Please use this identifier to cite or link to this item: https://doi.org/10.1038/s41598-018-21198-z
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dc.titleThe NLRP3 Inflammasome May Contribute to Pathologic Neovascularization in the Advanced Stages of Diabetic Retinopathy
dc.contributor.authorChaurasia, S.S
dc.contributor.authorLim, R.R
dc.contributor.authorParikh, B.H
dc.contributor.authorWey, Y.S
dc.contributor.authorTun, B.B
dc.contributor.authorWong, T.Y
dc.contributor.authorLuu, C.D
dc.contributor.authorAgrawal, R
dc.contributor.authorGhosh, A
dc.contributor.authorMortellaro, A
dc.contributor.authorRackoczy, E
dc.contributor.authorMohan, R.R
dc.contributor.authorBarathi, V.A
dc.date.accessioned2020-10-20T03:28:53Z
dc.date.available2020-10-20T03:28:53Z
dc.date.issued2018
dc.identifier.citationChaurasia, S.S, Lim, R.R, Parikh, B.H, Wey, Y.S, Tun, B.B, Wong, T.Y, Luu, C.D, Agrawal, R, Ghosh, A, Mortellaro, A, Rackoczy, E, Mohan, R.R, Barathi, V.A (2018). The NLRP3 Inflammasome May Contribute to Pathologic Neovascularization in the Advanced Stages of Diabetic Retinopathy. Scientific Reports 8 (1) : 2847. ScholarBank@NUS Repository. https://doi.org/10.1038/s41598-018-21198-z
dc.identifier.issn20452322
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/177828
dc.description.abstractDiabetic retinopathy (DR) is a retinal microvascular disease characterized by inflammatory and angiogenic pathways. In this study, we evaluated NLRP3 inflammasome in a double transgenic mouse model, Akimba (Ins2 Akita xVEGF +/-), which demonstrates hyperglycemia, vascular hyperpermeability and neovascularization seen in the proliferative DR. Retinal structural integrity, vascular leakage and function were examined by fundus photography, fluorescein angiography, optical coherence tomography, retinal flat mounts, laser speckle flowgraphy (LSFG), and electroretinography in Akimba and its parental strains, Akita (Ins2 Akita ) and Kimba (trVEGF029) mice. Inflammatory mechanisms involving NLRP3 inflammasome were investigated using real time-PCR, immunohistochemistry, ELISA and western blots. We observed an increased vascular leakage, reduced retinal thickness, and function in Akimba retina. Also, Akimba retina depicts decreased relative flow volume measured by LSFG. Most importantly, high levels of IL-1? along with increased NLRP3, ASC, and Caspase-1 at mRNA and protein levels were observed in Akimba retina. However, the in vivo functional role remains undefined. In conclusion, increased activation of macroglia (GFAP), microglia (Iba-1 and OX-42) and perivascular macrophages (F4/80 and CD14) together with pro-inflammatory (IL-1? and IL-6) and pro-angiogenic markers (PECAM-1, ICAM-1, VEGF, Flt-1, and Flk-1), suggested a critical role for NLRP3 inflammasome in the Akimba mouse model depicting advanced stages of DR pathogenesis. © 2018 The Author(s).
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjectcryopyrin
dc.subjectcytokine
dc.subjectglial fibrillary acidic protein
dc.subjectglial fibrillary astrocytic protein, mouse
dc.subjectIns2 protein, mouse
dc.subjectinsulin
dc.subjectNlrp3 protein, mouse
dc.subjectvascular endothelial growth factor A, mouse
dc.subjectvasculotropin A
dc.subjectanimal
dc.subjectdiabetic retinopathy
dc.subjectdiagnostic imaging
dc.subjectdisease model
dc.subjectelectroretinography
dc.subjectfluorescence angiography
dc.subjectgenetics
dc.subjecthuman
dc.subjectmetabolism
dc.subjectmouse
dc.subjectneovascularization (pathology)
dc.subjectoptical coherence tomography
dc.subjectpathology
dc.subjectretina
dc.subjecttransgenic mouse
dc.subjectAnimals
dc.subjectCytokines
dc.subjectDiabetic Retinopathy
dc.subjectDisease Models, Animal
dc.subjectElectroretinography
dc.subjectFluorescein Angiography
dc.subjectGlial Fibrillary Acidic Protein
dc.subjectHumans
dc.subjectInsulin
dc.subjectMice
dc.subjectMice, Transgenic
dc.subjectNeovascularization, Pathologic
dc.subjectNLR Family, Pyrin Domain-Containing 3 Protein
dc.subjectRetina
dc.subjectTomography, Optical Coherence
dc.subjectVascular Endothelial Growth Factor A
dc.typeArticle
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.contributor.departmentOPHTHALMOLOGY
dc.description.doi10.1038/s41598-018-21198-z
dc.description.sourcetitleScientific Reports
dc.description.volume8
dc.description.issue1
dc.description.page2847
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