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Endothelial Jak3 expression enhances pro-hematopoietic angiocrine function in mice
José Gabriel Barcia Durán1, Tyler Lu1,2, Sean Houghton1
1Ansary Stem Cell Institute, Division of Regenerative Medicine, Department of Medicine, Weill Cornell Medicine, New York, NY, 10065, USA.
Communications Biology
|March 26, 2021
Summary
Janus kinase 3 (JAK3) is expressed in bone marrow endothelial cells, impacting hematopoietic stem cell maintenance. Loss of JAK3 impairs the niche, while JAK3 overexpression expands stem cells.
Area of Science:
- Immunology
- Cell Biology
- Hematology
Background:
- Janus kinase 3 (JAK3) is primarily studied for its role in immunity.
- Functional JAK3 expression outside the immune system is largely unknown.
- The bone marrow niche regulates hematopoietic stem cell function.
Purpose of the Study:
- To investigate JAK3 expression in non-hematopoietic cells.
- To determine the role of JAK3 in the bone marrow niche.
- To explore JAK3's impact on long-term repopulating hematopoietic stem cells (LT-HSCs).
Main Methods:
- Immunohistochemistry to detect JAK3 expression in endothelial cells.
- Analysis of JAK3 knockout mouse models.
- In vitro expansion of LT-HSCs with JAK3-overexpressing endothelial cells.
Main Results:
- JAK3 is expressed in endothelial cells of various organs, notably the bone marrow.
- The bone marrow niche in JAK3-deficient mice is detrimental to LT-HSC maintenance.
- Endothelial cells overexpressing JAK3 enhance LT-HSC expansion in vitro.
Conclusions:
- JAK3 has a novel function in the bone marrow vascular niche.
- Endothelial JAK3 plays a critical role in regulating LT-HSC function.
- Targeting endothelial JAK3 may offer new therapeutic strategies for hematopoiesis.
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