Proliferative Retinopathy

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Carl-david Agardh - One of the best experts on this subject based on the ideXlab platform.

  • Platelet aggregation in Type I diabetics with and without Proliferative Retinopathy
    Acta ophthalmologica, 2009
    Co-Authors: Carl-david Agardh, Elisabet Agardh, Birgitta Bauer
    Abstract:

    The cause of Retinopathy in diabetes mellitus is unknown. Among factors suggested to be involved in the development of Retinopathy is altered platelet function. In the present study, platelet aggregation was measured in vitro after stimulation with adenosine diphosphate (ADP) and collagen in patients with and without Proliferative Retinopathy. The results show that patients with Proliferative Retinopathy have an increased platelet aggregation in vitro after stimulation with collagen and ADP. However, the increased platelet aggregation was also found to be correlated to the duration of diabetes. Thus, the present study does not support the opinion that abnormal platelet function can be regarded as a primary cause of diabetic Retinopathy. Increased platelet aggregation seems to be coupled to the duration of diabetes and to still unknown factors developing with prolonged duration of the disease.

  • Plasma lipids and plasma lipoproteins in diabetics with and without Proliferative Retinopathy
    Acta medica Scandinavica, 2009
    Co-Authors: Carl-david Agardh, Elisabeth Agardh, Birgitta Bauer, Peter Nilsson-ehle
    Abstract:

    The single most important factor related to the development of diabetic Retinopathy is the duration of diabetes. Little is known about the underlying mechanisms, but many factors have been suggested to be involved, among them derangements in plasma lipids and plasma lipoproteins. In the present study we examined the relation between plasma lipids, plasma lipoproteins, and the duration of diabetes in Type I diabetics with and without Proliferative Retinopathy. The duration of diabetes in the two groups was 12.2 +/- 2.8 and 21.5 +/- 9.0 years, respectively (mean +/- SD; p less than 0.01). Except for moderately low HDL levels, plasma lipid and lipoprotein concentrations were normal in both groups of patients. The levels of lipids and lipoproteins did not correlate with the duration of diabetes. Furthermore, no differences were seen between patients with and without Proliferative Retinopathy. Thus, the present study does not indicate that plasma lipids and plasma lipoproteins play any major role in the development of diabetic Proliferative Retinopathy.

  • tnf alpha is an independent serum marker for Proliferative Retinopathy in type 1 diabetic patients
    Journal of Diabetes and Its Complications, 2008
    Co-Authors: Carin Gustavsson, Elisabet Agardh, Boel Bengtsson, Carl-david Agardh
    Abstract:

    PURPOSE: This study aimed to determine if there are any associations between serum levels of inflammatory markers and Proliferative Retinopathy (PDR) in type 1 diabetic patients. DESIGN: A cross-sectional design was utilized for this study. METHODS: One hundred twenty-eight type 1 diabetic patients underwent stereo fundus photography according to the Early Treatment Diabetic Retinopathy Study and were divided into two Retinopathy groups: no or nonProliferative Retinopathy (NDR/NPDR; n=62) and PDR (n=66). Serum levels of tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, IL-6, soluble vascular cellular adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 (sICAM-1), P-selectin, and high-sensitivity C-reactive protein (hsCRP) were analyzed. Statistical analysis was performed using nonparametric Mann-Whitney U test and multivariate logistic regression analysis. RESULTS: Patients with PDR had higher levels of TNF-alpha [7.0 pg/ml (<4-17) vs. 6.0 pg/ml (<4-25); P=.009], sVCAM-1 [860 ng/ml (360-2120) vs. 700 ng/ml (310-1820); P<.001], and P-selectin [180 ng/ml (39-400) vs. 150 ng/ml (42-440); P=.017; figures are expressed as median (range)]. There were no differences in serum levels of sICAM-1 or hsCRP. IL-1beta was not detectable in any patient, and IL-6 was detectable in only 22.7% of the patients. In multivariate logistic regression analysis, TNF-alpha was the single, persistent, independent determinant inflammatory marker for PDR. CONCLUSION: The association between TNF-alpha and PDR in type 1 diabetic patients suggests that inflammation might play a role in the pathogenesis of Proliferative diabetic Retinopathy. (Less)

  • Type 1 diabetes patients with severe non‐Proliferative Retinopathy may benefit from panretinal photocoagulation
    Acta ophthalmologica Scandinavica, 2003
    Co-Authors: Monica Lövestam-adrian, Carl-david Agardh, Ole Torffvit, Elisabet Agardh
    Abstract:

    Purpose: To examine whether panretinal photocoagulation for severe nonProliferative Retinopathy in type 1 diabetes patients could halt the progression of Retinopathy with subsequent vitreous haemorrhages and visual impairment. Methods: During a 10-year follow-up study period of 344 type 1 diabetes patients, 81 subjects went through panretinal photocoagulation. Forty patients were treated for severe non-Proliferative Retinopathy (age at onset of diabetes 14 � 8 years, diabetes duration 18 þ 10 years) and 41 for Proliferative Retinopathy (age at onset 15 � 10 years, diabetes duration 22 þ 13 years). One randomly selected eye per patient forms the basis for the study. Metabolic control, systolic and diastolic blood pressure, serum creatinine and urinary albumin levels were measured and analysed yearly during the follow-up period. Results: A total of 35% (14/40) of eyes treated for severe non-Proliferative Retinopathy developed neovascularizations during a mean time of 2.9 � 1.5 years. Vitreous haemorrhages were more frequent in eyes with Proliferative Retinopathy at treatment than in eyes with severe non-Proliferative Retinopathy (12/41 versus 2/40; p ¼ 0.007). The number of vitrectomies due to vitreous haemorrhages in eyes treated for severe non-Proliferative Retinopathy tended to be lower (1/40 versus 6/41; p ¼ 0.052). Before photocoagulation, visual acuity (VA) was similar in eyes with severe non-Proliferative Retinopathy and in those with Proliferative Retinopathy (1.0, 0.4–1.0 versus 1.0, 0.1–1.0; median and range). Visual impairment and blindness tended to develop more often in eyes treated for Proliferative Retinopathy compared to those treated for severe non-Proliferative Retinopathy (10/40 versus 4/40; p ¼ 0.056). Eyes with neovascularizations at follow-up were more often visually impaired (VA < 0.5) than eyes without neovascularizations (15/55 versus 1/26; p ¼ 0.016). Conclusion: In type 1 diabetes, panretinal photocoagulation may be beneficial even at the severe non-Proliferative Retinopathy stage in terms of preventing vitreous haemorrhage, subsequent vitrectomy and visual impairment.

  • The incidence of nephropathy in type 1 diabetic patients with Proliferative Retinopathy: a 10-year follow-up study
    Diabetes research and clinical practice, 1998
    Co-Authors: Monica Lövestam-adrian, Elisabet Agardh, Carl-david Agardh
    Abstract:

    Patients with type 1 diabetes mellitus and with Proliferative Retinopathy often have a concomitant diabetic nephropathy. However, in cross-sectional studies it has been shown that 35% of patients with Proliferative Retinopathy do not show signs of diabetic nephropathy. The aim of the present study was to examine the incidence of diabetic nephropathy in type 1 diabetic patients with Proliferative Retinopathy but without signs of nephropathy. To that end, out of 102 consecutive patients with Proliferative Retinopathy attending the University Hospital, Lund, in 1986, 24 patients did not show any clinical signs of nephropathy, and were followed for 10 years regarding the development of nephropathy. Their age was 36.7 +/- 9.8 years, age at onset 11.8 +/- 7.5 years, diabetes duration 25.7 +/- 6.9 years and duration of Proliferative Retinopathy 4.6 +/- 3.8 years (mean +/- S.D.). At entry, no patient had albuminuria ( or = 30 mg/l). Two patients died before follow-up, but none of these had developed microalbuminuria at the time for death. Based on mean annual measurements, there were no increases in HbA1c, systolic and diastolic blood pressure, and serum creatinine levels. At entry, seven of the patients were treated with antihypertensive drugs and another three patients received such treatment during the study period. In conclusion, in a subgroup of patients with Proliferative Retinopathy, i.e. without clinical signs of diabetic nephropathy, no patient developed persistent microalbuminuria during a 10-year follow-up period. These results indicate further evidence for at least partly different pathogenic mechanisms behind diabetic Retinopathy and nephropathy.

Elisabet Agardh - One of the best experts on this subject based on the ideXlab platform.

  • Platelet aggregation in Type I diabetics with and without Proliferative Retinopathy
    Acta ophthalmologica, 2009
    Co-Authors: Carl-david Agardh, Elisabet Agardh, Birgitta Bauer
    Abstract:

    The cause of Retinopathy in diabetes mellitus is unknown. Among factors suggested to be involved in the development of Retinopathy is altered platelet function. In the present study, platelet aggregation was measured in vitro after stimulation with adenosine diphosphate (ADP) and collagen in patients with and without Proliferative Retinopathy. The results show that patients with Proliferative Retinopathy have an increased platelet aggregation in vitro after stimulation with collagen and ADP. However, the increased platelet aggregation was also found to be correlated to the duration of diabetes. Thus, the present study does not support the opinion that abnormal platelet function can be regarded as a primary cause of diabetic Retinopathy. Increased platelet aggregation seems to be coupled to the duration of diabetes and to still unknown factors developing with prolonged duration of the disease.

  • tnf alpha is an independent serum marker for Proliferative Retinopathy in type 1 diabetic patients
    Journal of Diabetes and Its Complications, 2008
    Co-Authors: Carin Gustavsson, Elisabet Agardh, Boel Bengtsson, Carl-david Agardh
    Abstract:

    PURPOSE: This study aimed to determine if there are any associations between serum levels of inflammatory markers and Proliferative Retinopathy (PDR) in type 1 diabetic patients. DESIGN: A cross-sectional design was utilized for this study. METHODS: One hundred twenty-eight type 1 diabetic patients underwent stereo fundus photography according to the Early Treatment Diabetic Retinopathy Study and were divided into two Retinopathy groups: no or nonProliferative Retinopathy (NDR/NPDR; n=62) and PDR (n=66). Serum levels of tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, IL-6, soluble vascular cellular adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 (sICAM-1), P-selectin, and high-sensitivity C-reactive protein (hsCRP) were analyzed. Statistical analysis was performed using nonparametric Mann-Whitney U test and multivariate logistic regression analysis. RESULTS: Patients with PDR had higher levels of TNF-alpha [7.0 pg/ml (<4-17) vs. 6.0 pg/ml (<4-25); P=.009], sVCAM-1 [860 ng/ml (360-2120) vs. 700 ng/ml (310-1820); P<.001], and P-selectin [180 ng/ml (39-400) vs. 150 ng/ml (42-440); P=.017; figures are expressed as median (range)]. There were no differences in serum levels of sICAM-1 or hsCRP. IL-1beta was not detectable in any patient, and IL-6 was detectable in only 22.7% of the patients. In multivariate logistic regression analysis, TNF-alpha was the single, persistent, independent determinant inflammatory marker for PDR. CONCLUSION: The association between TNF-alpha and PDR in type 1 diabetic patients suggests that inflammation might play a role in the pathogenesis of Proliferative diabetic Retinopathy. (Less)

  • Type 1 diabetes patients with severe non‐Proliferative Retinopathy may benefit from panretinal photocoagulation
    Acta ophthalmologica Scandinavica, 2003
    Co-Authors: Monica Lövestam-adrian, Carl-david Agardh, Ole Torffvit, Elisabet Agardh
    Abstract:

    Purpose: To examine whether panretinal photocoagulation for severe nonProliferative Retinopathy in type 1 diabetes patients could halt the progression of Retinopathy with subsequent vitreous haemorrhages and visual impairment. Methods: During a 10-year follow-up study period of 344 type 1 diabetes patients, 81 subjects went through panretinal photocoagulation. Forty patients were treated for severe non-Proliferative Retinopathy (age at onset of diabetes 14 � 8 years, diabetes duration 18 þ 10 years) and 41 for Proliferative Retinopathy (age at onset 15 � 10 years, diabetes duration 22 þ 13 years). One randomly selected eye per patient forms the basis for the study. Metabolic control, systolic and diastolic blood pressure, serum creatinine and urinary albumin levels were measured and analysed yearly during the follow-up period. Results: A total of 35% (14/40) of eyes treated for severe non-Proliferative Retinopathy developed neovascularizations during a mean time of 2.9 � 1.5 years. Vitreous haemorrhages were more frequent in eyes with Proliferative Retinopathy at treatment than in eyes with severe non-Proliferative Retinopathy (12/41 versus 2/40; p ¼ 0.007). The number of vitrectomies due to vitreous haemorrhages in eyes treated for severe non-Proliferative Retinopathy tended to be lower (1/40 versus 6/41; p ¼ 0.052). Before photocoagulation, visual acuity (VA) was similar in eyes with severe non-Proliferative Retinopathy and in those with Proliferative Retinopathy (1.0, 0.4–1.0 versus 1.0, 0.1–1.0; median and range). Visual impairment and blindness tended to develop more often in eyes treated for Proliferative Retinopathy compared to those treated for severe non-Proliferative Retinopathy (10/40 versus 4/40; p ¼ 0.056). Eyes with neovascularizations at follow-up were more often visually impaired (VA < 0.5) than eyes without neovascularizations (15/55 versus 1/26; p ¼ 0.016). Conclusion: In type 1 diabetes, panretinal photocoagulation may be beneficial even at the severe non-Proliferative Retinopathy stage in terms of preventing vitreous haemorrhage, subsequent vitrectomy and visual impairment.

  • The incidence of nephropathy in type 1 diabetic patients with Proliferative Retinopathy: a 10-year follow-up study
    Diabetes research and clinical practice, 1998
    Co-Authors: Monica Lövestam-adrian, Elisabet Agardh, Carl-david Agardh
    Abstract:

    Patients with type 1 diabetes mellitus and with Proliferative Retinopathy often have a concomitant diabetic nephropathy. However, in cross-sectional studies it has been shown that 35% of patients with Proliferative Retinopathy do not show signs of diabetic nephropathy. The aim of the present study was to examine the incidence of diabetic nephropathy in type 1 diabetic patients with Proliferative Retinopathy but without signs of nephropathy. To that end, out of 102 consecutive patients with Proliferative Retinopathy attending the University Hospital, Lund, in 1986, 24 patients did not show any clinical signs of nephropathy, and were followed for 10 years regarding the development of nephropathy. Their age was 36.7 +/- 9.8 years, age at onset 11.8 +/- 7.5 years, diabetes duration 25.7 +/- 6.9 years and duration of Proliferative Retinopathy 4.6 +/- 3.8 years (mean +/- S.D.). At entry, no patient had albuminuria ( or = 30 mg/l). Two patients died before follow-up, but none of these had developed microalbuminuria at the time for death. Based on mean annual measurements, there were no increases in HbA1c, systolic and diastolic blood pressure, and serum creatinine levels. At entry, seven of the patients were treated with antihypertensive drugs and another three patients received such treatment during the study period. In conclusion, in a subgroup of patients with Proliferative Retinopathy, i.e. without clinical signs of diabetic nephropathy, no patient developed persistent microalbuminuria during a 10-year follow-up period. These results indicate further evidence for at least partly different pathogenic mechanisms behind diabetic Retinopathy and nephropathy.

Jakob Grauslund - One of the best experts on this subject based on the ideXlab platform.

  • Proliferative Retinopathy predicts nephropathy: a 25-year follow-up study of type 1 diabetic patients
    Acta diabetologica, 2011
    Co-Authors: Charlotte Karlberg, Christine Falk, Anders Green, Anne Katrin Sjølie, Jakob Grauslund
    Abstract:

    We wanted to examine Proliferative Retinopathy as a marker of incident nephropathy in a 25-year follow-up study of a population-based cohort of Danish type 1 diabetic patients and to examine cross-sectional associations between nephropathy and Retinopathy in long-term surviving patients of the same cohort. All type 1 diabetic patients from Fyn County, Denmark, were identified as of 1 July 1973. One hundred and eighty four patients were examined in 1981–1982 (baseline) and in 2007–2008 (follow-up). The level of Retinopathy was graded by ophthalmoscopy at baseline and nine-field digital colour fundus photographs at follow-up. Single spot urine was used to evaluate nephropathy at both examinations. Proliferative Retinopathy was present in 29 patients (15.8%) at baseline. At follow-up, these patients were more likely to macroalbuminuria (20.7% vs. 6.5%) than patients without Proliferative Retinopathy at baseline. In a multivariate logistic regression adjusted for baseline age, sex, duration of diabetes, smoking, HbA1, systolic and diastolic blood pressure, odds ratio of nephropathy (micro- and macroalbuminuria combined) was 2.98 (95% confidence interval 1.18–7.51, p = 0.02) for patients with Proliferative Retinopathy at baseline as compared to those without. At follow-up, there was a close relation between Retinopathy and nephropathy. The level of macroalbuminuria was 4.3, 4.6 and 13.0% for patients with no or mild non-Proliferative Retinopathy, moderate non-Proliferative Retinopathy and Proliferative Retinopathy, respectively. In conclusion, Proliferative Retinopathy is an independent marker of long-term nephropathy in type 1 diabetes. Upcoming studies should examine whether these microvascular complications are also causally linked in type 1 diabetes.

  • Prevalence and 25 year incidence of Proliferative Retinopathy among Danish type 1 diabetic patients.
    Diabetologia, 2009
    Co-Authors: Jakob Grauslund, Anders Green, Anne Katrin Sjølie
    Abstract:

    Aims/hypothesis This study aimed to evaluate the prevalence of Retinopathy in long-surviving type 1 diabetic patients. It also investigated the 25 year incidence of Proliferative Retinopathy and associated risk factors in a Danish population-based cohort.

Anne Katrin Sjølie - One of the best experts on this subject based on the ideXlab platform.

  • Proliferative Retinopathy predicts nephropathy: a 25-year follow-up study of type 1 diabetic patients
    Acta diabetologica, 2011
    Co-Authors: Charlotte Karlberg, Christine Falk, Anders Green, Anne Katrin Sjølie, Jakob Grauslund
    Abstract:

    We wanted to examine Proliferative Retinopathy as a marker of incident nephropathy in a 25-year follow-up study of a population-based cohort of Danish type 1 diabetic patients and to examine cross-sectional associations between nephropathy and Retinopathy in long-term surviving patients of the same cohort. All type 1 diabetic patients from Fyn County, Denmark, were identified as of 1 July 1973. One hundred and eighty four patients were examined in 1981–1982 (baseline) and in 2007–2008 (follow-up). The level of Retinopathy was graded by ophthalmoscopy at baseline and nine-field digital colour fundus photographs at follow-up. Single spot urine was used to evaluate nephropathy at both examinations. Proliferative Retinopathy was present in 29 patients (15.8%) at baseline. At follow-up, these patients were more likely to macroalbuminuria (20.7% vs. 6.5%) than patients without Proliferative Retinopathy at baseline. In a multivariate logistic regression adjusted for baseline age, sex, duration of diabetes, smoking, HbA1, systolic and diastolic blood pressure, odds ratio of nephropathy (micro- and macroalbuminuria combined) was 2.98 (95% confidence interval 1.18–7.51, p = 0.02) for patients with Proliferative Retinopathy at baseline as compared to those without. At follow-up, there was a close relation between Retinopathy and nephropathy. The level of macroalbuminuria was 4.3, 4.6 and 13.0% for patients with no or mild non-Proliferative Retinopathy, moderate non-Proliferative Retinopathy and Proliferative Retinopathy, respectively. In conclusion, Proliferative Retinopathy is an independent marker of long-term nephropathy in type 1 diabetes. Upcoming studies should examine whether these microvascular complications are also causally linked in type 1 diabetes.

  • Prevalence and 25 year incidence of Proliferative Retinopathy among Danish type 1 diabetic patients.
    Diabetologia, 2009
    Co-Authors: Jakob Grauslund, Anders Green, Anne Katrin Sjølie
    Abstract:

    Aims/hypothesis This study aimed to evaluate the prevalence of Retinopathy in long-surviving type 1 diabetic patients. It also investigated the 25 year incidence of Proliferative Retinopathy and associated risk factors in a Danish population-based cohort.

Jing Chen - One of the best experts on this subject based on the ideXlab platform.

  • Retinal expression of small non-coding RNAs in a murine model of Proliferative Retinopathy.
    Scientific reports, 2016
    Co-Authors: Chi-hsiu Liu, Zhongxiao Wang, Ye Sun, John Paul Sangiovanni, Jing Chen
    Abstract:

    Ocular neovascularization is a leading cause of blindness in Proliferative Retinopathy. Small non-coding RNAs (sncRNAs) play critical roles in both vascular and neuronal development of the retina through post-transcriptional regulation of target gene expression. To identify the function and therapeutic potential of sncRNAs in Retinopathy, we assessed the expression profile of retinal sncRNAs in a mouse model of oxygen-induced Retinopathy (OIR) with pathologic proliferation of neovessels. Approximately 2% of all analyzed sncRNAs were significantly altered in OIR retinas compared with normoxic controls. Twenty three microRNAs with substantial up- or down-regulation were identified, including miR-351, -762, -210, 145, -155, -129-5p, -150, -203, and -375, which were further analyzed for their potential target genes in angiogenic, hypoxic, and immune response-related pathways. In addition, nineteen small nucleolar RNAs also revealed differential expression in OIR retinas compared with control retinas. A decrease of overall microRNA expression in OIR retinas was consistent with reduced microRNA processing enzyme Dicer, and increased expression of Alu element in OIR. Together, our findings elucidated a group of differentially expressed sncRNAs in a murine model of Proliferative Retinopathy. These sncRNAs may exert critical post-transcriptional regulatory roles in regulating pathological neovascularization in eye diseases.

  • Wnt Signaling Mediates Pathological Vascular Growth in Proliferative Retinopathy
    Circulation, 2011
    Co-Authors: Jing Chen, Andreas Stahl, Nathan M. Krah, Molly R. Seaward, Roberta J. Dennison, Przemyslaw Sapieha, Jing Hua, Colman J. Hatton, Aimee M. Juan, C. M. Aderman
    Abstract:

    Background—Ischemic Proliferative Retinopathy, characterized by pathological retinal neovascularization, is a major cause of blindness in working-age adults and children. Defining the molecular pathways distinguishing pathological neovascularization from normal vessels is critical to controlling these blinding diseases with targeted therapy. Because mutations in Wnt signaling cause defective retinal vasculature in humans with some characteristics of the pathological vessels in Retinopathy, we investigated the potential role of Wnt signaling in pathological retinal vascular growth in Proliferative Retinopathy. Methods and Results—In this study, we show that Wnt receptors (Frizzled4 and low-density lipoprotein receptor–related protein5 [Lrp5]) and activity are significantly increased in pathological neovascularization in a mouse model of oxygen-induced Proliferative Retinopathy. Loss of Wnt coreceptor Lrp5 and downstream signaling molecule dishevelled2 significantly decreases the formation of pathological r...

  • postnatal weight gain modifies severity and functional outcome of oxygen induced Proliferative Retinopathy
    American Journal of Pathology, 2010
    Co-Authors: Andreas Stahl, Jing Chen, Nathan M. Krah, Molly R. Seaward, Roberta J. Dennison, Przemyslaw Sapieha, Tara L Favazza, Felicitas Bucher, Chatarina Lofqvist
    Abstract:

    In clinical studies, postnatal weight gain is strongly associated with Retinopathy of prematurity (ROP). However, animal studies are needed to investigate the pathophysiological mechanisms of how postnatal weight gain affects the severity of ROP. In the present study, we identify nutritional supply as one potent parameter that affects the extent of Retinopathy in mice with identical birth weights and the same genetic background. Wild-type pups with poor postnatal nutrition and poor weight gain (PWG) exhibit a remarkably prolonged phase of Retinopathy compared to medium weight gain or extensive weight gain pups. A high (r2 = 0.83) parabolic association between postnatal weight gain and oxygen-induced Retinopathy severity is observed, as is a significantly prolonged phase of Proliferative Retinopathy in PWG pups (20 days) compared with extensive weight gain pups (6 days). The extended Retinopathy is concomitant with prolonged overexpression of retinal vascular endothelial growth factor in PWG pups. Importantly, PWG pups show low serum levels of nonfasting glucose, insulin, and insulin-like growth factor-1 as well as high levels of ghrelin in the early postoxygen-induced Retinopathy phase, a combination indicative of poor metabolic supply. These differences translate into visual deficits in adult PWG mice, as demonstrated by impaired bipolar and proximal neuronal function. Together, these results provide evidence for a pathophysiological correlation between poor postnatal nutritional supply, slow weight gain, prolonged retinal vascular endothelial growth factor overexpression, protracted Retinopathy, and reduced final visual outcome.

  • Suppression of retinal neovascularization by erythropoietin siRNA in a mouse model of Proliferative Retinopathy.
    Investigative ophthalmology & visual science, 2008
    Co-Authors: Jing Chen, C. M. Aderman, Kip M. Connor, Keirnan L. Willett, O. P. Aspegren, Lois E. H. Smith
    Abstract:

    Purpose Erythropoietin (EPO), an oxygen-regulated hormone stimulating erythrocyte production, was recently found to be critical for retinal angiogenesis. EPO mRNA expression levels in retina are highly elevated during the hypoxia-induced proliferation phase of Retinopathy. The authors investigated the inhibition of retinal EPO mRNA expression with RNA interference as a potential strategy to suppress retinal neovascularization and to prevent Proliferative Retinopathy.