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The Role of LncRNAs in Pulmonary Fibrosis

Award Number: R01HL135152
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 07/01/2017
PERIOD OF PERFORMANCE END DATE: 05/31/2023

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The Role of LncRNAs in Pulmonary Fibrosis - PROJECT SUMMARY Idiopathic pulmonary fibrosis (IPF) is a progressive and irreversible interstitial lung disease with a mean life expectancy of only 3 to 5 years after diagnosis. It is one of approximately 7,000 rare diseases. The disease typically occurs in individuals between the ages of 50 and 70 years old. The abnormal activation of local resident pulmonary fibroblasts is believed to be a major factor driving the fibrotic progression in IPF. However, the molecular mechanisms leading to the fibroblast activation are not fully understood. The long-term goal of this project is to elucidate the pathogenesis of IPF and thus to advance the development of an effective pharmacological therapy. The objective of the current application is to understand how long non-coding RNAs (lncRNAs) regulate pulmonary fibroblast activation in IPF. lncRNAs are non-protein-coding RNAs with a size of > 200 nucleotides that have been increasingly recognized for their importance in regulating various biological processes. Although small non-coding RNAs, such as microRNAs, have been extensively studied in IPF, very little is known regarding the roles of lncRNAs in the pathogenesis of pulmonary diseases, such as IPF. Through the analyses of RNA_seq datasets, we have identified human fetal-lethal non-coding developmental regulatory RNA (FENDRR) as an lncRNA that is down-regulated in the fibrotic lungs of patients with IPF. Our preliminary studies have shown that TGFβ1 and hypoxia reduce FENDRR expression in pulmonary fibroblasts and that the overexpression of FENDRR inhibits fibroblast activation. We have also demonstrated that FENDRR reduces cellular iron content, and that iron depletion decreases pro-fibrotic miR- 214 expression. In addition, we have shown that FENDRR is a competing endogenous RNA (ceRNA) that functions as a sponge for miR-214. Finally, we have provided evidence that adenovirus-mediated gene transfer of FENDRR into mouse lungs attenuates bleomycin-induced pulmonary fibrosis in preventive and therapeutic modes. The central hypothesis of this project is that the down-regulation of FENDRR in IPF contributes to pulmonary fibrosis by promoting fibroblast activation via increased expression and activity of pro-fibrotic miR-214 due to iron overload and a reduced competition between FENDRR and miR-214, respectively. Aim I will delineate the transcriptional regulation of FENDRR by the TGFβ and hypoxia signaling pathways. Aim II will define the functional roles and molecular mechanisms of FENDRR in fibroblast activation. Aim III will determine the therapeutic efficacy and mechanisms of action of Fendrr in pre-clinical pulmonary fibrosis mouse models. The proposed studies will define novel mechanisms involved in the pathogenesis of IPF.


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: 2024 ( Subtotal = $0 )
2024	2020	OKLAHOMA STATE UNIVERSITY	401 WHITEHURST HALL	STILLWATER	OK	74078	PAYNE	USA	Lung Diseases Research	000	4	1/18/2024	NON-COMPETING CONTINUATION	$0
														Subtotal = $0

Issue Date FY: 2022 ( Subtotal = $0 )
2022	2020	OKLAHOMA STATE UNIVERSITY	401 WHITEHURST HALL	STILLWATER	OK	74078	PAYNE	USA	Lung Diseases Research	000	4	4/14/2022	NON-COMPETING CONTINUATION	$0
														Subtotal = $0

Issue Date FY: 2020 ( Subtotal = $374,000 )
2020	2020	OKLAHOMA STATE UNIVERSITY	401 WHITEHURST HALL	STILLWATER	OK	74078	PAYNE	USA	Lung Diseases Research	000	4	5/15/2020	NON-COMPETING CONTINUATION	$374,000
														Subtotal = $374,000

Issue Date FY: 2019 ( Subtotal = $374,000 )
2019	2019	OKLAHOMA STATE UNIVERSITY	401 WHITEHURST HALL	STILLWATER	OK	74078	PAYNE	USA	Lung Diseases Research	000	3	5/20/2019	NON-COMPETING CONTINUATION	$374,000
														Subtotal = $374,000

Issue Date FY: 2018 ( Subtotal = $374,000 )
2018	2018	OKLAHOMA STATE UNIVERSITY	401 WHITEHURST HALL	STILLWATER	OK	74078	PAYNE	USA	Lung Diseases Research	002	2	5/18/2018	NON-COMPETING CONTINUATION	$374,000
2018	2017	OKLAHOMA STATE UNIVERSITY	401 WHITEHURST HALL	STILLWATER	OK	74078	PAYNE	USA	Lung Diseases Research	001	1	11/16/2017	NEW	$374,000
2018	2017	OKLAHOMA STATE UNIVERSITY	401 WHITEHURST HALL	STILLWATER	OK	74078	PAYNE	USA	Lung Diseases Research	000	1	11/8/2017	NEW	-$374,000
														Subtotal = $374,000

Issue Date FY: 2017 ( Subtotal = $374,000 )
2017	2017	OKLAHOMA STATE UNIVERSITY	401 WHITEHURST HALL	STILLWATER	OK	74078	PAYNE	USA	Lung Diseases Research	000	1	6/21/2017	NEW	$374,000
														Subtotal = $374,000

Grand Total All Awards = $1,496,000

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The Role of LncRNAs in Pulmonary Fibrosis

Award Number: R01HL135152

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

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

PERIOD OF PERFORMANCE START DATE: 07/01/2017

PERIOD OF PERFORMANCE END DATE: 05/31/2023

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