Tumor-derived interleukin-1α and leukemia inhibitory factor promote extramedullary hematopoiesis.
Extramedullary hematopoiesis (EMH) expands hematopoietic capacity outside of the bone marrow in response to inflammatory conditions, including infections and cancer. Because of its inducible nature, EMH offers a unique opportunity to study the interaction between hematopoietic stem and progenitor ce...
| Main Authors: | , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2023-05-01
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| Series: | PLoS Biology |
| Online Access: | https://doi.org/10.1371/journal.pbio.3001746 |
| _version_ | 1827951581754032128 |
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| author | Derek A G Barisas Ashraf Ul Kabir Jun Wu Karen Krchma Minseo Kim Madhav Subramanian Bernd H Zinselmeyer Colin L Stewart Kyunghee Choi |
| author_facet | Derek A G Barisas Ashraf Ul Kabir Jun Wu Karen Krchma Minseo Kim Madhav Subramanian Bernd H Zinselmeyer Colin L Stewart Kyunghee Choi |
| author_sort | Derek A G Barisas |
| collection | DOAJ |
| description | Extramedullary hematopoiesis (EMH) expands hematopoietic capacity outside of the bone marrow in response to inflammatory conditions, including infections and cancer. Because of its inducible nature, EMH offers a unique opportunity to study the interaction between hematopoietic stem and progenitor cells (HSPCs) and their niche. In cancer patients, the spleen frequently serves as an EMH organ and provides myeloid cells that may worsen pathology. Here, we examined the relationship between HSPCs and their splenic niche in EMH in a mouse breast cancer model. We identify tumor produced IL-1α and leukemia inhibitory factor (LIF) acting on splenic HSPCs and splenic niche cells, respectively. IL-1α induced TNFα expression in splenic HSPCs, which then activated splenic niche activity, while LIF induced proliferation of splenic niche cells. IL-1α and LIF display cooperative effects in activating EMH and are both up-regulated in some human cancers. Together, these data expand avenues for developing niche-directed therapies and further exploring EMH accompanying inflammatory pathologies like cancer. |
| first_indexed | 2024-04-09T13:44:34Z |
| format | Article |
| id | doaj.art-37118693b3bf4b4f9fb28f88c9c22c5b |
| institution | Directory Open Access Journal |
| issn | 1544-9173 1545-7885 |
| language | English |
| last_indexed | 2024-04-09T13:44:34Z |
| publishDate | 2023-05-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS Biology |
| spelling | doaj.art-37118693b3bf4b4f9fb28f88c9c22c5b2023-05-09T05:30:43ZengPublic Library of Science (PLoS)PLoS Biology1544-91731545-78852023-05-01215e300174610.1371/journal.pbio.3001746Tumor-derived interleukin-1α and leukemia inhibitory factor promote extramedullary hematopoiesis.Derek A G BarisasAshraf Ul KabirJun WuKaren KrchmaMinseo KimMadhav SubramanianBernd H ZinselmeyerColin L StewartKyunghee ChoiExtramedullary hematopoiesis (EMH) expands hematopoietic capacity outside of the bone marrow in response to inflammatory conditions, including infections and cancer. Because of its inducible nature, EMH offers a unique opportunity to study the interaction between hematopoietic stem and progenitor cells (HSPCs) and their niche. In cancer patients, the spleen frequently serves as an EMH organ and provides myeloid cells that may worsen pathology. Here, we examined the relationship between HSPCs and their splenic niche in EMH in a mouse breast cancer model. We identify tumor produced IL-1α and leukemia inhibitory factor (LIF) acting on splenic HSPCs and splenic niche cells, respectively. IL-1α induced TNFα expression in splenic HSPCs, which then activated splenic niche activity, while LIF induced proliferation of splenic niche cells. IL-1α and LIF display cooperative effects in activating EMH and are both up-regulated in some human cancers. Together, these data expand avenues for developing niche-directed therapies and further exploring EMH accompanying inflammatory pathologies like cancer.https://doi.org/10.1371/journal.pbio.3001746 |
| spellingShingle | Derek A G Barisas Ashraf Ul Kabir Jun Wu Karen Krchma Minseo Kim Madhav Subramanian Bernd H Zinselmeyer Colin L Stewart Kyunghee Choi Tumor-derived interleukin-1α and leukemia inhibitory factor promote extramedullary hematopoiesis. PLoS Biology |
| title | Tumor-derived interleukin-1α and leukemia inhibitory factor promote extramedullary hematopoiesis. |
| title_full | Tumor-derived interleukin-1α and leukemia inhibitory factor promote extramedullary hematopoiesis. |
| title_fullStr | Tumor-derived interleukin-1α and leukemia inhibitory factor promote extramedullary hematopoiesis. |
| title_full_unstemmed | Tumor-derived interleukin-1α and leukemia inhibitory factor promote extramedullary hematopoiesis. |
| title_short | Tumor-derived interleukin-1α and leukemia inhibitory factor promote extramedullary hematopoiesis. |
| title_sort | tumor derived interleukin 1α and leukemia inhibitory factor promote extramedullary hematopoiesis |
| url | https://doi.org/10.1371/journal.pbio.3001746 |
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