Role of the Adiponectin Binding Protein, T-Cadherin (Cdh13), in Allergic Airways Responses in Mice

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Role of the Adiponectin Binding Protein, T-Cadherin (Cdh13), in Allergic Airways Responses in Mice

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Title: Role of the Adiponectin Binding Protein, T-Cadherin (Cdh13), in Allergic Airways Responses in Mice
Author: 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

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Citation: 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.
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Abstract: 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.
Published Version: doi:10.1371/journal.pone.0041088
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3398886/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:10461895
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