June 2015
Volume 56, Issue 7
ARVO Annual Meeting Abstract  |   June 2015
The role of SOCS3/STAT3 axis in myeloid cells in the development of diabetic retinopathy
Author Affiliations & Notes
  • Mei Chen
    Centre for Experimental Medicine, Queens University of Belfast, Belfast, United Kingdom
  • Footnotes
    Commercial Relationships Mei Chen, None
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Investigative Ophthalmology & Visual Science June 2015, Vol.56, 5849. doi:
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      Mei Chen; The role of SOCS3/STAT3 axis in myeloid cells in the development of diabetic retinopathy. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):5849.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: Suppressor of cytokine signalling (SOCS) proteins are feedback inhibitors of the JAK/STAT pathway. SOCS3 critically controls STAT3 activation, cytokine signalling and inflammatory gene expression in macrophages and microglia. In this study, we investigated the role of SOCS3/STAT3 in myeloid cells in the initiation and progression of diabetic retinopathy (DR).<br />

Methods: Mice with a conditional deletion of SOCS3 in myeloid cells (LysMCre-SOCS3 fl/fl) and C57BL/6J (as control) were rendered diabetic by a low-dose multiple intraperitoneal injections of Stroptozocine. Diabetes related retinal changes, including leukostasis, acellular capilliaries, and microglial activation were assessed at different stages of disease.<br /> Bone marrow derived macrophages (BMDMs) from LysMCre-SOCS3 fl/fl and C57BL/6J mice were cultured in high glucose (HG) medium, and cell activation was evaluated by real-time RT-PCR.<br />

Results: In C57BL/6J diabetic mice the expression of phosphorylated STAT3 (pSTAT3) was increased and SOCS3 was decreased in the retina. Interleukin 6 (IL-6), the main cytokine that stimulates STAT3 activation, was increased in the plamsa in diabetic mice. Although blood glucose levels and Hbac-1 were comparable between LysMCre-SOCS3fl/fl and WT mice after STZ injection, the LysMCre-SOCS3 fl/fl diabetic mice developed severe retinal vasculopathy, including increased leukostasis and microglial activation at one month and enhanced acellular capillary formation at 6 months after diabetes induction. <br />

Conclusions: our study suggests that the JAK/STAT3 pathway is involved in the initiation and progression of DR, and uncontrolled STAT3 activation results in accelerated DR progression. Targeting the STAT3 pathway may be a novel approach for the management of DR.<br />


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