دورية أكاديمية
أعرض في EDS

The Expression of Water and Ion Channels in Diffuse Alveolar Damage Is Not Dependent on DAD Etiology.

التفاصيل البيبلوغرافية
العنوان: The Expression of Water and Ion Channels in Diffuse Alveolar Damage Is Not Dependent on DAD Etiology.
المؤلفون: Pires-Neto RC; Departamento de Patologia da Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, Brazil., Del Carlo Bernardi F; Departamento de Patologia da Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, Brazil., Alves de Araujo P; Departamento de Patologia da Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, Brazil., Mauad T; Departamento de Patologia da Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, Brazil., Dolhnikoff M; Departamento de Patologia da Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, Brazil.
المصدر: PloS one [PLoS One] 2016 Nov 11; Vol. 11 (11), pp. e0166184. Date of Electronic Publication: 2016 Nov 11 (Print Publication: 2016).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science
مواضيع طبية MeSH: Aquaporin 1/*metabolism , Aquaporin 5/*metabolism , Epithelial Sodium Channels/*metabolism , Pulmonary Alveoli/*metabolism , Sodium-Potassium-Exchanging ATPase/*metabolism, Acute Lung Injury/etiology ; Acute Lung Injury/metabolism ; Adult ; Aged ; Aged, 80 and over ; Aquaporin 3/metabolism ; Autopsy ; Female ; Humans ; Immunohistochemistry ; Influenza A Virus, H1N1 Subtype/physiology ; Influenza, Human/complications ; Influenza, Human/virology ; Leptospirosis/complications ; Male ; Middle Aged ; Pulmonary Alveoli/pathology ; Respiration Disorders/etiology ; Respiration Disorders/metabolism ; Sepsis/complications ; Young Adult
مستخلص: Introduction: Aquaporins and ion channels are membrane proteins that facilitate the rapid movement of water and solutes across biological membranes. Experimental and in vitro studies reported that the function of these channels and pulmonary edema resolution are impaired in acute lung injury (ALI). Although current evidence indicates that alveolar fluid clearance is impaired in patients with ALI/diffuse alveolar damage (DAD), few human studies have addressed the alterations in pulmonary channels in this clinical condition. Additionally, it is not known whether the primary cause of DAD is a relevant variable for the channel dysfunction.
Methods: Autopsied lungs of 43 patients with acute respiratory failure (ARF) due to DAD of three different etiologies, non-pulmonary sepsis, H1N1 viral infection and leptospirosis, were compared to 18 normal lungs. We quantified the expression of aquaporin (AQP) 1, AQP3, AQP5, epithelial Na+ channel (ENaC) and sodium potassium ATPase (Na-K-ATPase) in the alveolar septum using immunohistochemistry and image analysis.
Results: The DAD group presented with increased expression of AQP3, AQP5 and Na-K-ATPase and decreased expression of ENaC compared to controls. However, there was no difference in protein expression within the DAD groups of different etiologies.
Conclusion: Water and ion channels are altered in patients with ARF due to DAD. The cause of DAD does not seem to influence the level of impairment of these channels.
Competing Interests: The authors have declared that no competing interests exist.
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المشرفين على المادة: 0 (AQP1 protein, human)
0 (AQP3 protein, human)
0 (AQP5 protein, human)
0 (Aquaporin 5)
0 (Epithelial Sodium Channels)
146410-94-8 (Aquaporin 1)
158801-98-0 (Aquaporin 3)
EC 7.2.2.13 (Sodium-Potassium-Exchanging ATPase)
تواريخ الأحداث: Date Created: 20161112 Date Completed: 20170710 Latest Revision: 20240327
رمز التحديث: 20240327
مُعرف محوري في PubMed: PMC5106024
DOI: 10.1371/journal.pone.0166184
PMID: 27835672
قاعدة البيانات: MEDLINE
الوصف
تدمد:1932-6203
DOI:10.1371/journal.pone.0166184