About: Angiotensin converting enzyme 2 abrogates bleomycin-induced lung injury

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Angiotensin converting enzyme 2 abrogates bleomycin-induced lung injury
Creator	Penninger, J Coltan, L Eaton, F Hall, A Kassiri, Z Loibner, H Oudit, G Rey-Parra, G Schuster, M Thébaud, B Vadivel, A
Source	Medline; PMC
abstract	Despite substantial progress, mortality and morbidity of the acute respiratory distress syndrome (ARDS), a severe form of acute lung injury (ALI), remain unacceptably high. There is no effective treatment for ARDS/ALI. The renin–angiotensin system (RAS) through Angiotensin-converting enzyme (ACE)-generated Angiotensin II contributes to lung injury. ACE2, a recently discovered ACE homologue, acts as a negative regulator of the RAS and counterbalances the function of ACE. We hypothesized that ACE2 prevents Bleomycin (BLM)-induced lung injury. Fourteen to 16-week-old ACE2 knockout mice—male (ACE2(−/y)) and female (ACE2(−/−))—and age-matched wild-type (WT) male mice received intratracheal BLM (1.5U/kg). Male ACE2(−/y) BLM injured mice exhibited poorer exercise capacity, worse lung function and exacerbated lung fibrosis and collagen deposition compared with WT. These changes were associated with increased expression of the profibrotic genes α-smooth muscle actin (α-SMA) and Transforming Growth Factor ß1. Compared with ACE2(−/y) exposed to BLM, ACE2(−/−) exhibited better lung function and architecture and decreased collagen deposition. Treatment with intraperitoneal recombinant human (rh) ACE2 (2 mg/kg) for 21 days improved survival, exercise capacity, and lung function and decreased lung inflammation and fibrosis in male BLM-WT mice. Female BLM WT mice had mild fibrosis and displayed a possible compensatory upregulation of the AT2 receptor. We conclude that ACE2 gene deletion worsens BLM-induced lung injury and more so in males than females. Conversely, ACE2 protects against BLM-induced fibrosis. rhACE2 may have therapeutic potential to attenuate respiratory morbidity in ALI/ARDS.
has issue date	2012-01-14(xsd:dateTime)
bibo:doi	10.1007/s00109-012-0859-2
bibo:pmid	22246130
has license	no-cc
sha1sum (hex)	d6e5282c9d180b459c54d6a82ff60fcfcfe99636
schema:url	https://doi.org/10.1007/s00109-012-0859-2
resource representing a document's title	Angiotensin converting enzyme 2 abrogates bleomycin-induced lung injury
has PubMed Central identifier	PMC7080102
has PubMed identifier	22246130
schema:publication	J Mol Med (Berl)
resource representing a document's body	covid:d6e5282c9d180b459c54d6a82ff60fcfcfe99636#body_text
is schema:about of	named entity 'human' named entity 'fibrosis' named entity 'Male' named entity 'ARDS' named entity 'gene' named entity 'ALI' named entity 'BLM' named entity 'lung function' named entity 'lung injury' named entity 'BLM' named entity 'INCREASED EXPRESSION' named entity 'GENES' named entity 'ACE' named entity 'FUNCTION' named entity 'AGE' named entity 'LUNG FIBROSIS' covid:arg/d6e5282c9d180b459c54d6a82ff60fcfcfe99636 named entity 'TREATMENT' named entity 'UPREGULATION' named entity 'CHANGES' named entity 'WORSE' named entity 'TRANSFORMING GROWTH FACTOR' named entity 'ENZYME' named entity 'ASSOCIATED WITH' named entity 'CONCLUDE' named entity 'LUNG FUNCTION' named entity '282' named entity 'EXACERBATED' named entity 'PROGRESS' named entity 'INDUCED' named entity 'ANGIOTENSIN II' named entity 'POSSIBLE' named entity 'INDUCED' named entity 'LUNG INJURY' named entity 'MATCHED' named entity 'RECEIVED' named entity 'RESPIRATORY MORBIDITY' named entity 'ACUTE LUNG INJURY' named entity 'ANGIOTENSIN CONVERTING ENZYME 2' named entity 'WILD-TYPE' named entity 'MG%' named entity 'INTRATRACHEAL' named entity 'DISPLAYED' named entity 'ARCHITECTURE' named entity 'RECOMBINANT' named entity 'SMOOTH MUSCLE ACTIN' named entity 'FEMALE' named entity 'EXPOSED TO' named entity 'BLEOMYCIN' named entity 'THESE' named entity 'POTENTIAL' named entity 'DAYS' named entity 'MORTALITY' named entity 'FIBROSIS' named entity 'MILD' named entity 'SEVERE' named entity 'INJURED' named entity 'MICE' named entity 'INTRAPERITONEAL' named entity 'HIGH' named entity 'AT2 RECEPTOR' named entity 'MORBIDITY' named entity 'LUNG INFLAMMATION' named entity 'RENIN-ANGIOTENSIN SYSTEM' named entity 'NEGATIVE REGULATOR' named entity 'PREVENTS' named entity 'SMA' named entity 'DECREASED' named entity 'ACUTE RESPIRATORY DISTRESS SYNDROME' named entity 'HUMAN' named entity 'LUNG INJURY'

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