Co-expression of the collagen receptors leukocyte-associated immunoglobulin-like receptor-1 and glycoprotein VI on a subset of megakaryoblasts

Steevels, Tessa A. M.; Westerlaken, Geertje H. A.; Tijssen, Marloes R.; Coffer, Paul J.; Lenting, Peter J.; Akkerman, Jan Willem N.; Meyaard, Linde

doi:10.3324/haematol.2010.026120

Cited by 23 publications

(18 citation statements)

References 37 publications

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“…They are regarded as late megakaryocyte lineage markers as compared to αIIbβ3 or GPIb, GPV and GPIX, which mark earlier stages of megakaryocyte maturation (Lagrue-Lak-Hal et al, 2001;Lepage et al, 2000). In addition, LAIR1 has been described as an early megakaryocyte inhibitory receptor for collagen, with reduced expression on mature megakaryocytes and no expression on platelets (Steevels et al, 2010). DDR1 has most recently been reported to be expressed on early megakaryocytes and to modulate their motility on collagen I (Abbonante et al, 2013) and, finally, GPV on platelets can also bind to collagen (Moog et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

“…Although these receptors are expressed by megakaryocytes from relatively early stages in their maturation (Lagrue-Lak-Hal et al, 2001), their function on PPF is ill-defined. Moreover, other collagen receptors, such as leukocyte-associated immunoglobulin-like receptor-1 (LAIR1) (Steevels et al, 2010) and discoidin domain receptor 1 (DDR1) (Abbonante et al, 2013) have been proposed as inhibitory collagen receptors on early megakaryocytes, whose expression decreases during maturation and thus are absent from circulating platelets. Accordingly, once released from megakaryocytes, collagens are strong platelet agonists, with their binding leading to adhesion, aggregation and granule secretion, suggesting that collagen receptors in megakaryocytes are capable of transducing distinct signaling cascades.…”

Section: Introductionmentioning

confidence: 99%

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Proplatelet formation is selectively inhibited by collagen type I through Syk-independent GPVI signaling

Semeniak

Kulawig

Stegner

et al. 2016

Journal of Cell Science

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Collagen receptors GPVI (also known as GP6) and integrin α2β1 are highly expressed on blood platelets and megakaryocytes, their immediate precursors. After vessel injury, subendothelial collagen becomes exposed and induces platelet activation to prevent blood loss. Collagen types I and IV are thought to have opposite effects on platelet biogenesis, directing proplatelet formation (PPF) towards the blood vessels to prevent premature release within the marrow cavity. We used megakaryocytes lacking collagen receptors or treated megakaryocytes with blocking antibodies, and could demonstrate that collagen-I-mediated inhibition of PPF is specifically controlled by GPVI. Other collagen types competed for binding and diminished the inhibitory signal, which was entirely dependent on receptor-proximal Src family kinases, whereas Syk and LAT were dispensable. Adhesion assays indicate that megakaryocyte binding to collagens is mediated by α2β1, and that collagen IV at the vascular niche might displace collagen I from megakaryocytes and thus contribute to prevention of premature platelet release into the marrow cavity and thereby directionally promote PPF at the vasculature.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Proplatelet formation is selectively inhibited by collagen type I through Syk-independent GPVI signaling

Semeniak

Kulawig

Stegner

et al. 2016

Journal of Cell Science

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“…Since collagen has such a large role in ECM biomechanical properties, it has been the focus of research for the understanding of MK development and platelet formation [30,46,47]. MKs express two main receptors for collagen, integrin-α2β1 and glycoprotein VI [47]; however, MK expression of leukocyte-associated immunoglobulin-like 1 (LAIR1) and discoidin domain receptor (DDR1) that also bind collagen have been described in the literature [48,49]. Early MK progenitors (CFU-MK) have a lower affinity for adhering to collagen compared to later MK progenitors [50], which is interesting as integrin-α2β1 and glycoprotein VI expression occurs early in MK development [50,51].…”

Section: Integrins As Ecm Sensors In the Context Of Megakaryocytosismentioning

confidence: 99%

Matrix Mechanosensation in the Erythroid and Megakaryocytic Lineages

Ward

Ravid

2020

Cells

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The biomechanical properties of the bone marrow microenvironment emerge from a combination of interactions between various extracellular matrix (ECM) structural proteins and soluble factors. Matrix stiffness directs stem cell fate, and both bone marrow stromal and hematopoietic cells respond to biophysical cues. Within the bone marrow, the megakaryoblasts and erythroblasts are thought to originate from a common progenitor, giving rise to fully mature magakaryocytes (the platelet precursors) and erythrocytes. Erythroid and megakaryocytic progenitors sense and respond to the ECM through cell surface adhesion receptors such as integrins and mechanosensitive ion channels. While hematopoietic stem progenitor cells remain quiescent on stiffer ECM substrates, the maturation of the erythroid and megakaryocytic lineages occurs on softer ECM substrates. This review surveys the major matrix structural proteins that contribute to the overall biomechanical tone of the bone marrow, as well as key integrins and mechanosensitive ion channels identified as ECM sensors in context of megakaryocytosis or erythropoiesis.

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“…LAIR-1 is expressed on nearly all immune cells as well as on early hematopoietic stem and progenitor cells. In humans, it becomes downregulated concomitantly with CD34, when the stem cells differentiate into the megakaryocytic lineage [15][16][17].…”

Section: Introductionmentioning

confidence: 99%

Impact ofItga2-Gp6-double collagen receptor deficient mice for bone marrow megakaryocytes and platelets

Semeniak

Faber

Öftering

et al. 2019

Preprint

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The two main collagen receptors on platelets, GPVI and integrin α2β1, play an important role for the recognition of exposed collagen at sites of vessel injury, which leads to platelet activation and subsequently stable thrombus formation. Both receptors are already expressed on megakaryocytes, the platelet forming cells within the bone marrow. Megakaryocytes are in permanent contact with collagen filaments in the marrow cavity and at the basal lamina of sinusoids without obvious preactivation. The role of both collagen receptors for megakaryocyte maturation and thrombopoiesis is still poorly understood. To investigate the function of both collagen receptors, we generated mice that are double deficient for Gp6 and Itga2. Flow cytometric analyses revealed that the deficiency of both receptors had no impact on platelet number and the expected lack in GPVI responsiveness. Integrin activation

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Co-expression of the collagen receptors leukocyte-associated immunoglobulin-like receptor-1 and glycoprotein VI on a subset of megakaryoblasts

Cited by 23 publications

References 37 publications

Proplatelet formation is selectively inhibited by collagen type I through Syk-independent GPVI signaling

Proplatelet formation is selectively inhibited by collagen type I through Syk-independent GPVI signaling

Matrix Mechanosensation in the Erythroid and Megakaryocytic Lineages

Impact ofItga2-Gp6-double collagen receptor deficient mice for bone marrow megakaryocytes and platelets

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