Nonperfusion of retina and choroid in transgenic mouse models of sickle cell disease

Lutty, G. A.; Merges, Carol; McLeod, D. Scott; Wajer, Stephen D.; Suzuka, Sandra M.; Fabry, Mary E.; Nagel, Ronald L.

doi:10.1080/02713689808951225

Cited by 17 publications

(9 citation statements)

References 18 publications

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“…It is important to note that the staining pattern seen in whole-mount preparations was identical using both ADPase enzyme histochemistry (Lutty and McLeod, 1992;Chan-Ling et al, 2004) and CD39 immunohistochemistry in the fetal human as a marker for angioblasts and blood vessels. It is present in adult retinal endothelial cells of all species studied to date and we have used it to study pathological neovascularization in sickle cell and diabetic retinopathy as well as retinopathy of prematurity McLeod, 1992, 2005;McLeod et al, 1993McLeod et al, , 1996bMcLeod et al, , 1997Lutty et al, 1994Lutty et al, , 1996. CD39, or nucleoside triphosphate diphosphohydrolase-1 (NTPDase1), is the major vascular endothelial ecto-nucleotidase and hydrolyses nucleoside triphosphates and diphosphates, ultimately to the nucleoside analogues (Goepfert et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

The initial fetal human retinal vasculature develops by vasculogenesis

McLeod

Hasegawa

Prow

et al. 2006

Developmental Dynamics

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There is increasing evidence that the hemangioblast, a common progenitor for hematopoietic cells and endothelial cells, participates in embryonic and extra-embryonic vasculogenesis in some organs. Whether resident angioblasts or endothelial progenitor cells (EPCs) contribute to human retinal vasculogenesis is still a matter of controversy. To address this controversy, fetal human retinas of 6 -23 weeks gestation (WG) were examined using immunohistochemistry and a panel of antibodies against endothelial cell markers (CD34, CD31), a marker for retinal angioblasts and endothelium (CD39/ecto-ADPase), and a marker for precursors and hemangioblasts (CXCR4). Confocal microscopic spectral analysis and double labeling with Ki67 was used to identify the proliferating cell types. In the inner neuroblastic layer of the 6 -8 WG retina and in the putative ganglion cell layer in avascular regions of older eyes (14 WG-20 WG), scattered CD39 ؉ angioblasts were well in advance of forming vasculature. There was a layer of CXCR4 ؉ cells in the inner retina that was reduced in size with development. As blood vessels formed, CD39؉ cells were always well in advance of the vascular front and they expressed CXCR4. This demonstrates that a pool of resident angioblasts express CD39 and CXCR4 as they differentiate and participate in vasculogenesis in the fetal human. They retain expression of CD39 as endothelial cells in the newly formed retinal vasculature but they down-regulate CXCR4 expression. Developmental Dynamics 235:3336 -3347, 2006.

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Section: Introductionmentioning

confidence: 99%

The initial fetal human retinal vasculature develops by vasculogenesis

McLeod

Hasegawa

Prow

et al. 2006

Developmental Dynamics

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“…Reproducibility of existing models is limited, partly because of technical artifacts and because the induction of choroidal neovascularization was accompanied by a nonspecific, local inflammatory reaction. [21][22][23][24][25][26][27] Recent work reported a transgenic mouse model in which overexpression of VEGF in the photoreceptors was under the control of a constitutively active rhodopsin promoter. These mice developed retinal neovascularization but failed to develop choroidal neovascularization that is characteristic of ARMD.…”

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confidence: 99%

Intrachoroidal Neovascularization in Transgenic Mice Overexpressing Vascular Endothelial Growth Factor in the Retinal Pigment Epithelium

Schwesinger

Yee

Rohan

et al. 2001

The American Journal of Pathology

205

126

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“…20,21 The initial vascular occlusion which occurs in SCA involves the peripheral retinal capillaries and may progress to occlude all retinal vessels. 18 Mice from the a H b S (b MDD ) and a H b S (a MD b MDD ) transgenic lines have been reported to serve as models for SCA. 18 These mice develop red blood cell plugs in the eyes with ®brin sometimes present at sites of occlusion.…”

Section: Discussionmentioning

confidence: 99%

Ocular thrombosis and retinal degeneration induced in female F344 rats by 2-butoxyethanol

Nyska

Maronpot²,

Ghanayem

1999

Hum Exp Toxicol

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2-butoxyethanol, used extensively for domestic and industrial purposes, was tested in our experiments for its potential to cause damage to female rat ocular tissues. Female rats were previously found to be particularly sensitive to 2-butoxyethanol. A group of eight female F344 rats (2–3 months old) were exposed by gavage to 250 mg of 2-butoxyethanol/kg b.w. per day for 3 consecutive days and sacrificed 24 h after the last dose. Eight female rats received the dosing vehicle (water) and served as controls. At necropsy, petechial hemorrhages were noted on the sclera. Microscopic examination revealed treatmentrelated effects in the eyes, in addition to other known effects of BE exposure such as disseminated thrombosis and necrosis and infarction in various organs. The spectrum of histopathological changes noted in the eyes included hemorrhages localized in the posterior layers of the retina, leading to photoreceptor degeneration. Thrombi were identified in ciliary processes and limbal blood vessels. Histological changes suggestive of the retinal ischemic-infarctive process were also noted. Possible pathogenic mechanisms of 2-butoxyethanol-induced retinopathy are discussed.

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Nonperfusion of retina and choroid in transgenic mouse models of sickle cell disease

Cited by 17 publications

References 18 publications

The initial fetal human retinal vasculature develops by vasculogenesis

The initial fetal human retinal vasculature develops by vasculogenesis

Intrachoroidal Neovascularization in Transgenic Mice Overexpressing Vascular Endothelial Growth Factor in the Retinal Pigment Epithelium

Ocular thrombosis and retinal degeneration induced in female F344 rats by 2-butoxyethanol

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