Role of Surfactant Proteins A and D in Sepsis-Induced Acute Kidney Injury. Issue 1 (January 2015)
- Record Type:
- Journal Article
- Title:
- Role of Surfactant Proteins A and D in Sepsis-Induced Acute Kidney Injury. Issue 1 (January 2015)
- Main Title:
- Role of Surfactant Proteins A and D in Sepsis-Induced Acute Kidney Injury
- Authors:
- Liu, Jiao
Abdel-Razek, Osama
Liu, Zhiyong
Hu, Fengqi
Zhou, Qingshan
Cooney, Robert N.
Wang, Guirong - Abstract:
- <abstract> <title> <x xml:space="preserve">Abstract</x> </title> <sec> <title>ABSTRACT</title> <p>Sepsis is a major cause of acute kidney injury (AKI) with high rates of morbidity and mortality. Surfactant proteins A and D (SP-A, SP-D) play a critical role in host defense and regulate inflammation during infection. Recent studies indicate SP-A and SP-D are expressed in the kidney. The current study examines the role of SP-A and SP-D in the pathogenesis of sepsis-induced AKI. Wild-type (WT) and SP-A/SP-D double-knockout (KO) C57BL/6 mice were treated by cecal ligation and puncture (CLP) or sham surgery. Histological, cellular, and molecular indices of kidney injury were investigated in septic mice 6 and 24 h after CLP. Twenty-four hours after CLP, kidney injury was more severe, renal function was decreased, and blood creatinine and blood urea nitrogen were higher in septic SP-A/SP-D KO mice (<italic>P</italic> &lt; 0.05, versus septic WT mice). Kidney edema and vascular permeability were increased in septic SP-A/SP-D KO mice (<italic>P</italic> &lt; 0.01, versus septic WT mice). Apoptotic cells increased significantly (<italic>P</italic> &lt; 0.01) in the kidney of septic SP-A/SP-D KO mice compared with septic WT mice. Molecular analysis revealed levels of Bcl-2 (an inhibitor of apoptosis) were lower and levels of caspase 3 (a biomarker of apoptosis) were higher in the kidney of septic SP-A/SP-D KO mice (<italic>P</italic> &lt; 0.01, versus septic WT mice). Furthermore,<abstract> <title> <x xml:space="preserve">Abstract</x> </title> <sec> <title>ABSTRACT</title> <p>Sepsis is a major cause of acute kidney injury (AKI) with high rates of morbidity and mortality. Surfactant proteins A and D (SP-A, SP-D) play a critical role in host defense and regulate inflammation during infection. Recent studies indicate SP-A and SP-D are expressed in the kidney. The current study examines the role of SP-A and SP-D in the pathogenesis of sepsis-induced AKI. Wild-type (WT) and SP-A/SP-D double-knockout (KO) C57BL/6 mice were treated by cecal ligation and puncture (CLP) or sham surgery. Histological, cellular, and molecular indices of kidney injury were investigated in septic mice 6 and 24 h after CLP. Twenty-four hours after CLP, kidney injury was more severe, renal function was decreased, and blood creatinine and blood urea nitrogen were higher in septic SP-A/SP-D KO mice (<italic>P</italic> &lt; 0.05, versus septic WT mice). Kidney edema and vascular permeability were increased in septic SP-A/SP-D KO mice (<italic>P</italic> &lt; 0.01, versus septic WT mice). Apoptotic cells increased significantly (<italic>P</italic> &lt; 0.01) in the kidney of septic SP-A/SP-D KO mice compared with septic WT mice. Molecular analysis revealed levels of Bcl-2 (an inhibitor of apoptosis) were lower and levels of caspase 3 (a biomarker of apoptosis) were higher in the kidney of septic SP-A/SP-D KO mice (<italic>P</italic> &lt; 0.01, versus septic WT mice). Furthermore, levels of nuclear factor κB and phosphorylated IκB-α increased significantly in the kidney of septic SP-A/SP-D KO mice compared with septic WT mice, suggesting SP-A/SP-D KO mice have a more pronounced inflammatory response to sepsis. We conclude SP-A and SP-D attenuate kidney injury by modulating inflammation and apoptosis in sepsis-induced AKI.</p> </sec> </abstract> … (more)
- Is Part Of:
- Shock. Volume 43:Issue 1(2015:Jan.)
- Journal:
- Shock
- Issue:
- Volume 43:Issue 1(2015:Jan.)
- Issue Display:
- Volume 43, Issue 1 (2015)
- Year:
- 2015
- Volume:
- 43
- Issue:
- 1
- Issue Sort Value:
- 2015-0043-0001-0000
- Page Start:
- Page End:
- Publication Date:
- 2015-01
- Subjects:
- Shock -- Periodicals
Shock -- Periodicals
Choc (Pathologie) -- Périodiques
Shock
Periodicals
616.0475 - Journal URLs:
- http://www.shockjournal.com ↗
http://ovidsp.ovid.com/ovidweb.cgi?T=JS&NEWS=n&CSC=Y&PAGE=toc&D=yrovft&AN=00024382-000000000-00000 ↗
http://journals.lww.com ↗ - DOI:
- 10.1097/SHK.0000000000000270 ↗
- Languages:
- English
- ISSNs:
- 1073-2322
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 8267.443000
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 3951.xml