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2 edition of Modulating the expression of growth factors in neovascular models of retinal injury. found in the catalog.

Modulating the expression of growth factors in neovascular models of retinal injury.

Tara Alexandra Young

Modulating the expression of growth factors in neovascular models of retinal injury.

by Tara Alexandra Young

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Published .
Written in English


About the Edition

Growth factors in the eye exist in a critical balance in order to maintain retinal homeostasis. Aberrant regulation of both pro- and anti-angiogenic molecules results in the formation of abnormal vessels, or neovascularization. Neovascularization of the choroid or retina plays a significant role in blindness and contributes to the pathogenesis of diabetic retinopathy, age-related macular degeneration and retinal detachment. We hypothesized that the expression of key growth factors in neovascular models of retinal injury can be modulated to influence the disease process. Through the use of primary cultured rat retinal pigment epithelial cells and rat models of laser-induced neovascular retinal injury, choroidal neovascularization and surgically-induced retinal detachment, we investigated the role of vascular endothelial growth factor regulation in high glucose and hypoxia and the role of pigment epithelial derived factor in influencing models of neovascular retinal disease. We showed that the protein kinase C isozymes are important in vascular endothelial growth factor-mediated signaling in the retinal pigment epithelial cell type, and that protein kinase C-delta and protein kinase C-zeta exhibit differential responses to vascular endothelial growth factor, high glucose and hypoxic stimulation. Furthermore, we demonstrated that pigment epithelial derived factor may influence photodynamic therapy enhanced angiographic choroidal neovascular lesion closure. Finally we examined growth factors involved in experimentally-induced retinal detachment and the specific effect of pigment epithelial derived factor on this model of retinal injury. We found that pigment epithelial derived factor had little influence on this model. We conclude that the mechanisms of vascular endothelial growth factor production and regulation in the retinal pigment epithelial cell type are mediated by protein kinase C. Further study of this cell type in the regulation of angiogenesis in the eye is warranted. Additionally, the modification of growth factors in the ocular milieu of our in vivo models of retinal injury may have an influential role in the modification of the disease process which underscores the importance of developing new therapeutic strategies for ocular neovascular eye disease.

The Physical Object
Pagination209 leaves.
Number of Pages209
ID Numbers
Open LibraryOL21549526M
ISBN 109780494219805

Ophthotech Anti-PGDF in AMD Study Group () Combined inhibition of platelet-derived (PDGF) and vascular endothelial (VEGF) growth factors for the treatment of neovascular age-related macular degeneration (NV-AMD). Results of a phase 1 study. Introduction. Retinal neovascularization is one of the vision-threatening complications of ocular vascular diseases. Recently, the incidence rate of these diseases, such as diabetic retinopathy, central retinal vein occlusion, neovascular glaucoma and retinopathy of prematurity has shown an increasing trend due to the aging of society and the improvement of living conditions ().

(B) IB4-stained retinal whole mounts from littermate P16 wild-type mice housed in normoxia (naive) or subjected to OIR and analyzed on day 5 (D5) after return to normoxia. Red squares indicate areas shown at higher magnification. Note central vaso-obliteration (VO) and the presence of neovascular tufts (NV) in the OIR model. Scale bars: μm. @article{osti_, title = {Retinal hypoxia induces vascular endothelial growth factor through induction of estrogen-related receptor γ}, author = {Do, Ji Yeon and Choi, Young Keun and Kook, Hyun and Suk, Kyoungho and Lee, In-Kyu and Division of Endocrinology and Metabolism, Department of Internal Medicine, Research Institute of Aging and.

Integrin α v β3 has been found localized in retinal neovascular tissue removed from patients with proliferative diabetic retinopathy. 78 In the mouse model of OIR, inhibition of α v β3 and α v β5 using a nonpeptidic antagonist reduced neovascular area, and VEGF and VEGFR2 expression in the retina. 79 Intraperitoneal or intravitreal. TNF-α tumor necrosis factor-α VEGF vascular endothelial growth factor Figure 1. A low-salt (LS) diet reduced neovascular-ization and vaso-obliteration in rats with oxygen-induced retinopathy (OIR). A, Wholemounts from rats with OIR and immunolabeled with .


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Modulating the expression of growth factors in neovascular models of retinal injury by Tara Alexandra Young Download PDF EPUB FB2

Increased expression of VEGF in CNVM suggested the controversial hypothesis that tissue hypoxia may be an etiologic factor for this disorder, since hypoxia stimulates VEGF expression in RPE.

It has been suggested that drusen deposits between Bruch's membrane and RPE or thickening of Bruch's membrane could mediate outer retinal hypoxia even. The oxygen-induced retinopathy (OIR) mouse model was chosen for these studies because it is a well‑established model for studying pathological angiogenesis in the eye and, similar to human ischemic retinopathies (e.g., ROP and PDR), neovascular pathology in this model involves multiple growth factors, including VEGF, bFGF, HGF, and IGF-1 (27 Cited by: 3.

Mark S. Blumenkranz, Darius M. Moshfeghi, in Retina (Fourth Edition), Fibroblast growth factor. Basic fibroblast growth factor (FGF2) has been found to be elevated in excised choroidal neovascular membranes from patients undergoing surgery for ARMD, and is capable when implanted within the eye or adjacent to the retina of inducing pathologic neovascularization.

65, 66 Laser models of. Nishijima, K. et al. Vascular endothelial growth factor-A is a survival factor for retinal neurons and a critical neuroprotectant during the adaptive response to ischemic injury.

by: 2. Vazquez-Chona F, Song BK, Geisert EE, Jr. () Temporal changes in gene expression after injury in the rat retina. Invest Ophthalmol Vis Sci – PubMed CrossRef Google Scholar Vazquez-Chona FR, Lu L, Williams RW et al () Genomic loci modulating the retinal transcriptome in wound by: 2.

PurposePlacental growth factor (PlGF) is a member of the VEGF family that plays an important role in experimental models of diabetic retinopathy and retinal neovascularization.

the expression of T-cell chemokine receptors [9,10]. Murine models of experimental CNV find systemic activation of T helper cells [25]. In vitro studies of activated T-cells and their cytokines have demonstrated two important mediators in the etiology by modulating the protein expression and secretion in retinal.

Explore the latest full-text research PDFs, articles, conference papers, preprints and more on GROWTH FACTORS. Find methods information, sources, references or conduct a literature review on. Retinal hypoxia increases the expression of all Vegfa isoforms.

To determine whether specific VEGF isoforms are differentially regulated in neovascular eye disease caused by tissue ischemia, we studied their expression in a mouse model of oxygen-induced retinopathy (OIR), which has the hallmarks of retinopathy of prema.

Over-expression of BMP4 was associated with less severe CNV as characterized by fluorescein angiography, CNV volume measurement and histology.

While control mice showed increased levels of vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP)-9 after laser injury, Vmd2-Bmp4 Tg showed no increase in either VEGF or MMP but vascular endothelial growth factors (VEGFs) have been found to play important roles in its development [1].

Among them, VEGF-A can promote the division and proliferation of vascular endothelial cells and neovascularization and main-tain the survival of new vessels.

Furthermore, VEGF-A is an inflammatory cell chemotactic factor [2,3]. The secretion of all growth factors was significantly increased in both tissues after laser injury, but strongly reduced in XBDtreated mice especially at early time points of the analysis (Fig.

Vascular endothelial growth factor (VEGF)mRNA undergoes alternative splicing events that generate four different homodimeric isoforms, VEGF, VEGF, VEGF, or VEGF VEGF is a. Retinal and choroidal neovascularization are a major cause of significant visual impairment, worldwide.

Understanding the various factors involved in the accompanying physiopathology is vital for development of novel treatments, and most important, for preserving patient vision. The intraocular use of anti-vascular endothelial growth factor therapeutics has improved management of the retinal.

Photobiomodulation has also gained interest for the treatment of retinal disorders, having had positive effects in several mouse retinopathy models such as in light induced injury [,], OIR [,], streptozotocin-induced diabetes, methanol induced degeneration, and a model of complement factor H related degeneration.

These promising. CNV model, a well-established and one of the most commonly used angiogenesis models (27). In this model, we detect up-regulation of RIP kinases and caspases in retinal pigment epithelium (RPE)-choroid-sclera tissue containing CNV lesions during the phase of ongoing neovascular response with macrophage infiltration (Fig.

1A and SI Appendix,Fig.S1). Interestingly, CCN2 expression pattern is somewhat similar to that of CCN1. CCN2 expression coincides with the formation of primary, intermediary and deep capillary plexuses (Chintala et al.

).When the retinal vasculature is completely established, the expression of CCN2 decline but maintains relatively high basal levels in the adult vasculature. coherence tomography (OCT).

Eyes with neovascular lesions comprised of less than 50% active CNV, sub-retinal hemor-rhage greater than 25% of the lesion size, or the presence of other retinal diseases were excluded from the study.

Specifi - cally, eyes with any other potential cause for CNV, such as. 17]. Using this model, we previously demonstrated that the transcription nuclear factor-B plays a significant role in reg-ulating the expression of many genes, including chemokines [18, 19]. However, it still remains unclear what roles the chemotactic mediators play in ischemia-associated retinal.

This generates substantial expression of VEGF and other growth factors to initiate a rapid, yet faulty and pathological neovascularization.

The neovascular response peaks at postnatal day 18 in the form of “tufts” and then regresses between P19 and P. retinal vasculature following ischemic insult. miR binds to the 3 -UTR and represses the expression of the CCN1 gene, which encodes an extracellular matrix-associated integrin-binding protein that both promotes physiological angiogenesis and harnesses growth factor-induced abnormal angiogenic responses.

Single CCN1 deficiency or double CCN1.Objective. To evaluate the role of CCAAT/enhancer-binding protein β (C/EBP β) in retinal neovascularization (RNV) in an oxygen-induced retinopathy (OIR) model.

Methods. Rats with OIR were exposed to alternating hypoxic and hyperopic conditions for 14 days. Then, the rats with OIR were assigned randomly to groups that received intravitreal injections of either shRNA lentiviral particles.Ocular angiogenesis, characterized by the formation of new blood vessels in the avascular area in eyes, is a highly coordinated process involved in retinal vasculature formation and several ocular diseases such as age-related macular degeneration, proliferative diabetic retinopathy and retinopathy of prematurity.

This process is orchestrated by complicated cellular interactions and vascular.