiency are reduced. Phospholipids increased and triglycerides decreased. Mucosal repair after injury is impaired in Cd36-/- and EC-Cd36-/-, not in PC-Cd36-/- mice, and is due to defect of progenitor differentiation to PCs, not of progenitor proliferation or mature PC dysfunction. Relevance to humans is explored in the Vanderbilt BioVu using PrediXcan that links genetically-determined gene expression to clinical phenotypes, which associates low CD36 mRNA with gastritis, gastric ulcer, and gastro-intestinal hemorrhage. A CD36 variant predicted to disrupt an enhancer site associates (p < 10-17) to death from gastro-intestinal hemorrhage in the UK Biobank. The findings support role of CD36 in gastric tissue repair, and its deletion associated with chronic diseases that can predispose to malignancy.
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$a Miao, Zhi-Feng $u Department of Surgical Oncology, Laboratory of Precision Diagnosis and Treatment of Gastrointestinal Tumors, First Hospital of China Medical University, Shenyang, China $u Division of Gastroenterology, Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA
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$a Peche, Vivek S $u Center for Human Nutrition, Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA
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$a Love-Gregory, Latisha $u Department of Pathology & Immunology, Washington University School of Medicine, St Louis, MO, USA
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$a Kuda, Ondrej $u Institute of Physiology, Czech Academy of Sciences, Videnska 1083, 14220 Prague 4, Czech Republic
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$a Gamazon, Eric R $u Division of Genetic Medicine, Vanderbilt University Medical Center, Nashville, TN, USA $u MRC Epidemiology Unit, University of Cambridge, Cambridge, UK
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$a Mills, Jason C $u Gastroenterology & Hepatology Section, Departments of Medicine and of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA. Jason.Mills@bcm.edu
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$a Abumrad, Nada A $u Center for Human Nutrition, Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA. nabumrad@wustl.edu $u Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO, USA. nabumrad@wustl.edu
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