Role of the adiponectin binding protein, T-cadherin (cdh13), in pulmonary responses to subacute ozone.

Adiponectin, an adipose derived hormone with pleiotropic functions, binds to several proteins, including T-cadherin. We have previously reported that adiponectin deficient (Adipo(-/-)) mice have increased IL-17A-dependent neutrophil accumulation in their lungs after subacute exposure to ozone (0.3 p...

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Autores principales:	David I Kasahara, Alison S Williams, Leandro A Benedito, Barbara Ranscht, Lester Kobzik, Christopher Hug, Stephanie A Shore
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/670afc39aa1445eeb8add390567d3314
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spelling	oai:doaj.org-article:670afc39aa1445eeb8add390567d33142021-11-18T07:42:52ZRole of the adiponectin binding protein, T-cadherin (cdh13), in pulmonary responses to subacute ozone.1932-620310.1371/journal.pone.0065829https://doaj.org/article/670afc39aa1445eeb8add390567d33142013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23755285/?tool=EBIhttps://doaj.org/toc/1932-6203Adiponectin, an adipose derived hormone with pleiotropic functions, binds to several proteins, including T-cadherin. We have previously reported that adiponectin deficient (Adipo(-/-)) mice have increased IL-17A-dependent neutrophil accumulation in their lungs after subacute exposure to ozone (0.3 ppm for 72 hrs). The purpose of this study was to determine whether this anti-inflammatory effect of adiponectin required adiponectin binding to T-cadherin. Wildtype, Adipo(-/-) , T-cadherin deficient (T-cad(-/-) ), and bideficient (Adipo(-/-)/T-cad(-/-) ) mice were exposed to subacute ozone or air. Compared to wildtype mice, ozone-induced increases in pulmonary IL-17A mRNA expression were augmented in T-cad(-/-) and Adipo(-/-) mice. Compared to T-cad(-/-) mice, there was no further increase in IL-17A in Adipo(-/-)/T-cad(-/-) mice, indicating that adiponectin binding to T-cadherin is required for suppression of ozone-induced IL-17A expression. Similar results were obtained for pulmonary mRNA expression of saa3, an acute phase protein capable of inducing IL-17A expression. Comparison of lung histological sections across genotypes also indicated that adiponectin attenuation of ozone-induced inflammatory lesions at bronchiolar branch points required T-cadherin. BAL neutrophils and G-CSF were augmented in T-cad(-/-) mice and further augmented in Adipo(-/-)/T-cad(-/-) mice. Taken together with previous observations indicating that augmentation of these moieties in ozone exposed Adipo(-/-) mice is partially IL-17A dependent, the results indicate that effects of T-cadherin deficiency on BAL neutrophils and G-CSF are likely secondary to changes in IL-17A, but that adiponectin also acts via T-cadherin independent pathways. Our results indicate that T-cadherin is required for the ability of adiponectin to suppress some but not all aspects of ozone-induced pulmonary inflammation.David I KasaharaAlison S WilliamsLeandro A BeneditoBarbara RanschtLester KobzikChristopher HugStephanie A ShorePublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 6, p e65829 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q David I Kasahara Alison S Williams Leandro A Benedito Barbara Ranscht Lester Kobzik Christopher Hug Stephanie A Shore Role of the adiponectin binding protein, T-cadherin (cdh13), in pulmonary responses to subacute ozone.
description	Adiponectin, an adipose derived hormone with pleiotropic functions, binds to several proteins, including T-cadherin. We have previously reported that adiponectin deficient (Adipo(-/-)) mice have increased IL-17A-dependent neutrophil accumulation in their lungs after subacute exposure to ozone (0.3 ppm for 72 hrs). The purpose of this study was to determine whether this anti-inflammatory effect of adiponectin required adiponectin binding to T-cadherin. Wildtype, Adipo(-/-) , T-cadherin deficient (T-cad(-/-) ), and bideficient (Adipo(-/-)/T-cad(-/-) ) mice were exposed to subacute ozone or air. Compared to wildtype mice, ozone-induced increases in pulmonary IL-17A mRNA expression were augmented in T-cad(-/-) and Adipo(-/-) mice. Compared to T-cad(-/-) mice, there was no further increase in IL-17A in Adipo(-/-)/T-cad(-/-) mice, indicating that adiponectin binding to T-cadherin is required for suppression of ozone-induced IL-17A expression. Similar results were obtained for pulmonary mRNA expression of saa3, an acute phase protein capable of inducing IL-17A expression. Comparison of lung histological sections across genotypes also indicated that adiponectin attenuation of ozone-induced inflammatory lesions at bronchiolar branch points required T-cadherin. BAL neutrophils and G-CSF were augmented in T-cad(-/-) mice and further augmented in Adipo(-/-)/T-cad(-/-) mice. Taken together with previous observations indicating that augmentation of these moieties in ozone exposed Adipo(-/-) mice is partially IL-17A dependent, the results indicate that effects of T-cadherin deficiency on BAL neutrophils and G-CSF are likely secondary to changes in IL-17A, but that adiponectin also acts via T-cadherin independent pathways. Our results indicate that T-cadherin is required for the ability of adiponectin to suppress some but not all aspects of ozone-induced pulmonary inflammation.
format	article
author	David I Kasahara Alison S Williams Leandro A Benedito Barbara Ranscht Lester Kobzik Christopher Hug Stephanie A Shore
author_facet	David I Kasahara Alison S Williams Leandro A Benedito Barbara Ranscht Lester Kobzik Christopher Hug Stephanie A Shore
author_sort	David I Kasahara
title	Role of the adiponectin binding protein, T-cadherin (cdh13), in pulmonary responses to subacute ozone.
title_short	Role of the adiponectin binding protein, T-cadherin (cdh13), in pulmonary responses to subacute ozone.
title_full	Role of the adiponectin binding protein, T-cadherin (cdh13), in pulmonary responses to subacute ozone.
title_fullStr	Role of the adiponectin binding protein, T-cadherin (cdh13), in pulmonary responses to subacute ozone.
title_full_unstemmed	Role of the adiponectin binding protein, T-cadherin (cdh13), in pulmonary responses to subacute ozone.
title_sort	role of the adiponectin binding protein, t-cadherin (cdh13), in pulmonary responses to subacute ozone.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/670afc39aa1445eeb8add390567d3314
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Role of the adiponectin binding protein, T-cadherin (cdh13), in pulmonary responses to subacute ozone.

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