Journal
SCIENCE
Volume 348, Issue 6240, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aaa2340
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Categories
Funding
- NIH [P50 CA150964, P30 CA043703, R25CA148052, U54HL119810, 1P01CA95471-09, 5P30 CA142543-03]
- Harrington Discovery Institute
- Marguerite Wilson Foundation
- Inje University
- National Research Foundation, Ministry of Science, ICT and Future Planning of Korea [2014002213]
- Welch Foundation [I-1612]
- Cancer Prevention Research Institute of Texas [RP110708]
- Howard Hughes Medical Institute
- [P50 CA130810]
- [P30 DK097948]
- National Research Foundation of Korea [2014R1A1A1002213] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Agents that promote tissue regeneration could be beneficial in a variety of clinical settings, such as stimulating recovery of the hematopoietic system after bone marrow transplantation. Prostaglandin PGE2, a lipid signaling molecule that supports expansion of several types of tissue stem cells, is a candidate therapeutic target for promoting tissue regeneration in vivo. Here, we show that inhibition of 15-hydroxyprostaglandin dehydrogenase (15-PGDH), a prostaglandin-degrading enzyme, potentiates tissue regeneration in multiple organs in mice. In a chemical screen, we identify a small-molecule inhibitor of 15-PGDH (SW033291) that increases prostaglandin PGE2 levels in bone marrow and other tissues. SW033291 accelerates hematopoietic recovery in mice receiving a bone marrow transplant. The same compound also promotes tissue regeneration in mouse models of colon and liver injury. Tissues from 15-PGDH knockout mice demonstrate similar increased regenerative capacity. Thus, 15-PGDH inhibition may be a valuable therapeutic strategy for tissue regeneration in diverse clinical contexts.
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