NDLI: Disruption of cyclooxygenase type 2 exacerbates apoptosis and renal damage during obstructive nephropathy.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Nilsson, Line Madsen, Kirsten Krag, Søren Frøkiær, Jørgen Jensen, Boye L. Nørregaard, Rikke
Description	Author Affiliation: Nilsson L ( Department of Clinical Medicine, Aarhus University, Aarhus, Denmark); Madsen K ( Cardiovascular and Renal Research, University of Southern Denmark, Odense, Denmark); Krag S ( Department of Pathology, Aarhus University Hospital, Aarhus, Denmark); Frøkiær J ( Department of Clinical Medicine, Aarhus University, Aarhus, Denmark); Jensen BL ( Cardiovascular and Renal Research, University of Southern Denmark, Odense, Denmark); Nørregaard R ( Department of Clinical Medicine, Aarhus University, Aarhus, Denmark)
Abstract	Renal oxidative stress is increased in response to ureteral obstruction. In vitro, cyclooxygenase (COX)-2 activity contributes to protection against oxidants. In the present study, we tested the hypothesis that COX-2 activity counters oxidative stress and apoptosis in an in vivo model of obstructive nephropathy. Renal oxidative stress markers, antioxidant enzymes, and markers of tubular injury, tubular dilation, and apoptosis were investigated in COX-2 knockout (COX-2(-/-)) and wild-type (WT) mice subjected to 3 or 7 days of unilateral ureteral obstruction (UUO). In a separate series, WT sham-operated and UUO mice were treated with a selective COX-2 inhibitor, parecoxib. COX-2 increased in response to UUO; the oxidative stress markers 4-hydroxynonenal and nitrotyrosine protein residues increased in kidney tissue with no genotype difference after UUO, whereas the antioxidant enzymes heme oxygenase-1 and SOD2 displayed higher levels in COX-2(-/-) mice. Tubular injury was aggravated by COX-2 deletion, as measured by tubular dilatation, an increase in kidney injury molecule-1, cortical caspase-3 content, and apoptosis index. In conclusion, COX-2 is necessary to protect against tubular injury and apoptosis after UUO but not necessary to protect against oxidative stress. COX-2 is not likely to directly regulate antioxidant enzymes heme oxygenase-1 and SOD in the kidney.
File Format	HTM / HTML
ISSN	1931857X
Issue Number	12
Volume Number	309
e-ISSN	15221466
Journal	AJP: Renal Physiology
Language	English
Publisher	American Physiological Society
Publisher Date	2015-12-15
Publisher Place	United States
Access Restriction	Subscribed
Subject Keyword	Kidney Diseases Research Support, Non-u.s. Gov't Oxidative Stress Cyclooxygenase 2 Drug Therapy Discipline Nephrology Pharmacology Metabolism Drug Effects Journal Article Mice, Knockout Antioxidants Discipline Physiology Pathology Ureteral Obstruction Animals Cyclooxygenase 2 Inhibitors Mice Enzymology Apoptosis
Content Type	Text
Resource Type	Article
Subject	Physiology Urology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in