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Conference Paper: Activation of microglia/macrophages determines the fate of retinal ganglion cell survival in rat chronic ocular hypertension model

TitleActivation of microglia/macrophages determines the fate of retinal ganglion cell survival in rat chronic ocular hypertension model
Authors
Issue Date2006
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSG
Citation
The 25th Annual Scientific Meeting of the Hong Kong Society of Neurosciences, Hong Kong, 5-6 December 2005. In Neurosignals, 2006, v. 15 n. 3, p. 139, abstract no. OP-3/25 How to Cite?
AbstractAlthough it has been demonstrated that microglia/macrophages produce neuroprotective effects in acute injury, whether they do the same in chronic neurodegeneration such as glaucoma is largely unknown. Using a laser-induced chronic ocular hypertension (COH) model, we systematically studied the influences of microglia in RGC loss. Adult female SD rats were anesthetized with intra-peritoneal injection of a ketamine/xylazine mixture. Proparacaine hydrochloride was applied to the eyes as topical anesthetics. The limbal vein and the three radial episcleral aqueous humor drainage veins of the right eye were photocoagulated twice with a 7-day interval using an Argon laser. While a small number of microglial cells (10 3 ) did not produce significant influence, injection of large number of microglial cells (10 5 ) into the vitreous significantly increased RGC loss. Appropriate quantity (10 4 ) microglial cells per intraocular injection markedly reduced RGC loss in the COH model. Monocyte chemoattractant protein 1 at low concentration (10 and 100 ng), but not at high concentration (1,000 ng), provided significant neuroprotective effect on RGCs, which may attribute to the chemoattractive property on microglia/macrophages to the retina. Immunocytochemical staining on flat mounted retinas displayed high immunoreactivity for ionized calcium binding adapter molecular 1 (Iba1), indicating high number of microglia/macrophages. Potent stimulation of micro glia/macrophages by lipopolysaccharide (LPS) significantly increased the death of RGCs in the COH model. Iba1-immunoreactive positive microglia/macrophages in the LPS group were activated with enlarged cell body and thickened short process. These results advance our understanding of the roles of microglia in chronic neurodegeneration. Our results can demonstrate that microglia/macrophages can be either protective or harmful depending on the stimulation in chronic neurological disorder like glaucoma. Acknowledgement: The study is supported by The American Health Assistant Foundation to R.C.C. Chang and K.-F. So.
Persistent Identifierhttp://hdl.handle.net/10722/67401
ISSN
2015 Impact Factor: 1.593
2015 SCImago Journal Rankings: 0.763

 

DC FieldValueLanguage
dc.contributor.authorChiu, Ken_HK
dc.contributor.authorJi, JZen_HK
dc.contributor.authorYu, MSen_HK
dc.contributor.authorSo, KFen_HK
dc.contributor.authorChang, RCCen_HK
dc.date.accessioned2010-09-06T05:54:49Z-
dc.date.available2010-09-06T05:54:49Z-
dc.date.issued2006en_HK
dc.identifier.citationThe 25th Annual Scientific Meeting of the Hong Kong Society of Neurosciences, Hong Kong, 5-6 December 2005. In Neurosignals, 2006, v. 15 n. 3, p. 139, abstract no. OP-3/25en_HK
dc.identifier.issn1424-862Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/67401-
dc.description.abstractAlthough it has been demonstrated that microglia/macrophages produce neuroprotective effects in acute injury, whether they do the same in chronic neurodegeneration such as glaucoma is largely unknown. Using a laser-induced chronic ocular hypertension (COH) model, we systematically studied the influences of microglia in RGC loss. Adult female SD rats were anesthetized with intra-peritoneal injection of a ketamine/xylazine mixture. Proparacaine hydrochloride was applied to the eyes as topical anesthetics. The limbal vein and the three radial episcleral aqueous humor drainage veins of the right eye were photocoagulated twice with a 7-day interval using an Argon laser. While a small number of microglial cells (10 3 ) did not produce significant influence, injection of large number of microglial cells (10 5 ) into the vitreous significantly increased RGC loss. Appropriate quantity (10 4 ) microglial cells per intraocular injection markedly reduced RGC loss in the COH model. Monocyte chemoattractant protein 1 at low concentration (10 and 100 ng), but not at high concentration (1,000 ng), provided significant neuroprotective effect on RGCs, which may attribute to the chemoattractive property on microglia/macrophages to the retina. Immunocytochemical staining on flat mounted retinas displayed high immunoreactivity for ionized calcium binding adapter molecular 1 (Iba1), indicating high number of microglia/macrophages. Potent stimulation of micro glia/macrophages by lipopolysaccharide (LPS) significantly increased the death of RGCs in the COH model. Iba1-immunoreactive positive microglia/macrophages in the LPS group were activated with enlarged cell body and thickened short process. These results advance our understanding of the roles of microglia in chronic neurodegeneration. Our results can demonstrate that microglia/macrophages can be either protective or harmful depending on the stimulation in chronic neurological disorder like glaucoma. Acknowledgement: The study is supported by The American Health Assistant Foundation to R.C.C. Chang and K.-F. So.-
dc.languageengen_HK
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSGen_HK
dc.relation.ispartofNeurosignals-
dc.rightsNeurosignals. Copyright © S Karger AG.en_HK
dc.titleActivation of microglia/macrophages determines the fate of retinal ganglion cell survival in rat chronic ocular hypertension modelen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailSo, KF: hrmaskf@hkucc.hku.hken_HK
dc.identifier.emailChang, RCC: rccchang@hkucc.hku.hken_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.identifier.authorityChang, RCC=rp00470en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1159/000095356-
dc.identifier.hkuros112873en_HK
dc.identifier.volume15-
dc.identifier.issue3-
dc.identifier.spage139, abstract no. OP-3/25-
dc.identifier.epage139, abstract no. OP-3/25-
dc.publisher.placeSwitzerland-

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