Upregulation of Retinal Vascular Endothelial Growth Factor mRNAs in Spontaneously Diabetic Rats without Ophthalmoscopic Retinopathy

1998 ◽  
Vol 30 (6) ◽  
pp. 333-339 ◽  
Author(s):  
Yasunori Segawa ◽  
Yutaka Shirao ◽  
Sho-ichi Yamagishi ◽  
Tomomi Higashide ◽  
Miho Kobayashi ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Diabetic Rats ◽  
Vascular Endothelial ◽  
Spontaneously Diabetic Rats ◽  
Endothelial Growth Factor

Fracture Healing and Biomarker Expression in a Diabetic Zucker Rat Model

2014 ◽  
Vol 104 (5) ◽  
pp. 428-433 ◽  
Author(s):  
Javier La Fontaine ◽  
Nathan A. Hunt ◽  
Stacey Curry ◽  
Tyler Kearney ◽  
Daniel Jupiter ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Fracture Healing ◽  
Bone Healing ◽  
Rat Model ◽  
Healing Process ◽  
Diabetic Rats ◽  
Vascular Endothelial ◽  
Delayed Healing ◽  
Endothelial Growth Factor

Background Persons with diabetes have a higher incidence of fractures compared with persons without diabetes. However, there is little published information concerning the deleterious effect of late-stage diabetes on fracture healing. There are no studies using animal models that evaluate the effect of advanced diabetes on fracture healing. The purpose of our study was to evaluate cytokine expression, specifically macrophage inflammatory protein 1 (MIP-1) and vascular endothelial growth factor, in fracture healing in a type 2 diabetes rat model. Methods We evaluated biomarker expression after femur fracture using a rat model. The two groups consisted of 24 Zucker diabetic rats (study group) and 12 Zucker lean rats (control group). An independent reviewer was used to assess delayed union. We evaluated serum samples 2, 4, 7, and 14 days after surgery for MIP-1, vascular endothelial growth factor, leptin, and other cytokine levels. Results At 3 weeks, Kaplan-Meier estimates showed that 45.8% of femur fractures in Zucker diabetic rats had healed, whereas 81.8% of those in Zucker lean rats had healed (P = .02). A logistic regression model to predict fast healing that included the three cytokines and diabetes status showed that the only factor achieving significance was MIP-1α. Vascular endothelial growth factor was the only biomarker to show significance compared with delayed healing. Conclusions These results confirm significant differences in biomarker expression between diabetic and nondiabetic rats during bone healing. The key factors for bone healing may appear early in the healing process, whereas differences in diabetes versus nondiabetes are seen later in the healing process. Increased levels of MIP-1α were associated with the likelihood of delayed healing.

scholarly journals Antibodies against Vascular Endothelial Growth Factor Improve Early Renal Dysfunction in Experimental Diabetes

2001 ◽  
Vol 12 (5) ◽  
pp. 993-1000 ◽  
Author(s):  
AN S. DE VRIESE ◽  
RONALD G. TILTON ◽  
MARLIES ELGER ◽  
CLIFFORD C. STEPHAN ◽  
WILHELM KRIZ ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Renal Dysfunction ◽  
Diabetic Rats ◽  
Renal Physiology ◽  
Vascular Endothelial ◽  
Binding Studies ◽  
Anti Vegf ◽  
Endothelial Growth Factor

Abstract. Vascular endothelial growth factor (VEGF) is a cytokine that potently stimulates angiogenesis, microvascular hyperpermeability, and endothelium-dependent vasodilation, effects that are largely mediated by endothelial nitric oxide synthase (eNOS). The expression of VEGF is pronounced in glomerular visceral epithelial cells, but its function in renal physiology and pathophysiology is unknown. VEGF expression is upregulated by high ambient glucose concentrations in several cell typesin vitroand in glomeruli of diabetic rats. To assess the role of VEGF in the pathophysiology of early renal dysfunction in diabetes, monoclonal anti-VEGF antibodies (Ab) were administered to control and streptozotocin-induced diabetic rats for 6 wk after induction of diabetes. Based onin vitrobinding studies, an adequate serum VEGF inhibitory activity was achieved during the entire course of anti-VEGF Ab administration. Anti-VEGF Ab treatment but not administration of isotype-matched control Ab decreased hyperfiltration, albuminuria, and glomerular hypertrophy in diabetic rats. VEGF blockade also prevented the upregulation of eNOS expression in glomerular capillary endothelial cells of diabetic rats. Antagonism of VEGF had no effect on GFR and glomerular volume in control rats. These results identify VEGF as a pathogenetic link between hyperglycemia and early renal dysfunction in diabetes. Targeting VEGF may prove useful as a therapeutic strategy for the treatment of early diabetic nephropathy.

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