期刊
JCI INSIGHT
卷 4, 期 16, 页码 -出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/jci.insight.126982
关键词
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资金
- MD Anderson Cancer Center Support Grant [5 P30 CA016672-40]
- NYU Cancer Center Support Grant [NIH/NCI P30CA016087]
- National Blood Foundation Early Career Scientific Research Grants Program
- Rose M. Badgeley Residuary Charitable Trust
- NIH [R21HL139695, R01HL122788]
The complex process of platelet formation originates with the hematopoietic stem cell, which differentiates through the myeloid lineage, matures, and releases proplatelets into the BM sinusoids. How formed platelets maintain a low basal activation state in the circulation remains unknown. We identify Lepr(+) stromal cells lining the BM sinusoids as important contributors to sustaining low platelet activation. Ablation of murine Lepr(+) cells led to a decreased number of platelets in the circulation with an increased activation state. We developed a potentially novel culture system for supporting platelet formation in vitro using a unique population of CD51(+)PDGFR alpha(+) perivascular cells, derived from human umbilical cord tissue, which display numerous mesenchymal stem cell (MSC) properties. Megakaryocytes cocultured with MSCs had altered LAT and Rap1b gene expression, yielding platelets that are functional with low basal activation levels, a critical consideration for developing a transfusion product. Identification of a regulatory cell that maintains low baseline platelet activation during thrombopoiesis opens up new avenues for improving blood product production ex vivo.
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