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The neuroprotective role of DPSC EVs overexpressing microRNA-22-3p

Award Number: F31EY039675
ORGANIZATION: NATIONAL EYE INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 08/24/2026
PERIOD OF PERFORMANCE END DATE: 08/23/2028

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The neuroprotective role of DPSC EVs overexpressing microRNA-22-3p - PROJECT SUMMARY/ ABSTRACT Central retinal arterial occlusion (CRAO) is a form of retinal ischemia that causes vision loss and cellular damage characterized by inflammation and apoptosis of retinal cells. There is no current therapy for CRAO, and its severity is amplified by the retina’s inability to regenerate. Bone marrow mesenchymal stem cell (BMSC)-based therapy reduces inflammation and cell death in the retina. Yet, the neuroprotective effect is limited due to the challenging isolation of cells and low cell integration into the retina. Extracellular vesicles (EVs) derived from BMSCs are a neuroprotective alternative. This proposal will characterize a distinct source of MSCs derived from dental pulp, known as dental pulp stem cells (DPSCs), isolated from discarded teeth. DPSCs originate from the neural crest and are highly anti-inflammatory, making them potentially superior as an EV for translational treatment of CRAO. There are critical knowledge gaps in the mechanisms responsible for the anti-inflammatory and anti-apoptotic action of DPSC EVs. Inflammatory preconditioning of DPSC EVs enhanced the neuroprotective effects and altered the microRNA (miR) profile responsible for EV functionality. Upregulating enriched miR from preconditioned DPSC EVs further enhanced neuroprotection; our group termed this method “functionally engineered EVs (FEEs).” Preliminary data showed that inflammatory preconditioning of DPSC EVs increased levels of anti-inflammatory and anti-apoptosis miR-22-3p by approximately 10-fold in preconditioned DPSC EVs. Based on these preliminary results, I hypothesize that FEEs with enhanced levels of miRNA-22-3p will increase their anti-inflammatory and anti-apoptotic properties in the retina superior to EVs from native DPSCs (N-EVs). To test my hypothesis, I propose two integrated aims. First, I will determine the role of FEE-22 and N-EV from DPSCs in neuroinflammation and neuronal cell death in the retina in vitro. Second, I will determine the neuroprotective effect of FEE-22 and N-EVs in a rodent model of CRAO. This work is expected to uncover the fundamental mechanisms of miR-mediated EV therapeutics in the retina, underlying novel translational therapy for CRAO.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $50,114 )
2026	2026	UNIVERSITY OF ILLINOIS	809 S MARSHFIELD AVE M/C 551	CHICAGO	IL	60612	COOK	USA	Vision Research	000	1	8/24/2026	NEW	$50,114
2026	2026	UNIVERSITY OF ILLINOIS	809 S MARSHFIELD AVE M/C 551	CHICAGO	IL	60612	COOK	USA	Vision Research	001	1	8/24/2026	NEW	$0
														Subtotal = $50,114

Grand Total All Awards = $50,114

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The neuroprotective role of DPSC EVs overexpressing microRNA-22-3p

Award Number: F31EY039675

ORGANIZATION: NATIONAL EYE INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 08/24/2026

PERIOD OF PERFORMANCE END DATE: 08/23/2028

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