Steven Abcouwer

Personal Information
Title Associate Professor
Expertise Retinopathy
Institution University of Michigan-Ann Arbor
Data Summary
TypeCount
Grants/SubContracts 1
Progress Reports 0
Presentations 1
Publications 12
Protocols 0
Committees 1
Experiments 0
Strains 0
Models 0

SubContract(s)


Monitoring microglial inflammatory phenotype in diabetic retinopathy models
We hypothesize that flow cytometry can be used to efficiently monitor the activation and inflammatory status of retinal microglia during diabetic retinopathy (DR). The Specific Aim is to demonstrate the feasibility of methods to measure the activation and inflammatory status of retinal microglia during the progression of DR. Microglia are resident macrophage cells in the central and peripheral nervous system, and the sole immune cell of the retina. They perform innate immune surveillance, becoming “activated” upon infection or tissue damage. During acute and chronic neurodegenerative diseases microglia become activated, exhibiting an altered phenotype that includes changes in morphology, increased phagocytosis, surface marker expression, and gene expression. Fully activated microglia produce inflammatory and toxic molecules that contribute to neuronal inflammation, neuronal toxicity and vascular dysfunction. Microglia exhibiting an activated morphology have been observed in both human diabetic retinas and experimental models of DR. Immunohistochemical co-staining for inflammatory proteins and microglial marker proteins have qualitatively cemonstrated that activated microglia are a potential source of inflammatory proteins during retinopathies. However, during some neurodegenerative diseases microglia assume an alternative activation phenotype that coincides with the expression of anti-inflammatory proteins. These microglia may actually play a beneficial adaptive role that minimizes the inflammatory response to neuronal damage. Given that inflammation is now thought to play a key role in the progression of DR, it is vital to define the activation and inflammatory status of retinal microglia. The goal is to perfect methods enabling the expression of several inflammatory proteins, including TNFa, IL-6, IL-1ß, and iNOS, as well as anti-inflammatory proteins, including TGFß, IL-1Ra, IL-27, and arginase, to be quantified in subsets of retinal microglia by flow cytometry. To accomplish this we will: 1) use cultured microglia to initially test and develop antibody combinations for use in flow cytometry, 2) further test these combinations using the retinal IR model, and 3) apply these methods to retinas of diabetic animals.


Progress Reports

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 PublicationAltmetricsSubmitted ByPubMed IDStatus

Year: 2016; Items: 3

 
Protective Effect of a GLP-1 Analog on Ischemia-Reperfusion Induced Blood-Retinal Barrier Breakdown and Inflammation.
Gonçalves A, Lin CM, Muthusamy A, Fontes-Ribeiro C, Ambrósio AF, Abcouwer SF, Fernandes R, Antonetti DA
Investigative ophthalmology & visual science, 2016 (57), 2584 - 92
27163772
Published
 
CX3CR1 deficiency accelerates the development of retinopathy in a rodent model of type 1 diabetes.
Beli E, Dominguez JM, Hu P, Thinschmidt JS, Caballero S, Li Calzi S, Luo D, Shanmugam S, Salazar TE, Duan Y, Boulton ME, Mohr S, Abcouwer SF, Saban DR, Harrison JK, Grant MB
Journal of molecular medicine (Berlin, Germany), 2016
27344677
Published
 
Tissue-specific metabolic reprogramming drives nutrient flux in diabetic complications.
Sas KM, Kayampilly P, Byun J, Nair V, Hinder LM, Hur J, Zhang H, Lin C, Qi NR, Michailidis G, Groop PH, Nelson RG, Darshi M, Sharma K, Schelling JR, Sedor JR, Pop-Busui R, Weinberg JM, Soleimanpour SA, Abcouwer SF, Gardner TW, Burant CF, Feldman EL, Kretzler M, Brosius FC, Pennathur S
JCI insight, 2016 (1), e86976
27699244
Published

Year: 2014; Items: 2

 
Diabetic retinopathy: loss of neuroretinal adaptation to the diabetic metabolic environment.
Abcouwer SF, Gardner TW
Annals of the New York Academy of Sciences, 2014 (1311), 174 - 190
Submitted Externally
24673341
Published
 
mTORC1-independent reduction of retinal protein synthesis in type 1 diabetes.
Fort PE, Losiewicz MK, Pennathur S, Jefferson LS, Kimball SR, Abcouwer SF, Gardner TW
Diabetes, 2014 (63), 3077 - 3090
Submitted Externally
24740573
Published

Year: 2013; Items: 3

 
23258912
Published
 
A role for systemic inflammation in diabetic retinopathy.
Abcouwer SF, Antonetti DA
Investigative ophthalmology & visual science, 2013 (54), 2384
Submitted Externally
23539166
Published
 
Angiogenic Factors and Cytokines in Diabetic Retinopathy.
Abcouwer SF
Journal of clinical & cellular immunology, 2013 (Suppl 1)
24319628
Published

Year: 2011; Items: 3

 
An integrated approach to diabetic retinopathy research.
Gardner TW, Abcouwer SF, Barber AJ, Jackson GR
Archives of ophthalmology, 2011 (129), 230 - 235
Submitted Externally
21320973
Published
 
The significance of vascular and neural apoptosis to the pathology of diabetic retinopathy.
Barber AJ, Gardner TW, Abcouwer SF
Investigative ophthalmology & visual science, 2011 (52), 1156 - 1163
21357409
Published
 
Differential roles of hyperglycemia and hypoinsulinemia in diabetes induced retinal cell death: evidence for retinal insulin resistance.
Fort PE, Losiewicz MK, Reiter CE, Singh RS, Nakamura M, Abcouwer SF, Barber AJ, Gardner TW
PLoS ONE, 2011 (6), e26498
Submitted Externally
22046295
Published

Year: 2010; Items: 1

 
TNF-a signals through PKC?/NF-?B to alter the tight junction complex and increase retinal endothelial cell permeability.
Aveleira CA, Lin CM, Abcouwer SF, Ambrósio AF, Antonetti DA
Diabetes, 2010 (59), 2872 - 2882
Submitted Externally
20693346
Published

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Title YearTypeOptions
Abcouwer, Steven (2009 P&F)
2009Presentation
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No protocols found.

No experiments found.

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No models found.