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Article: The RhoA GTPase-activating protein DLC2 modulates RhoA activity and hyperalgesia to noxious thermal and inflammatory stimuli

TitleThe RhoA GTPase-activating protein DLC2 modulates RhoA activity and hyperalgesia to noxious thermal and inflammatory stimuli
Authors
KeywordsDeleted in liver cancer 2
ERK
Hyperalgesia
Inflammation
Nerve conduction velocity
Pain
RhoA
Issue Date2012
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSG
Citation
Neurosignals, 2012, v. 20 n. 2, p. 112-126 How to Cite?
AbstractDeleted in liver cancer 2 (DLC2) is a novel Rho GTPase-activating protein that regulates RhoA activity. DLC2 is ubiquitously expressed in most tissues, including the brain, spinal cord and peripheral nerves, and is thought to be involved in actin cytoskeletal reorganization. Unlike DLC1-deficient mice, DLC2-deficient mice (DLC2 -/-) are viable and without gross anatomical abnormalities. Interestingly, DLC2 -/- mice exhibit hyperalgesia to noxious thermal stimuli and inflammation-inducing chemicals, such as formalin and acetic acid. There was no difference in the structure or morphology of cutaneous or sural nerves between DLC2 +/+ and DLC2 -/- mice. However, sensory nerve conduction velocity in DLC2 -/- mice was significantly higher than that in DLC2 +/+ mice, whereas motor nerve conduction velocity was not affected. After formalin injection, DLC2 -/- mice showed increased RhoA activity in the spinal cord and an increased number of phosphorylated ERK1/2-positive cells. The inflammatory hyperalgesia in DLC2 -/- mice appeared to be mediated through the activation of RhoA and ERK1/2. Taken together, DLC2 plays a key role in pain modulation during inflammation by suppressing the activation of RhoA and ERK to prevent an exaggerated pain response, and DLC2 -/- mice provide a valuable tool for further understanding the regulation of inflammatory pain. Copyright © 2011 S. Karger AG, Basel.
Persistent Identifierhttp://hdl.handle.net/10722/148690
ISSN
2015 Impact Factor: 1.593
2015 SCImago Journal Rankings: 0.763
ISI Accession Number ID
Funding AgencyGrant Number
CRCG
CRCG funding, The University of Hong Kong
Funding Information:

We thank Dr. T.O. Yau, Dr. Amy K.M. Lam and Mr. James Y.B. Lau for technical assistance in generating DLC2-/- mice and Dr. Thomas H.Y. Leung for technical advice on Rhotekin binding assay. I.O. Ng is Loke Yew Professor in Pathology. This project is supported by CRCG funding, The University of Hong Kong, to S.K. Chung.

References

 

DC FieldValueLanguage
dc.contributor.authorChan, FKCen_HK
dc.contributor.authorChung, SSMen_HK
dc.contributor.authorNg, IOen_HK
dc.contributor.authorChung, SKen_HK
dc.date.accessioned2012-05-29T06:14:42Z-
dc.date.available2012-05-29T06:14:42Z-
dc.date.issued2012en_HK
dc.identifier.citationNeurosignals, 2012, v. 20 n. 2, p. 112-126en_HK
dc.identifier.issn1424-862Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/148690-
dc.description.abstractDeleted in liver cancer 2 (DLC2) is a novel Rho GTPase-activating protein that regulates RhoA activity. DLC2 is ubiquitously expressed in most tissues, including the brain, spinal cord and peripheral nerves, and is thought to be involved in actin cytoskeletal reorganization. Unlike DLC1-deficient mice, DLC2-deficient mice (DLC2 -/-) are viable and without gross anatomical abnormalities. Interestingly, DLC2 -/- mice exhibit hyperalgesia to noxious thermal stimuli and inflammation-inducing chemicals, such as formalin and acetic acid. There was no difference in the structure or morphology of cutaneous or sural nerves between DLC2 +/+ and DLC2 -/- mice. However, sensory nerve conduction velocity in DLC2 -/- mice was significantly higher than that in DLC2 +/+ mice, whereas motor nerve conduction velocity was not affected. After formalin injection, DLC2 -/- mice showed increased RhoA activity in the spinal cord and an increased number of phosphorylated ERK1/2-positive cells. The inflammatory hyperalgesia in DLC2 -/- mice appeared to be mediated through the activation of RhoA and ERK1/2. Taken together, DLC2 plays a key role in pain modulation during inflammation by suppressing the activation of RhoA and ERK to prevent an exaggerated pain response, and DLC2 -/- mice provide a valuable tool for further understanding the regulation of inflammatory pain. Copyright © 2011 S. Karger AG, Basel.en_HK
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSGen_HK
dc.relation.ispartofNeuroSignalsen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectDeleted in liver cancer 2en_HK
dc.subjectERKen_HK
dc.subjectHyperalgesiaen_HK
dc.subjectInflammationen_HK
dc.subjectNerve conduction velocityen_HK
dc.subjectPainen_HK
dc.subjectRhoAen_HK
dc.titleThe RhoA GTPase-activating protein DLC2 modulates RhoA activity and hyperalgesia to noxious thermal and inflammatory stimulien_HK
dc.typeArticleen_HK
dc.identifier.emailChung, SSM:skchung@hkucc.hku.hken_HK
dc.identifier.emailNg, IO:iolng@hkucc.hku.hken_HK
dc.identifier.emailChung, SK:skchung@hkucc.hku.hken_HK
dc.identifier.authorityChung, SSM=rp00381en_HK
dc.identifier.authorityNg, IO=rp00335en_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.description.naturepostprinten_US
dc.identifier.doi10.1159/000331240en_HK
dc.identifier.pmid22204965-
dc.identifier.scopuseid_2-s2.0-84858998423en_HK
dc.identifier.hkuros204801-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84858998423&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume20en_HK
dc.identifier.issue2en_HK
dc.identifier.spage112en_HK
dc.identifier.epage126en_HK
dc.identifier.isiWOS:000301762700005-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridChan, FKC=54792657600en_HK
dc.identifier.scopusauthoridChung, SSM=7404292976en_HK
dc.identifier.scopusauthoridNg, IO=7102753722en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK

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