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The Role of DPP in Dental Pulp Stem Cells and its Potential in Tissue Regeneration

Award Number: R56DE028531
ORGANIZATION: NATIONAL INSTITUTE OF DENTAL AND CRANIOFACIAL RESEARCH
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 04/01/2019
PERIOD OF PERFORMANCE END DATE: 09/17/2028

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The Role of DPP in Dental Pulp Stem Cells and its Potential in Tissue Regeneration - PROJECT SUMMARY Deep caries and pulp exposures are normally treated by pulp capping or partial pulp amputation to preserve the vitality of the pulp. Control of dental caries is a major public health program. Discovery of the dental pulp stem cells (DPSCs) have opened up new avenues for regeneration or repair of the pulp-dentin complex. The use of adult stem cells for tissue regeneration and repair is important in regenerative medicine. Another important component for tissue engineering is a bioactive signaling molecule. For the last two decades we have been studying the acidic phosphoproteins of the organic matrix of bone and dentin. Besides their function in the extracellular matrix, many of these proteins are now implicated in stimulating signaling events. One such protein identified in the dentin matrix is dentin phosphophoryn (DPP). Recently we discovered that DPP can stimulate the release of intracellular calcium in DPSCs. Depletion of intracellular calcium from the endoplasmic reticulum leads to ER stress. Cells cope with ER-stress by activating “autophagy” a tightly regulated degradation and recycling process crucial for cellular homeostasis. One of our recent observations is that DPP stimulation can activate the process of autophagy in DPSCs. Preliminary data indicate that DPP-mediated ER-stress can induce autophagy to serve as a cytoprotective mechanism in a stressful environment to promote the differentiation of DPSCs to functional odontoblast like cells which make dentin, a mineralized tissue. To test this hypothesis, we propose to use molecular and structural approaches in the following 3 aims: (a) Demonstrate DPP-mediated ER-stress induces autophagy to promote odontogenic differentiation of DPSCs; (b) Establish DPP-mediated stress-primed autophagy activates adenosine signaling to promote odontogenic differentiation; (c) Assess DPP-mediated autophagy promotes the secretion of autophagic LC3+ extracellular vesicles enriched with a molecular cargo that mediates matrix mineralization. Overall, results from these studies would reveal an unprecedented signaling framework modulated by DPP that could be utilized in the future to develop therapies to restore lost, damaged or diseased dentin-pulp complex with a vital pulp leading to tooth survival.


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 = $1,269,872 )
2026	2026	UNIVERSITY OF ILLINOIS	809 S MARSHFIELD AVE M/C 551	CHICAGO	IL	60612	COOK	USA	Oral Diseases and Disorders Research	000	6	9/17/2026	COMPETING CONTINUATION	$1,269,872
														Subtotal = $1,269,872

Grand Total All Awards = $1,269,872

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The Role of DPP in Dental Pulp Stem Cells and its Potential in Tissue Regeneration

Award Number: R56DE028531

ORGANIZATION: NATIONAL INSTITUTE OF DENTAL AND CRANIOFACIAL RESEARCH

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 04/01/2019

PERIOD OF PERFORMANCE END DATE: 09/17/2028

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