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Overactive EGFR Signaling Leads to L...
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Venkataraman, Thiagarajan.
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Overactive EGFR Signaling Leads to Lung Fibrosis After SARS-CoV Infection.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Overactive EGFR Signaling Leads to Lung Fibrosis After SARS-CoV Infection./
作者:
Venkataraman, Thiagarajan.
出版者:
Ann Arbor : ProQuest Dissertations & Theses, : 2017,
面頁冊數:
143 p.
附註:
Source: Dissertation Abstracts International, Volume: 78-10(E), Section: B.
Contained By:
Dissertation Abstracts International78-10B(E).
標題:
Virology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10259261
ISBN:
9781369822786
Overactive EGFR Signaling Leads to Lung Fibrosis After SARS-CoV Infection.
Venkataraman, Thiagarajan.
Overactive EGFR Signaling Leads to Lung Fibrosis After SARS-CoV Infection.
- Ann Arbor : ProQuest Dissertations & Theses, 2017 - 143 p.
Source: Dissertation Abstracts International, Volume: 78-10(E), Section: B.
Thesis (Ph.D.)--University of Maryland, Baltimore, 2017.
SARS coronavirus (SARS-CoV) is a pathogenic respiratory virus that causes acute lung injury in humans. In turn, the host mounts a wound healing response to repair the injury. One of the major sequelae caused by SARS-CoV is pulmonary fibrosis (PF), which occurs more frequently in older patients. Fibrosis is caused by a dysregulated wound healing response and the molecular pathways underlying the development of fibrosis are not completely understood. Using mouse models of SARS-CoV pathogenesis, we have identified that the wound healing pathway, controlled by the epidermal growth factor receptor (EGFR) is critical to recovery from SARS-CoV induced tissue damage. In mice with constitutively active EGFR, [EGFR(DSK5) mice], we find that SARS-CoV infection causes enhanced lung disease. Importantly, we show that during infection the EGFR ligands amphiregulin and HB-EGF are upregulated and exogenous addition of these ligands during infection of wildtype mice leads to enhanced lung disease and altered wound healing dynamics. Our data demonstrate a key role of EGFR in the host response to SARS-CoV and how it may be implicated in lung disease induced by other highly pathogenic respiratory viruses.
ISBN: 9781369822786Subjects--Topical Terms:
642304
Virology.
Overactive EGFR Signaling Leads to Lung Fibrosis After SARS-CoV Infection.
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SARS coronavirus (SARS-CoV) is a pathogenic respiratory virus that causes acute lung injury in humans. In turn, the host mounts a wound healing response to repair the injury. One of the major sequelae caused by SARS-CoV is pulmonary fibrosis (PF), which occurs more frequently in older patients. Fibrosis is caused by a dysregulated wound healing response and the molecular pathways underlying the development of fibrosis are not completely understood. Using mouse models of SARS-CoV pathogenesis, we have identified that the wound healing pathway, controlled by the epidermal growth factor receptor (EGFR) is critical to recovery from SARS-CoV induced tissue damage. In mice with constitutively active EGFR, [EGFR(DSK5) mice], we find that SARS-CoV infection causes enhanced lung disease. Importantly, we show that during infection the EGFR ligands amphiregulin and HB-EGF are upregulated and exogenous addition of these ligands during infection of wildtype mice leads to enhanced lung disease and altered wound healing dynamics. Our data demonstrate a key role of EGFR in the host response to SARS-CoV and how it may be implicated in lung disease induced by other highly pathogenic respiratory viruses.
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