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Article: Fractalkine receptor regulates microglial neurotoxicity in an experimental mouse glaucoma model

TitleFractalkine receptor regulates microglial neurotoxicity in an experimental mouse glaucoma model
Authors
Issue Date2014
PublisherWiley Periodicals, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/37090
Citation
Glia, 2014, v. 62, p. 1943-1954 How to Cite?
AbstractNeuroinflammation underlies a wide variety of pathological processes in the central nerve system (CNS). Although previous experimental and clinical studies indicate that activation of neuroinflammatory signaling occurs early in glaucoma, the mechanisms controlling microglia activation are still poorly defined. In the present study, we investigated the role of the chemokine receptor Cx3cr1 in microglia activation and retinal ganglion cell (RGC) death in an experimental mouse glaucoma model with transient elevation of intraocular pressure (IOP). We demonstrated that retinal microglia played a pathogenic role in RGC death. Conversely, pharmacological suppression of microglia activation by minocycline increased RGC survival. Moreover, we found that Cx3cr1 deficiency enhanced microglial neurotoxicity and subsequently induced more extensive RGC loss, suggesting that Cx3cr1 suppressed microglial activation under elevated IOP. Overall, these findings provided novel insight into the mechanisms by which Cx3cr1 modulated microglia activation under elevated IOP. Suppression of microglia activation might be a potential treatment for slowing down the course of the disease and for increasing RGC survival in glaucoma patients.
Persistent Identifierhttp://hdl.handle.net/10722/207220

 

DC FieldValueLanguage
dc.contributor.authorWANG, Ken_US
dc.contributor.authorPENG, Ben_US
dc.contributor.authorLin, Ben_US
dc.date.accessioned2014-12-19T08:57:28Z-
dc.date.available2014-12-19T08:57:28Z-
dc.date.issued2014en_US
dc.identifier.citationGlia, 2014, v. 62, p. 1943-1954en_US
dc.identifier.urihttp://hdl.handle.net/10722/207220-
dc.description.abstractNeuroinflammation underlies a wide variety of pathological processes in the central nerve system (CNS). Although previous experimental and clinical studies indicate that activation of neuroinflammatory signaling occurs early in glaucoma, the mechanisms controlling microglia activation are still poorly defined. In the present study, we investigated the role of the chemokine receptor Cx3cr1 in microglia activation and retinal ganglion cell (RGC) death in an experimental mouse glaucoma model with transient elevation of intraocular pressure (IOP). We demonstrated that retinal microglia played a pathogenic role in RGC death. Conversely, pharmacological suppression of microglia activation by minocycline increased RGC survival. Moreover, we found that Cx3cr1 deficiency enhanced microglial neurotoxicity and subsequently induced more extensive RGC loss, suggesting that Cx3cr1 suppressed microglial activation under elevated IOP. Overall, these findings provided novel insight into the mechanisms by which Cx3cr1 modulated microglia activation under elevated IOP. Suppression of microglia activation might be a potential treatment for slowing down the course of the disease and for increasing RGC survival in glaucoma patients.en_US
dc.languageengen_US
dc.publisherWiley Periodicals, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/37090en_US
dc.relation.ispartofGliaen_US
dc.titleFractalkine receptor regulates microglial neurotoxicity in an experimental mouse glaucoma modelen_US
dc.typeArticleen_US
dc.identifier.emailLin, B: blin@hku.hken_US
dc.identifier.authorityLin, B=rp01356en_US
dc.identifier.hkuros241844en_US
dc.identifier.volume62en_US
dc.identifier.spage1943en_US
dc.identifier.epage1954en_US

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