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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004263naa a2200337 4500
001oai:lup.lub.lu.se:33b3ae83-9c8f-4f55-98dd-9ac490384b0b
003SwePub
008160401s2015 | |||||||||||000 ||eng|
024a https://lup.lub.lu.se/record/54533072 URI
024a https://doi.org/10.1186/s12974-015-0312-x2 DOI
040 a (SwePub)lu
041 a engb eng
042 9 SwePub
072 7a art2 swepub-publicationtype
072 7a ref2 swepub-contenttype
100a Manouchehrian, Oscaru Lund University,Lunds universitet,Oftalmologi, Lund,Sektion IV,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Retinal Molekylär Homeostas,Forskargrupper vid Lunds universitet,Ophthalmology, Lund,Section IV,Department of Clinical Sciences, Lund,Faculty of Medicine,Retinal Molecular Homeostasi,Lund University Research Groups4 aut0 (Swepub:lu)med-omo
2451 0a Who let the dogs out?: detrimental role of Galectin-3 in hypoperfusion-induced retinal degeneration.
264 c 2015-05-14
264 1b Springer Science and Business Media LLC,c 2015
520 a BackgroundRetinal ischemia results in a progressive degeneration of neurons and a pathological activation of glial cells, resulting in vision loss. In the brain, progressive damage after ischemic insult has been correlated to neuroinflammatory processes involving microglia. Galectin-3 has been shown to mediate microglial responses to ischemic injury in the brain. Therefore, we wanted to explore the contribution of Galectin-3 (Gal-3) to hypoperfusion-induced retinal degeneration in mice.MethodsGal-3 knockout (Gal-3 KO) and wildtype (WT) C57BL/6 mice were subjected to chronic cerebral hypoperfusion by bilateral narrowing of the common carotid arteries using metal coils resulting in a 30% reduction of blood flow. Sham operated mice served as controls. After 17 weeks, the mice were sacrificed and the eyes were analyzed for retinal architecture, neuronal cell survival, and glial reactivity using morphological staining and immunohistochemistry.ResultsHypoperfusion caused a strong increase in Gal-3 expression and microglial activation in WT mice, coupled with severe degenerative damage to all retinal neuronal subtypes, remodeling of the retinal lamination and Müller cell gliosis. In contrast, hypoperfused Gal-3 KO mice displayed a retained laminar architecture, a significant preservation of photoreceptors and ganglion cell neurons, and an attenuation of microglial and Müller cell activation.ConclusionModerate cerebral blood flow reduction in the mouse results in severe retinal degenerative damage. In mice lacking Gal-3 expression, pathological changes are significantly attenuated. Gal-3 is thereby a potential target for treatment and prevention of hypoperfusion-induced retinal degeneration and a strong candidate for further research as a factor behind retinal degenerative disease.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Neurologi0 (SwePub)302072 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Neurology0 (SwePub)302072 hsv//eng
700a Arnér, Karinu Lund University,Lunds universitet,Oftalmologi, Lund,Sektion IV,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Ophthalmology, Lund,Section IV,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)oft-kar
700a Deierborg, Tomasu Lund University,Lunds universitet,Neuroinflammation,Forskargrupper vid Lunds universitet,Lund University Research Groups4 aut0 (Swepub:lu)expb-tol
700a Taylor, Linnéau Lund University,Lunds universitet,Oftalmologi, Lund,Sektion IV,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Ophthalmology, Lund,Section IV,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)med-lat
710a Oftalmologi, Lundb Sektion IV4 org
773t Journal of Neuroinflammationd : Springer Science and Business Media LLCg 12:1q 12:1x 1742-2094
856u http://dx.doi.org/10.1186/s12974-015-0312-xx freey FULLTEXT
856u https://jneuroinflammation.biomedcentral.com/track/pdf/10.1186/s12974-015-0312-x
8564 8u https://lup.lub.lu.se/record/5453307
8564 8u https://doi.org/10.1186/s12974-015-0312-x

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