April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Spleen as the source of infiltrating monocytes in the diabetic retina
Author Affiliations & Notes
  • Eleni Beli
    Ophthalmology, Indiana University School of Medicine, Indianapolis, IN
    Physiology, Michigan State University, Lansing, MI
  • Svetlana Bozack
    Physiology, Michigan State University, Lansing, MI
  • Harshini Chakravarthy
    Physiology, Michigan State University, Lansing, MI
  • Qi Wang
    Physiology, Michigan State University, Lansing, MI
  • Nermin Kady
    Physiology, Michigan State University, Lansing, MI
  • Tatiana Salazar
    Ophthalmology, Indiana University School of Medicine, Indianapolis, IN
    School of Medicine, University of Florida, Gainesville, FL
  • James M Dominguez
    Ophthalmology, Indiana University School of Medicine, Indianapolis, IN
    School of Medicine, University of Florida, Gainesville, FL
  • Ashay D Bhatwadekar
    Ophthalmology, Indiana University School of Medicine, Indianapolis, IN
    School of Medicine, University of Florida, Gainesville, FL
  • Maria Grant
    Ophthalmology, Indiana University School of Medicine, Indianapolis, IN
    School of Medicine, University of Florida, Gainesville, FL
  • Julia V Busik
    Physiology, Michigan State University, Lansing, MI
  • Footnotes
    Commercial Relationships Eleni Beli, None; Svetlana Bozack, None; Harshini Chakravarthy, None; Qi Wang, None; Nermin Kady, None; Tatiana Salazar, None; James Dominguez, None; Ashay Bhatwadekar, None; Maria Grant, None; Julia Busik, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 4907. doi:
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      Eleni Beli, Svetlana Bozack, Harshini Chakravarthy, Qi Wang, Nermin Kady, Tatiana Salazar, James M Dominguez, Ashay D Bhatwadekar, Maria Grant, Julia V Busik; Spleen as the source of infiltrating monocytes in the diabetic retina. Invest. Ophthalmol. Vis. Sci. 2014;55(13):4907.

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

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Abstract

Purpose: We have previously identified that increased infiltration of inflammatory monocytes contributes to retinal pathology in diabetes. Moreover, diurnal fluctuations of monocytes in both rodents and humans with type 1 diabetes (T1D) are altered and diabetes results in an increase in peak release as well as a phase shift of circulating monocytes compared to age-matched controls. In this study, we asked if the spleen has a role in regulating monocyte phenotype and trafficking thus contributing to the pathogenesis of diabetic retinopathy.

Methods: Control (n=4) and 4 months STZ diabetic (n=4) mice were euthanized at ZT4-16. Single cell suspensions from spleen, retina, bone marrow and blood were analyzed by flow cytometry. Patrolling monocytes were identified as GR1(1A8)-, CD3-, CD19-, NK1.1-, CD11b+, CD115+, F480-, Ly6Clo cells. Inflammatory monocytes were identified as GR1-, CD3-, CD19-, NK1.1-, CD11b+, F480-, CD115+, Ly6Chi cells.

Results: The levels of monocytes in the peripheral circulation were reduced from 49,064 ± 14,051 to 2,742 ± 834 (p=0.03) between ZT4 and ZT13 concurrent with an increase in adhesion molecules expression in the retina: CCL2 mRNA expression changed from 0.023 ± 0.01 at ZT4 to 0.011 ± 0.00 at ZT13 (p=0.051) and VCAM mRNA expression from 0.035 ± 0.01 at ZT4 to 0.14 ± 0.01 at ZT13 (p< 0.05). Both patrolling and inflammatory monocytes were decreased in the spleen at the active phase (ZT16). Patrolling monocytes accumulated in the bone marrow during the active phase, while the inflammatory monocytes increased in the circulation in diabetic, but not control animals.

Conclusions: Monocytes released from spleen may be an important source of infiltrating inflammatory monocytes in the retina contributing to the pathogenesis of diabetic retinopathy.

Keywords: 499 diabetic retinopathy • 498 diabetes  
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