Publications by authors named "C Ghevaert"
Article Synopsis
- Understanding how platelets influence oligodendrocyte progenitor cell (OPC) function is crucial for developing treatments for multiple sclerosis (MS).
- Research shows that platelets aggregate near OPCs in demyelinated areas, and reducing platelets leads to impaired OPC differentiation and remyelination.
- The study indicates that platelets have a dual role in remyelination, enhancing OPC differentiation initially but suppressing it with prolonged exposure, providing insights into remyelination challenges in MS.
Hematopoietic stem cells (HSCs) residing in specialized niches in the bone marrow are responsible for the balanced output of multiple short-lived blood cell lineages in steady-state and in response to different challenges. However, feedback mechanisms by which HSCs, through their niches, sense acute losses of specific blood cell lineages remain to be established. While all HSCs replenish platelets, previous studies have shown that a large fraction of HSCs are molecularly primed for the megakaryocyte-platelet lineage and are rapidly recruited into proliferation upon platelet depletion.
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- Platelets are tiny cells in our blood that help stop bleeding, and they come from larger cells called megakaryocytes.
- Researchers found that when they send megakaryocytes through mouse lungs, they can produce a huge number of platelets, sometimes up to 3000 from one cell!
- The study also looked at how things like oxygen and the lungs' structure help in making platelets, and they discovered that a special protein, Tropomyosin 4, is important for the final stage of making platelets.
Long-range interactions between regulatory elements and promoters are key in gene transcriptional control; however, their study requires large amounts of starting material, which is not compatible with clinical scenarios nor the study of rare cell populations. Here we introduce low input capture Hi-C (liCHi-C) as a cost-effective, flexible method to map and robustly compare promoter interactomes at high resolution. As proof of its broad applicability, we implement liCHi-C to study normal and malignant human hematopoietic hierarchy in clinical samples.
View Article and Find Full Text PDFAdult hematopoietic stem cells (HSCs) are predominantly quiescent and can be activated in response to acute stress such as infection or cytotoxic insults. STAT1 is a pivotal downstream mediator of interferon (IFN) signaling and is required for IFN-induced HSC proliferation, but little is known about the role of STAT1 in regulating homeostatic hematopoietic stem/progenitor cells (HSPCs). Here, we show that loss of STAT1 altered the steady state HSPC landscape, impaired HSC function in transplantation assays, delayed blood cell regeneration following myeloablation, and disrupted molecular programs that protect HSCs, including control of quiescence.
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