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Bidirectional control of keratinocyte differentiation and proliferation by transcription factor FOXQ1

Award Number: R01AR082911
ORGANIZATION: NATIONAL INSTITUTE OF ARTHRITIS & MUSCULOSKELETAL & SKIN DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 08/01/2023
PERIOD OF PERFORMANCE END DATE: 06/30/2028

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Bidirectional control of keratinocyte differentiation and proliferation by transcription factor FOXQ1 - The skin forms the first barrier against physical, biological and chemical insults and is essential for prevention of dehydration. To maintain this function epidermal keratinocytes undergo differentiation. During differentiation, the gene expression programs in keratinocytes switch from maintenance of cell proliferation to terminal differentiation. Calcium gradient formed between the basal and upper epidermal layers is a major factor underlying induction of terminal differentiation in keratinocytes. In addition, skin homeostasis relies on well- orchestrated intercellular communications mediated by cytokines that are produced by keratinocytes and other skin resident cells. We have identified that transcription factor FOXQ1 (a member of the Forkhead Box family of proteins) utilizes a novel, rheostat-like mechanism of transcriptional regulation of keratinocyte differentiation. Thus, in presence of low extracellular calcium, FOXQ1 repressed genes associated with epidermal differentiation in normal human keratinocytes (NHKs) and immortalized human keratinocytes (HaCaT). On the contrary, in calcium-treated (i.e. differentiation-induced) NHK and HaCaT cells, FOXQ1 activated the same set of genes. Therefore, in Specific Aim 1, we will identify the mechanisms underlying transcriptional regulation by FOXQ1 of keratinocyte differentiation. In addition, we demonstrated that under normal conditions, depletion of FOXQ1 in cultured keratinocytes decreased whereas its overexpression increased cell proliferation. Moreover, Foxq1-/- mice demonstrated decreased epidermal hyperplasia in response to treatment with imiquimod which induces psoriasis-like phenotypes in mouse epidermis. Therefore, in Specific Aim 2, we will generate keratinocyte-specific Foxq1 knock-out mice and identify the mechanisms of FOXQ1 regulation by pro-inflammatory cytokines and the role of Foxq1 in regulation of keratinocyte hyper-proliferation.


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: 2025 ( Subtotal = $449,379 )
2025	2025	DUKE UNIVERSITY	2200 W MAIN ST	DURHAM	NC	27705	DURHAM	USA	Arthritis, Musculoskeletal and Skin Diseases Research	000	3	7/16/2025	NON-COMPETING CONTINUATION	$449,379
														Subtotal = $449,379

Issue Date FY: 2024 ( Subtotal = $485,781 )
2024	2024	DUKE UNIVERSITY	2200 W MAIN ST	DURHAM	NC	27705	DURHAM	USA	Arthritis, Musculoskeletal and Skin Diseases Research	000	2	6/11/2024	NON-COMPETING CONTINUATION	$485,781
														Subtotal = $485,781

Issue Date FY: 2023 ( Subtotal = $513,064 )
2023	2023	DUKE UNIVERSITY	2200 W MAIN ST	DURHAM	NC	27705	DURHAM	USA	Arthritis, Musculoskeletal and Skin Diseases Research	000	1	7/27/2023	NEW	$513,064
														Subtotal = $513,064

Grand Total All Awards = $1,448,224

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Bidirectional control of keratinocyte differentiation and proliferation by transcription factor FOXQ1

Award Number: R01AR082911

ORGANIZATION: NATIONAL INSTITUTE OF ARTHRITIS & MUSCULOSKELETAL & SKIN DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

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

PERIOD OF PERFORMANCE START DATE: 08/01/2023

PERIOD OF PERFORMANCE END DATE: 06/30/2028

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