{"id":{"repo_id":"temple","oai_identifier":"oai:scholarshare.temple.edu:20.500.12613/517"},"canonical_url":"https://search.dev.ndltd.org/etd/temple/oai:scholarshare.temple.edu:20.500.12613/517","repository":{"repo_id":"temple","name":"Temple University","base_url":"https://scholarshare.temple.edu/server/oai/request"},"display":{"title":"YAP/TAZ REGULATES ALVEOLAR REGENERATION AND RESOLUTION OF LUNG INFLAMMATION","abstract":"Alveolar epithelium plays a pivotal role in protecting the lungs from inhaled infectious agents. Therefore, the regenerative capacity of the alveolar epithelium is critical for recovery from these insults to rebuild the epithelial barrier and restore pulmonary functions. Here, we show that sublethal infection of mice with Streptococcus pneumonia, the most common pathogen of community-acquired pneumonia, led to exclusive damage in lung alveoli, followed by alveolar epithelial regeneration and resolution of lung inflammation. We show that surfactant protein C-expressing (SPC-expressing) alveolar epithelial type II cells (AECIIs) underwent proliferation and differentiation after infection, which contributes to the newly formed alveolar epithelium. This increase in AECII activities was correlated with increased nuclear expression of Yap and Taz, the mediators of the Hippo pathway. Mice that lacked Yap/Taz in AECIIs exhibited prolonged inflammatory responses in the lung and were delayed in","abstract_html":"Alveolar epithelium plays a pivotal role in protecting the lungs from inhaled infectious agents. Therefore, the regenerative capacity of the alveolar epithelium is critical for recovery from these insults to rebuild the epithelial barrier and restore pulmonary functions. Here, we show that sublethal infection of mice with Streptococcus pneumonia, the most common pathogen of community-acquired pneumonia, led to exclusive damage in lung alveoli, followed by alveolar epithelial regeneration and resolution of lung inflammation. We show that surfactant protein C-expressing (SPC-expressing) alveolar epithelial type II cells (AECIIs) underwent proliferation and differentiation after infection, which contributes to the newly formed alveolar epithelium. This increase in AECII activities was correlated with increased nuclear expression of Yap and Taz, the mediators of the Hippo pathway. Mice that lacked Yap/Taz in AECIIs exhibited prolonged inflammatory responses in the lung and were delayed in","abstract_has_math":false,"creators":["LaCanna, Ryan"],"institution":"Temple University. Libraries","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":["Tian, Ying"],"committee_chairs":[],"committee_members":["Koch, Walter J.","Drosatos, Konstantinos","Kosmider, Beata"],"year":2019,"date_issued":"2019","date_published":"2019","updated_at":"2026-07-27T21:20:51Z","subjects":["Biology, Molecular"],"languages":["eng"],"rights":["IN COPYRIGHT- This Rights Statement can be used for an Item that is in copyright. Using this statement implies that the organization making this Item available has determined that the Item is in copyright and either is the rights-holder, has obtained permission from the rights-holder(s) to make their Work(s) available, or makes the Item available under an exception or limitation to copyright (including Fair Use) that entitles it to make the Item available."],"rights_urls":["http://rightsstatements.org/vocab/InC/1.0/"],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/20.500.12613/517","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Tian, Ying"]},{"key":"dc:contributor.committeemember","label":"Committee Member","values":["Koch, Walter J.","Drosatos, Konstantinos","Kosmider, Beata"]},{"key":"dc:creator","label":"Author","values":["LaCanna, Ryan"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2020-10-16T13:08:25Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2020-10-16T13:08:25Z"]},{"key":"dc:date.issued","label":"Date","values":["2019"]},{"key":"dc:publisher","label":"Institution","values":["Temple University. 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Using this statement implies that the organization making this Item available has determined that the Item is in copyright and either is the rights-holder, has obtained permission from the rights-holder(s) to make their Work(s) available, or makes the Item available under an exception or limitation to copyright (including Fair Use) that entitles it to make the Item available."]},{"key":"dc:rights.uri","label":"Rights URI","values":["http://rightsstatements.org/vocab/InC/1.0/"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/20.500.12613/517"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Alveolar epithelium plays a pivotal role in protecting the lungs from inhaled infectious agents. Therefore, the regenerative capacity of the alveolar epithelium is critical for recovery from these insults to rebuild the epithelial barrier and restore pulmonary functions. Here, we show that sublethal infection of mice with Streptococcus pneumonia, the most common pathogen of community-acquired pneumonia, led to exclusive damage in lung alveoli, followed by alveolar epithelial regeneration and resolution of lung inflammation. We show that surfactant protein C-expressing (SPC-expressing) alveolar epithelial type II cells (AECIIs) underwent proliferation and differentiation after infection, which contributes to the newly formed alveolar epithelium. This increase in AECII activities was correlated with increased nuclear expression of Yap and Taz, the mediators of the Hippo pathway. Mice that lacked Yap/Taz in AECIIs exhibited prolonged inflammatory responses in the lung and were delayed in"]},{"key":"dc:description.degree","label":"Dc Description Degree","values":["Ph.D."]},{"key":"dc:title","label":"Title","values":["YAP/TAZ REGULATES ALVEOLAR REGENERATION AND RESOLUTION OF LUNG INFLAMMATION"]}]}],"canonical_facts":{"dc:contributor.advisor":["Tian, Ying"],"dc:contributor.committeemember":["Koch, Walter J.","Drosatos, Konstantinos","Kosmider, Beata"],"dc:creator":["LaCanna, Ryan"],"dc:date.accessioned":["2020-10-16T13:08:25Z"],"dc:date.available":["2020-10-16T13:08:25Z"],"dc:date.issued":["2019"],"dc:description.abstract":["Alveolar epithelium plays a pivotal role in protecting the lungs from inhaled infectious agents. Therefore, the regenerative capacity of the alveolar epithelium is critical for recovery from these insults to rebuild the epithelial barrier and restore pulmonary functions. Here, we show that sublethal infection of mice with Streptococcus pneumonia, the most common pathogen of community-acquired pneumonia, led to exclusive damage in lung alveoli, followed by alveolar epithelial regeneration and resolution of lung inflammation. We show that surfactant protein C-expressing (SPC-expressing) alveolar epithelial type II cells (AECIIs) underwent proliferation and differentiation after infection, which contributes to the newly formed alveolar epithelium. This increase in AECII activities was correlated with increased nuclear expression of Yap and Taz, the mediators of the Hippo pathway. Mice that lacked Yap/Taz in AECIIs exhibited prolonged inflammatory responses in the lung and were delayed in"],"dc:description.degree":["Ph.D."],"dc:identifier.uri":["http://hdl.handle.net/20.500.12613/517"],"dc:language.iso":["eng"],"dc:publisher":["Temple University. Libraries"],"dc:rights":["IN COPYRIGHT- This Rights Statement can be used for an Item that is in copyright. Using this statement implies that the organization making this Item available has determined that the Item is in copyright and either is the rights-holder, has obtained permission from the rights-holder(s) to make their Work(s) available, or makes the Item available under an exception or limitation to copyright (including Fair Use) that entitles it to make the Item available."],"dc:rights.uri":["http://rightsstatements.org/vocab/InC/1.0/"],"dc:subject":["Biology, Molecular"],"dc:title":["YAP/TAZ REGULATES ALVEOLAR REGENERATION AND RESOLUTION OF LUNG INFLAMMATION"],"dc:type":["Text"]},"updated_at":"2026-07-27T21:20:51Z"}