About: Pentraxin 3 deficiency enhances features of chronic rejection in a mouse orthotopic lung transplantation model

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About: Pentraxin 3 deficiency enhances features of chronic rejection in a mouse orthotopic lung transplantation model Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Pentraxin 3 deficiency enhances features of chronic rejection in a mouse orthotopic lung transplantation model
Creator	Liu, Mingyao Bai, Xiaohui Cho, Hae-Ra Cypel, Marcelo Guana, Zehong Juvet, Stephen Keshavjee, Shaf Lua, Christina Martinu, Tereza Oishi, Hisashi Sugihara, Junichi Takizawa, Hiromitsu Yoshida, Mitsuteru Hwang, David Mckee, Trevor
Source	Medline; PMC
abstract	Chronic lung allograft dysfunction (CLAD) is a serious complication after lung transplantation and thought to represent chronic rejection. Increased expression of Pentraxin 3 (PTX3), an acute phase protein, was associated with worse outcome in lung transplant patients. To determine the role of recipient PTX3 in development of chronic rejection, we used a minor alloantigen-mismatched murine orthotopic single lung transplant model. Male C57BL/10 mice were used as donors. Male PTX3 knockout (KO) mice and their wild type (WT) littermates on 129/SvEv/C57BL6/J background were used as recipients. In KO recipients, 7/13 grafted lungs were consolidated without volume recovery on CT scan, while only 2/9 WT mice showed similar graft consolidation. For grafts where lung volume could be reliably analyzed by CT scan, the lung volume recovery was significantly reduced in KO mice compared to WT. Interstitial inflammation, parenchymal fibrosis and bronchiolitis obliterans scores were significantly higher in KO mice. Presence of myofibroblasts and lymphoid aggregation was significantly enhanced in the grafts of PTX3 KO recipients. Recipient PTX3 deficiency enhanced chronic rejection-like lesions by promoting a fibrotic process in the airways and lung parenchyma. The underlying mechanisms and potential protective role of exogenous PTX3 as a therapy should be further explored.
has issue date	2018-01-03(xsd:dateTime)
bibo:doi	10.18632/oncotarget.23902
bibo:pmid	29492210
has license	cc-by
sha1sum (hex)	d84ac9fd44932276ccfa7da5add9776e7d56595a
schema:url	https://doi.org/10.18632/oncotarget.23902
resource representing a document's title	Pentraxin 3 deficiency enhances features of chronic rejection in a mouse orthotopic lung transplantation model
has PubMed Central identifier	PMC5823599
has PubMed identifier	29492210
schema:publication	Oncotarget
resource representing a document's body	covid:d84ac9fd44932276ccfa7da5add9776e7d56595a#body_text
is schema:about of	named entity 'Pentraxin' named entity 'patients' named entity 'Interstitial' named entity 'Presence' named entity 'background' covid:arg/d84ac9fd44932276ccfa7da5add9776e7d56595a named entity 'bronchiolitis obliterans' named entity 'lesions' named entity 'lung transplant' named entity 'scores' named entity 'represent' named entity 'Male' named entity 'grafts' named entity 'promoting' named entity 'lungs' named entity 'exogenous' named entity 'mechanisms' named entity 'graft' named entity 'CT scan' named entity 'CT scan' named entity 'enhanced' named entity 'bronchiolitis obliterans' named entity 'KO mice' named entity 'exogenous' named entity 'lung transplant' named entity 'myofibroblasts' named entity 'parenchymal' named entity 'mice' named entity 'lung transplant' named entity 'inflammation' named entity 'PTX3' named entity 'CT scan' named entity 'PTX3' named entity 'C57BL' named entity 'mice' named entity 'fibrosis' named entity 'positive staining' named entity 'pathology' named entity 'oncotarget' named entity 'Waterloo, Ontario' named entity 'lung transplantation' named entity 'histological' named entity 'KO mice' named entity 'allografts' named entity 'lung transplantation' named entity 'IL-6' named entity 'PGD' named entity 'PTX3' named entity '1:200' named entity 'KO mice' named entity 'KO mice' named entity 'inflammation' named entity 'staining' named entity 'London' named entity 'PTX3' named entity 'PTX3' named entity 'PTX3' named entity 'IFN-γ' named entity 'anatomical' named entity 'lungs' named entity 'PGD' named entity 'cytokine' named entity 'Molecular Probes' named entity 'gross appearance' named entity 'wild type' named entity 'immunofluorescent staining' named entity 'lung volume'

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