Altered Expression of Type-1 and Type-2 Cannabinoid Receptors in Celiac Disease
Anandamide (AEA) is the prominent member of the endocannabinoid family and its biological action is mediated through the binding to both type-1 (CB1) and type-2 (CB2) cannabinoid receptors (CBR). The presence of AEA and CBR in the gastrointestinal tract highlighted their pathophysiological role in s...
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| Published in | PloS one Vol. 8; no. 4; p. e62078 |
|---|---|
| Main Authors | , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Public Library of Science
19.04.2013
Public Library of Science (PLoS) |
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| Online Access | Get full text |
| ISSN | 1932-6203 1932-6203 |
| DOI | 10.1371/journal.pone.0062078 |
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| Abstract | Anandamide (AEA) is the prominent member of the endocannabinoid family and its biological action is mediated through the binding to both type-1 (CB1) and type-2 (CB2) cannabinoid receptors (CBR). The presence of AEA and CBR in the gastrointestinal tract highlighted their pathophysiological role in several gut diseases, including celiac disease. Here, we aimed to investigate the expression of CBR at transcriptional and translational levels in the duodenal mucosa of untreated celiac patients, celiac patients on a gluten-free diet for at least 12 months and control subjects. Also biopsies from treated celiac patients cultured ex vivo with peptic-tryptic digest of gliadin were investigated. Our data show higher levels of both CB1 and CB2 receptors during active disease and normal CBR levels in treated celiac patients. In conclusion, we demonstrate an up-regulation of CB1 and CB2 mRNA and protein expression, that points to the therapeutic potential of targeting CBR in patients with celiac disease. |
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| AbstractList | Anandamide (AEA) is the prominent member of the endocannabinoid family and its biological action is mediated through the binding to both type-1 (CB1) and type-2 (CB2) cannabinoid receptors (CBR). The presence of AEA and CBR in the gastrointestinal tract highlighted their pathophysiological role in several gut diseases, including celiac disease. Here, we aimed to investigate the expression of CBR at transcriptional and translational levels in the duodenal mucosa of untreated celiac patients, celiac patients on a gluten-free diet for at least 12 months and control subjects. Also biopsies from treated celiac patients cultured ex vivo with peptic-tryptic digest of gliadin were investigated. Our data show higher levels of both CB1 and CB2 receptors during active disease and normal CBR levels in treated celiac patients. In conclusion, we demonstrate an up-regulation of CB1 and CB2 mRNA and protein expression, that points to the therapeutic potential of targeting CBR in patients with celiac disease. Anandamide (AEA) is the prominent member of the endocannabinoid family and its biological action is mediated through the binding to both type-1 (CB.sub.1) and type-2 (CB.sub.2) cannabinoid receptors (CBR). The presence of AEA and CBR in the gastrointestinal tract highlighted their pathophysiological role in several gut diseases, including celiac disease. Here, we aimed to investigate the expression of CBR at transcriptional and translational levels in the duodenal mucosa of untreated celiac patients, celiac patients on a gluten-free diet for at least 12 months and control subjects. Also biopsies from treated celiac patients cultured ex vivo with peptic-tryptic digest of gliadin were investigated. Our data show higher levels of both CB.sub.1 and CB.sub.2 receptors during active disease and normal CBR levels in treated celiac patients. In conclusion, we demonstrate an up-regulation of CB.sub.1 and CB.sub.2 mRNA and protein expression, that points to the therapeutic potential of targeting CBR in patients with celiac disease. Anandamide (AEA) is the prominent member of the endocannabinoid family and its biological action is mediated through the binding to both type-1 (CB1) and type-2 (CB2) cannabinoid receptors (CBR). The presence of AEA and CBR in the gastrointestinal tract highlighted their pathophysiological role in several gut diseases, including celiac disease. Here, we aimed to investigate the expression of CBR at transcriptional and translational levels in the duodenal mucosa of untreated celiac patients, celiac patients on a gluten-free diet for at least 12 months and control subjects. Also biopsies from treated celiac patients cultured ex vivo with peptic-tryptic digest of gliadin were investigated. Our data show higher levels of both CB1 and CB2 receptors during active disease and normal CBR levels in treated celiac patients. In conclusion, we demonstrate an up-regulation of CB1 and CB2 mRNA and protein expression, that points to the therapeutic potential of targeting CBR in patients with celiac disease.Anandamide (AEA) is the prominent member of the endocannabinoid family and its biological action is mediated through the binding to both type-1 (CB1) and type-2 (CB2) cannabinoid receptors (CBR). The presence of AEA and CBR in the gastrointestinal tract highlighted their pathophysiological role in several gut diseases, including celiac disease. Here, we aimed to investigate the expression of CBR at transcriptional and translational levels in the duodenal mucosa of untreated celiac patients, celiac patients on a gluten-free diet for at least 12 months and control subjects. Also biopsies from treated celiac patients cultured ex vivo with peptic-tryptic digest of gliadin were investigated. Our data show higher levels of both CB1 and CB2 receptors during active disease and normal CBR levels in treated celiac patients. In conclusion, we demonstrate an up-regulation of CB1 and CB2 mRNA and protein expression, that points to the therapeutic potential of targeting CBR in patients with celiac disease. |
| Audience | Academic |
| Author | Lanzarotto, Francesco Di Tommaso, Monia Di Sabatino, Antonio Villanacci, Vincenzo Maccarrone, Mauro Papadia, Cinzia Pasini, Alessandra Giuffrida, Paolo Biancheri, Paolo Montana, Chiara Battista, Natalia Vanoli, Alessandro Corazza, Gino R. Rapino, Cinzia |
| AuthorAffiliation | 1 Department of Biomedical Sciences, University of Teramo, Teramo, Italy 2 European Center for Brain Research (CERC)/Santa Lucia Foundation, Rome, Italy 4 Gastroenterology Unit, Parma University Hospital, Parma, Italy 5 Department of Molecular Medicine, Fondazione IRCCS Policlinico S. Matteo, Centro per lo Studio e la Cura della Malattia Celiaca, University of Pavia, Pavia, Italy 3 Department of Internal Medicine, Fondazione IRCCS Policlinico S. Matteo, Centro per lo Studio e la Cura della Malattia Celiaca, University of Pavia, Pavia, Italy University of Cincinnati, United States of America 6 Department of Gastroenterology, Spedali Civili di Brescia, Brescia, Italy 7 Department of Pathology, Spedali Civili di Brescia, Brescia, Italy 8 Center of Integrated Research, Campus Bio-Medico University of Rome, Rome, Italy |
| AuthorAffiliation_xml | – name: 4 Gastroenterology Unit, Parma University Hospital, Parma, Italy – name: 6 Department of Gastroenterology, Spedali Civili di Brescia, Brescia, Italy – name: 3 Department of Internal Medicine, Fondazione IRCCS Policlinico S. Matteo, Centro per lo Studio e la Cura della Malattia Celiaca, University of Pavia, Pavia, Italy – name: 2 European Center for Brain Research (CERC)/Santa Lucia Foundation, Rome, Italy – name: 8 Center of Integrated Research, Campus Bio-Medico University of Rome, Rome, Italy – name: University of Cincinnati, United States of America – name: 1 Department of Biomedical Sciences, University of Teramo, Teramo, Italy – name: 5 Department of Molecular Medicine, Fondazione IRCCS Policlinico S. Matteo, Centro per lo Studio e la Cura della Malattia Celiaca, University of Pavia, Pavia, Italy – name: 7 Department of Pathology, Spedali Civili di Brescia, Brescia, Italy |
| Author_xml | – sequence: 1 givenname: Natalia surname: Battista fullname: Battista, Natalia – sequence: 2 givenname: Antonio surname: Di Sabatino fullname: Di Sabatino, Antonio – sequence: 3 givenname: Monia surname: Di Tommaso fullname: Di Tommaso, Monia – sequence: 4 givenname: Paolo surname: Biancheri fullname: Biancheri, Paolo – sequence: 5 givenname: Cinzia surname: Rapino fullname: Rapino, Cinzia – sequence: 6 givenname: Paolo surname: Giuffrida fullname: Giuffrida, Paolo – sequence: 7 givenname: Cinzia surname: Papadia fullname: Papadia, Cinzia – sequence: 8 givenname: Chiara surname: Montana fullname: Montana, Chiara – sequence: 9 givenname: Alessandra surname: Pasini fullname: Pasini, Alessandra – sequence: 10 givenname: Alessandro surname: Vanoli fullname: Vanoli, Alessandro – sequence: 11 givenname: Francesco surname: Lanzarotto fullname: Lanzarotto, Francesco – sequence: 12 givenname: Vincenzo surname: Villanacci fullname: Villanacci, Vincenzo – sequence: 13 givenname: Gino R. surname: Corazza fullname: Corazza, Gino R. – sequence: 14 givenname: Mauro surname: Maccarrone fullname: Maccarrone, Mauro |
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| CitedBy_id | crossref_primary_10_1002_cpt_568 crossref_primary_10_1152_physrev_00002_2016 crossref_primary_10_1097_MPG_0000000000002887 crossref_primary_10_3390_ijms20235875 crossref_primary_10_1177_1087057113498418 crossref_primary_10_1016_j_tips_2015_02_008 crossref_primary_10_1016_j_crfs_2023_100499 crossref_primary_10_1007_s00018_015_1924_0 crossref_primary_10_1152_ajpgi_00294_2015 |
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| ContentType | Journal Article |
| Copyright | COPYRIGHT 2013 Public Library of Science 2013 Battista et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2013 Battista et al 2013 Battista et al |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Competing Interests: The authors have declared that no competing interests exist. Conceived and designed the experiments: NB ADS GRC MM. Performed the experiments: MDT PB CR PG AP. Analyzed the data: NB ADS. Contributed reagents/materials/analysis tools: CP CM AV FL VV GRC MM. Wrote the paper: NB ADS GRC MM. |
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| Title | Altered Expression of Type-1 and Type-2 Cannabinoid Receptors in Celiac Disease |
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