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Hidetaka Noma, Kanako Yasuda, Masahiko Shimura; Role of Soluble Vascular Endothelial Growth Factor Receptor Signaling and Other Factors or Cytokines in Diabetic Macular Edema. Invest. Ophthalmol. Vis. Sci. 2016;57(12):3245.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate the association between aqueous humor levels of various growth/inflammatory factors or cytokines and the severity of macular edema in patients with diabetic macular edema (DME).
Fifty eyes with DME were performed intravitreal ranibizumab injection (IRI) or intravitreal aflibercept injection (IAI). After initial IRI or IAI, a mean volume of 0.1 mL of aqueous humor was collected by anterior chamber limbal paracentesis. All patients signed an informed consent form. Aqueous humor levels of 10 factors or cytokines were measured in DME patients (n=50) and in cataract patients (n=15) as controls. The levels of vascular endothelial growth factor (VEGF), its receptors, and other factors or cytokines were measured by the suspension array method (xMAP; Luminex Corp. Austin, TX). The severity of macular edema was determined by measuring the central macular thickness, neurosensory retinal thickness, and subfoveal serous retinal thickness with optical coherence tomography.
Aqueous humor levels of growth factors, soluble vascular endothelial growth factor receptor 1 (sVEGFR-1), sVEGFR-2, and inflammatory factors or cytokines were significantly higher in the DME group than in the control group. The aqueous level of sVEGFR-2 was significantly correlated with the neurosensory retinal thickness, as well as with the levels of growth factors (VEGF, placental growth factor, and platelet-derived growth factor-AA) and inflammatory factors/cytokines (monocyte chemotactic protein-1, interleukin-6, and interleukin-8). Aqueous humor levels of the 3 growth factors were also significantly correlated with each other, as were levels of the two sVEGFRs.
These findings suggest that growth/inflammatory factors and cytokines have an important role in DME. Better understanding of the mechanisms involved may lead to development of new treatments such as anti-VEGFR-2 therapy.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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