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- Onozato, Maristela LUniversity of Tokyo, Japan and Georgetown University, USA (author)
Expression of NG,NG-dimethylarginine dimethylaminohydrolase and protein arginine N-methyltransferase isoforms in diabetic rat kidney: effects of angiotensin II receptor blockers
- Article/chapterEnglish2008
Publisher, publication year, extent ...
- American Diabetes Association,2008
- printrdacarrier
Numbers
- LIBRIS-ID:oai:DiVA.org:uu-11924
- https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-11924URI
- https://doi.org/10.2337/db06-1772DOI
- https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-99787URI
Supplementary language notes
- Language:English
- Summary in:English
Part of subdatabase
- SwePubSwePub
Classification
Notes
- Objective: The nitric oxide (NO) synthase inhibitor, asymmetric dimethylarginine (ADMA) is generated by protein arginine N-methyltransferase (PRMT)-1 and is metabolized by NG, NG-dimethylarginine dimethylaminohydrolase (DDAH). We tested the hypothesis that increased serum ADMA (SADMA) in the streptozotocin (STZ)-induced rat model of diabetes mellitus (DM) is mediated by an angiotensin receptor blocker– sensitive change in DDAH or PRMT expression.Research design and Methods: Data were compared from 4 groups of rats: sham injected controls; untreated STZ- DM at 4 weeks; STZ-DM rats administered the angiotensin II receptor blocker telmisartan for 2 weeks; control rats administered telmisartan for 2 weeks.Results: Immunostaining and Western blotting of microdissected nephron segments localized DDAH I in the proximal tubules and DDAH II in the glomeruli, afferent arterioles, macula densa and distal nephron. Renal angiotensin II and SADMA increased with DM but were normalized by 2 weeks of telmisartan. DDAH I expression was decreased in DM kidneys while DDAH II expression was increased. These changes were reversed by telmisartan which also reduced expression of PRMT-1 and -5. Telmisartan increased expressions of DDAH I but decreased DDAH II in Ang II-stimulated kidney slices ex-vivo.Conclusion: Renal angiotensin II and SADMA are increased in insulinopenic DM. They are normalized by an angiotensin II receptor blocker which increases the renal expression of DDAH I, decreases PRMT-1 and increases renal NO metabolites.
Subject headings and genre
- MEDICINE
- MEDICIN
Added entries (persons, corporate bodies, meetings, titles ...)
- Tojo, AkihiroUniversity of Tokyo, Japan (author)
- Leiper, JamesUniversity College London, UK (author)
- Fujita, ToshiroUniversity of Tokyo, Japan (author)
- Palm, FredrikUppsala universitet,Institutionen för medicinsk cellbiologi,Division of Nephrology and Hypertension, Cardiovascular Kidney Hypertension Institutet, Georgetown University, USA(Swepub:liu)frepa35 (author)
- Wilcox, Christopher SGeorgetown University, USA (author)
- University of Tokyo, Japan and Georgetown University, USAUniversity of Tokyo, Japan (creator_code:org_t)
Related titles
- In:Diabetes: American Diabetes Association57:1, s. 172-1800012-17971939-327X
Internet link
- http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Retrieve&list_uids=17909098&dopt=Citation
- http://diabetes.diabetesjournals.org/content/57/1/172.full.pdf
- https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-11924
- https://doi.org/10.2337/db06-1772
- https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-99787
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