Determining the role of TP53 regulation in alveolar epithelial transitional cell state, and the contribution of alveolar epithelial transitional cell state to pulmonary fibrosis
Ended Project Grant Awarded Last action
- Award ID
- F31HL172360
- Recipient
-
Duke University UEI TP7EK8DZV6N5
- Awarding agency
-
National Heart Lung and Blood Institute
National Institutes of Health, Department of Health and Human Services
- Obligated
- $319,678
Award facts
- Assistance listing
- 93.837 Cardiovascular Diseases Research
- Completion date
- Place of performance
- Durham, NC 27705, USA
Award details come from USAspending.gov.
Description
- Abstract
- Respiratory disease is the third leading cause of death in the industrialized world. Pulmonary fibrosis (PF) is a progressively debilitating and terminal disease in which the normally pliable tissue of the lung is gradually replaced with rigid scar tissue. PF is an especially difficult respiratory disease, as there are no effective treatments and patients DIE within an average of three to five years of diagnosis. Current models suggest that alveolar injury and ineffective repair underlie the pathogenesis of PF and other lung diseases. However, the mechanisms by which injury in the alveolar epithelium contributes to fibrotic disease remain unclear. Single cell transcriptomics data demonstrate that a transitional state exists between the well characterized alveolar type 2 (AT2) and type 1 (AT1) epithelial cells. Furthermore, marker analysis of this transitional state in human PF lungs suggests that accumulation of transitional cells occurs in regions with dense myofibroblasts in fibrotic lungs. IT is unclear what molecular mechanisms regulate the state of alveolar epithelial cells, but data from our lab has shown that TP53 is transiently upregulated in normal differentiation of AT2 to AT1 cells. This proposal details approaches to uncover the role of TP53 in regulating alveolar epithelial cell states, and to determine the impact of an alveolar epithelial transition state on pulmonary fibrosis. Understanding the mechanisms that drive these transitional states and their potential role in PF disease pathogenesis offers new avenues for developing novel therapies for fibrotic and other lung diseases.
Transactions
| Action | Obligated | Date |
|---|---|---|
| Amendment | $288 | |
| Amendment | $20,890 | |
| Amendment | $20,890 | |
| Amendment | $564 | |
| Amendment | $41,215 | |
| Amendment | $41,215 | |
| Amendment | $1,280 | |
| Amendment | $0 | |
| Amendment | $1,280 | |
| Amendment | $0 | |
| Amendment | $0 | |
| Amendment | $1,280 | |
| Amendment | $47,694 | |
| Amendment | $47,694 | |
| Amendment | $47,694 | |
| Original award | $47,694 |
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Quick answers
Who received award F31HL172360?
F31HL172360 was awarded to Duke University by National Heart Lung and Blood Institute (National Institutes of Health) on September 1, 2024.
How much is award F31HL172360 worth?
$319,678 has been obligated on F31HL172360.
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