| CD206-positive M2 macrophages that express heme oxygenase-1 protect against diabetic gastroparesis in mice. | |
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MedLine Citation:
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PMID: 20178793 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND & AIMS: Gastroparesis is a well-recognized complication of diabetes. In diabetics, up-regulation of heme oxygenase-1 (HO1) in gastric macrophages protects against oxidative stress-induced damage. Loss of up-regulation of HO1, the subsequent increase in oxidative stress, and loss of Kit delays gastric emptying; this effect is reversed by induction of HO1. Macrophages have pro- and anti-inflammatory activities, depending on their phenotype. We investigated the number and phenotype of gastric macrophages in NOD/ShiLtJ (nonobese diabetic [NOD]) mice after onset of diabetes, when delayed gastric emptying develops, and after induction of HO1 to reverse delay. METHODS: Four groups of NOD and db/db mice were studied: nondiabetic, diabetic with normal emptying, diabetic with delayed gastric emptying, and diabetic with delayed gastric emptying reversed by the HO1 inducer hemin. Whole mount samples from stomach were labeled in triplicate with antisera against F4/80, HO1, and CD206, and macrophages were quantified in stacked confocal images. Markers for macrophage subtypes were measured by quantitative polymerase chain reaction. RESULTS: Development of diabetes was associated with an increased number of macrophages and up-regulation of HO1 in CD206(+) M2 macrophages. Onset of delayed gastric emptying did not alter the total number of macrophages, but there was a selective loss of CD206(+)/HO1(+) M2 macrophages. Normalization of gastric emptying was associated with repopulation of CD206(+)/HO1(+) M2 macrophages. CONCLUSIONS: CD206(+) M2 macrophages that express HO1 appear to be required for prevention of diabetes-induced delayed gastric emptying. Induction of HO1 in macrophages might be a therapeutic option for patients with diabetic gastroparesis. |
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Authors:
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Kyoung Moo Choi; Purna C Kashyap; Nirjhar Dutta; Gary J Stoltz; Tamas Ordog; Terez Shea Donohue; Anthony J Bauer; David R Linden; Joseph H Szurszewski; Simon J Gibbons; Gianrico Farrugia |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2010-02-20 |
Journal Detail:
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Title: Gastroenterology Volume: 138 ISSN: 1528-0012 ISO Abbreviation: Gastroenterology Publication Date: 2010 Jun |
Date Detail:
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Created Date: 2010-06-10 Completed Date: 2010-07-01 Revised Date: 2011-07-28 |
Medline Journal Info:
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Nlm Unique ID: 0374630 Medline TA: Gastroenterology Country: United States |
Other Details:
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Languages: eng Pagination: 2399-409, 2409.e1 Citation Subset: AIM; IM |
Copyright Information:
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Copyright 2010 AGA Institute. Published by Elsevier Inc. All rights reserved. |
Affiliation:
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Enteric Neuroscience Program and Department of Physiology, Mayo Clinic, Rochester, Minnesota, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Arginase / genetics Blood Glucose / analysis Diabetes Complications / prevention & control* Female Gastric Emptying Gastroparesis / prevention & control* Heme Oxygenase-1 / analysis, physiology* Interleukin-10 / genetics Lectins, C-Type / analysis* Macrophages / enzymology, physiology* Mannose-Binding Lectins / analysis* Membrane Proteins / analysis, physiology* Mice Mice, Inbred NOD Receptors, Cell Surface / analysis* |
| Grant Support | |
ID/Acronym/Agency:
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DK57061/DK/NIDDK NIH HHS; DK68055/DK/NIDDK NIH HHS; P01 DK068055-050001/DK/NIDDK NIH HHS; R01 DK057061-09/DK/NIDDK NIH HHS; R01 DK057061-12/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Blood Glucose; 0/Lectins, C-Type; 0/Mannose-Binding Lectins; 0/Membrane Proteins; 0/Receptors, Cell Surface; 0/mannose receptor; 130068-27-8/Interleukin-10; EC 1.14.99.3/Heme Oxygenase-1; EC 1.14.99.3/Hmox1 protein, mouse; EC 3.5.3.1/Arg1 protein, mouse; EC 3.5.3.1/Arginase |
| Comments/Corrections | |
Comment In:
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Gastroenterology. 2010 Jun;138(7):2219-23
[PMID:
20434508
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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