Please use this identifier to cite or link to this item: http://dl.umsu.ac.ir/handle/Hannan/26521
Title: Role of the Adiponectin Binding Protein, T-Cadherin (Cdh13), in Allergic Airways Responses in Mice
Authors: Verbout, Norah G.;Ranscht, Barbara;Williams, Alison S.;Kasahara, David I.;Fedulov, Alexey V.;Zhu, Ming;Si, Huiqing;Wurmbrand, Allison Patricia;Hug, Christopher;Shore, Stephanie Ann
subject: Biology;Anatomy and Physiology;Respiratory System;Respiratory Physiology;Immunology;Immune System;Cytokines;Immunity;Inflammation;Immunologic Subspecialties;Pulmonary Immunology;Allergy and Hypersensitivity;Model Organisms;Animal Models;Mouse;Medicine;Nutrition;Obesity;Pulmonology;Asthma
Year: 2012
Publisher: Public Library of Science
Description: Adiponectin is an adipose derived hormone that declines in obesity. We have previously shown that exogenous administration of adiponectin reduces allergic airways responses in mice. T-cadherin (T-cad; Cdh13) is a binding protein for the high molecular weight isoforms of adiponectin. To determine whether the beneficial effects of adiponectin on allergic airways responses require T-cad, we sensitized wildtype (WT), T-cadherin deficient (T-cad−/−) and adiponectin and T-cad bideficient mice to ovalbumin (OVA) and challenged the mice with aerosolized OVA or PBS. Compared to WT, T-cad−/− mice were protected against OVA-induced airway hyperresponsiveness, increases in BAL inflammatory cells, and induction of IL-13, IL-17, and eotaxin expression. Histological analysis of the lungs of OVA-challenged T-cad−/− versus WT mice indicated reduced inflammation around the airways, and reduced mucous cell hyperplasia. Combined adiponectin and T-cad deficiency reversed the effects of T-cad deficiency alone, indicating that the observed effects of T-cad deficiency require adiponectin. Compared to WT, serum adiponectin was markedly increased in T-cad−/− mice, likely because adiponectin that is normally sequestered by endothelial T-cad remains free in the circulation. In conclusion, T-cad does not mediate the protective effects of adiponectin. Instead, mice lacking T-cad have reduced allergic airways disease, likely because elevated serum adiponectin levels act on other adiponectin signaling pathways.
URI: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3398886/pdf/
http://nrs.harvard.edu/urn-3:HUL.InstRepos:10461895
Standard no: Williams, Alison S., David I. Kasahara, Norah G. Verbout, Alexey V. Fedulov, Ming Zhu, Huiqing Si, Allison P. Wurmbrand, Christopher Hug, Barbara Ranscht, and Stephanie A. Shore. 2012. Role of the adiponectin binding protein, T-cadherin (Cdh13), in allergic airways responses in mice. PLoS ONE 7(7): e41088.
1932-6203
Appears in Collections:HMS Scholarly Articles

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