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Article: Aldose reductase deficiency improves wallerian degeneration and nerve regeneration in diabetic thy1-YFP mice

TitleAldose reductase deficiency improves wallerian degeneration and nerve regeneration in diabetic thy1-YFP mice
Authors
KeywordsAldose reductase
Diabetes
Nerve regeneration
Thy1-YFP mice
Wallerian degeneration
Issue Date2010
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.jneuropath.com
Citation
Journal Of Neuropathology And Experimental Neurology, 2010, v. 69 n. 3, p. 294-305 How to Cite?
AbstractThis study examined the role of aldose reductase (AR) in diabetes-associated impaired nerve regeneration using thy1-YFP (YFP) mice. Sciatic nerves of nondiabetic and streptozotocin-induced diabetic AR +/+YFP and AR-/-YFP mice were transected after 4 weeks of diabetes. Wallerian degeneration and nerve regeneration were evaluated at 1 and 2 weeks postaxotomy by fluorescence microscopy. Motor nerve conduction velocity recovery and regenerating nerve morphometric parameters were determined at 10 and 20 weeks, respectively. There was no difference in the extent of Wallerian degeneration, size of regenerating stump, motor nerve conduction velocity recovery, or caliber of regenerating fibers between nondiabetic AR +/+YFP and AR-/-YFP mice. In diabetic AR+/+YFP mice, Wallerian degeneration was delayed, associated with slower macrophage invasion and abnormal vascularization. Those mice had smaller regenerating stumps, slower motor nerve conduction velocity, and smaller regenerating fibers compared with nondiabetic mice. These features of impaired nerve regeneration were largely attenuated in diabetic AR-/-YFP mice. Retarded macrophage invasion and vascularization associated with Wallerian degeneration were normalized in diabetic ARYFP mice. These results indicate that AR plays an important role in diabetes-associated impaired nerve regeneration, in part by affecting vascularization and macrophage invasion during Wallerian degeneration. The thy1-YFP mice are valuable tools for further investigation of the mechanism of diabetes-associated nerve regeneration. Copyright © 2010 by the American Association of Neuropathologists, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/124477
ISSN
2015 Impact Factor: 3.432
2015 SCImago Journal Rankings: 2.136
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChen, YSen_HK
dc.contributor.authorChung, SSen_HK
dc.contributor.authorChung, SKen_HK
dc.date.accessioned2010-10-31T10:36:36Z-
dc.date.available2010-10-31T10:36:36Z-
dc.date.issued2010en_HK
dc.identifier.citationJournal Of Neuropathology And Experimental Neurology, 2010, v. 69 n. 3, p. 294-305en_HK
dc.identifier.issn0022-3069en_HK
dc.identifier.urihttp://hdl.handle.net/10722/124477-
dc.description.abstractThis study examined the role of aldose reductase (AR) in diabetes-associated impaired nerve regeneration using thy1-YFP (YFP) mice. Sciatic nerves of nondiabetic and streptozotocin-induced diabetic AR +/+YFP and AR-/-YFP mice were transected after 4 weeks of diabetes. Wallerian degeneration and nerve regeneration were evaluated at 1 and 2 weeks postaxotomy by fluorescence microscopy. Motor nerve conduction velocity recovery and regenerating nerve morphometric parameters were determined at 10 and 20 weeks, respectively. There was no difference in the extent of Wallerian degeneration, size of regenerating stump, motor nerve conduction velocity recovery, or caliber of regenerating fibers between nondiabetic AR +/+YFP and AR-/-YFP mice. In diabetic AR+/+YFP mice, Wallerian degeneration was delayed, associated with slower macrophage invasion and abnormal vascularization. Those mice had smaller regenerating stumps, slower motor nerve conduction velocity, and smaller regenerating fibers compared with nondiabetic mice. These features of impaired nerve regeneration were largely attenuated in diabetic AR-/-YFP mice. Retarded macrophage invasion and vascularization associated with Wallerian degeneration were normalized in diabetic ARYFP mice. These results indicate that AR plays an important role in diabetes-associated impaired nerve regeneration, in part by affecting vascularization and macrophage invasion during Wallerian degeneration. The thy1-YFP mice are valuable tools for further investigation of the mechanism of diabetes-associated nerve regeneration. Copyright © 2010 by the American Association of Neuropathologists, Inc.en_HK
dc.languageengen_HK
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.jneuropath.comen_HK
dc.relation.ispartofJournal of Neuropathology and Experimental Neurologyen_HK
dc.subjectAldose reductaseen_HK
dc.subjectDiabetesen_HK
dc.subjectNerve regenerationen_HK
dc.subjectThy1-YFP miceen_HK
dc.subjectWallerian degenerationen_HK
dc.subject.meshAldehyde Reductase - deficiency - genetics-
dc.subject.meshAxons - enzymology - pathology-
dc.subject.meshDiabetic Neuropathies - enzymology - physiopathology - therapy-
dc.subject.meshNerve Regeneration - genetics-
dc.subject.meshWallerian Degeneration - enzymology - physiopathology - therapy-
dc.titleAldose reductase deficiency improves wallerian degeneration and nerve regeneration in diabetic thy1-YFP miceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-3069&volume=69&issue=3&spage=294&epage=305&date=2010&atitle=Aldose+reductase+deficiency+improves+wallerian+degeneration+and+nerve+regeneration+in+diabetic+thy1-YFP+mice-
dc.identifier.emailChung, SS: smchung@hkucc.hku.hken_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.authorityChung, SS=rp00376en_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1097/NEN.0b013e3181d26487en_HK
dc.identifier.pmid20142761-
dc.identifier.scopuseid_2-s2.0-77649262334en_HK
dc.identifier.hkuros181680en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77649262334&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume69en_HK
dc.identifier.issue3en_HK
dc.identifier.spage294en_HK
dc.identifier.epage305en_HK
dc.identifier.isiWOS:000275418600009-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChen, YS=34975255700en_HK
dc.identifier.scopusauthoridChung, SS=14120761600en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK
dc.identifier.citeulike6916153-

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