The role of novel and known extracellular matrix and adhesion molecules in the homeostatic and regenerative bone marrow microenvironment

Klamer, Sofieke; Voermans, Carlijn

doi:10.4161/19336918.2014.968501

Cited by 79 publications

(85 citation statements)

References 230 publications

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“…POSTN also enhances bone formation at the periosteum [20, reviewed in 14]. These effects of POSTN might add to the stability of the BM microenvironment, and might also facilitate the function of other niche factors.…”

Section: Discussionmentioning

confidence: 99%

“…POSTN, produced by OP-9 cells, has recently been reported to be required for optimal B lymphopoiesis in vitro [13], suggesting that POSTN, as well as CXCL12, are B cell-specific niche factors within the BM microenvironment. Moreover, increased expression of POSTN within BM stromal cells might correlate with myelofibrosis, leading to the interesting hypothesis that POSTN might be a niche factor for clonal expansion in some form of chronic myeloproliferative diseases [reviewed in 14]. …”

Section: Introductionmentioning

confidence: 99%

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Periostin supports hematopoietic progenitor cells and niche-dependent myeloblastoma cells in vitro

Tanaka

Maekawa

Matsubara

et al. 2016

Biochemical and Biophysical Research Communications

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The expression of extracellular matrix protein periostin (POSTN) was attenuated in Med1−/− mouse embryonic fibroblasts (MEFs), which exhibited a decreased capability to support hematopoietic progenitor cells (HPCs) in vitro. When bone marrow (BM) cells were cocultured with mitomycin C-treated Med1+/+ MEFs, or OP-9 or MS-5 BM stromal cells, in the presence of anti-POSTN antibody, the growth of BM cells and number of long-term culture-initiating cells (LTC-ICs) were attenuated. When BM cells were cocultured with Med1−/− MEFs in the presence of recombinant POSTN, the growth of BM cells and the number of LTC-ICs were restored. Moreover, antibody-mediated blockage of stromal cells-derived POSTN markedly reduced the growth and cobblestone formation, a leukemic stem cell feature, of stromal cell-dependent MB-1 myeloblastoma cells. POSTN was expressed both in BM cells and variably in different BM stromal cells. Expression in the latter cells was increased by physical interaction with hematopoietic cells. The receptor for POSTN, integrin αvβ3, was expressed abundantly in BM stromal cells. The addition of recombinant POSTN to BM stromal cells induced intracellular signaling downstream of integrin αvβ3. These results suggest that stromal cell POSTN supports both normal HPCs and leukemia-initiating cells in vitro, at least in part, indirectly by acting on stromal cells in an autocrine or paracrine manner.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Periostin supports hematopoietic progenitor cells and niche-dependent myeloblastoma cells in vitro

Tanaka

Maekawa

Matsubara

et al. 2016

Biochemical and Biophysical Research Communications

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“…HSCs show preferential adhesion to several extracellular matrix (ECM) proteins and proteoglycans [28, 59]. When HSCs were grown on top of poly(ethylene- alt -maleic anhydride) (PEMA) substrates chemically modified with proteins (fibronectin, type I collagen fibrils, tropocollagen I) and proteoglycans (heparin sulphate, heparin, hyaluronic acid), HSCs adhered most strongly to fibronectin while moderately adhered to heparin sulphate, heparin, and collagen I fibrils and insignificantly adhered to tropocollagen I and hyaluronic acid [59].…”

Section: Niche-mimicking Platforms For Modulating Stem Cell Behaviorsmentioning

confidence: 99%

“…Definite hematopoiesis then ensues in the aorta-gonad-mesonephros (AGM), placenta, fetal liver, spleen, and finally in the bone marrow, the primary site of hematopoiesis for adults [9, 16]. During adult hematopoiesis, HSCs are found primarily in the bone marrow HSC niches, where various cellular components (e.g., osteolineage cells, vascular endothelial cells, neurons, macrophages), extracellular proteins (e.g., fibronectin, laminin, collagen, proteoglycans), and secreted or immobilized biomolecules and growth factors (e.g., SCF, TPO, Ang-1, Flt3L, CXCL-12, G-CSF, IL-3, IL-6, IL-11) comprise the functional microenvironments with local gradients in cellular and extracellular content [2, 19, 14, 24–28]. Several discrete anatomical localizations within the marrow have been described for HSC niches (e.g., endosteal, perivascular and, more specifically, sinusoidal and arteriolar niches) [19, 24, 27, 29, 30].…”

Section: Introductionmentioning

confidence: 99%

Challenges and Opportunities to Harnessing the (Hematopoietic) Stem Cell Niche

Choi

Harley

2016

Curr Stem Cell Rep

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In our body, stem cells reside in a microenvironment termed the niche. While the exact composition and therefore the level of complexity of a stem cell niche can vary significantly tissue-to-tissue, the stem cell niche microenvironment is dynamic, typically containing spatial and temporal variations in both cellular, extracellular matrix, and biomolecular components. This complex flow of secreted or bound biomolecules, cytokines, extracellular matrix components, and cellular constituents all contribute to the regulation of stem cell fate specification events, making engineering approaches at the nano- and micro-scale of particular interest for creating an artificial niche environment in vitro. Recent advances in fabrication approaches have enabled biomedical researchers to capture and recreate the complexity of stem cell niche microenvironments in vitro. Such engineered platforms show promise as a means to enhance our understanding of the mechanisms underlying niche-mediated stem cell regulation as well as offer opportunities to precisely control stem cell expansion and differentiation events for clinical applications. While these principles generally apply to all adult stem cells and niches, in this review, we focus on recent developments in engineering synthetic niche microenvironments for one of the best-characterized stem cell populations, hematopoietic stem cells (HSC). Specifically, we highlight recent advances in platforms designed to facilitate the extrinsic control of HSC fate decisions.

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“…Eindringende Osteoklasten und Osteoblasten bauen die verkalkte Matrix an der osteochondralen Schnittstelle um und lagern eine Kollagen-I-reiche ECM ab, wodurch das Trabekelnetzwerk gebildet und der Markhöhle ihre Gestalt gegeben wird. Die Knochenmark-ECM bietet eine geeignete Mikroumgebung für die Häma-topoese (Übersicht in [2]). Welchen Beitrag ihr ECM-Vorläufer in der chondralen Epiphysenfuge leistet, ist jedoch noch ungeklärt.…”

Section: Enchondrale Ossifikationunclassified

Bedeutung der extrazellulären Matrix des Knorpels für die Entwicklung und Funktion des Immunsystems

Etich

Brachvogel

2015

Z Rheumatol

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Die extrazelluläre Matrix (ECM) des Knochenmarks sendet Überlebenssignale an hämatopoetische Stammzellen (HSC) und dient ihnen als Adhäsionssubstrat. Das Gerüst leitet sich von einem Knorpel-ECM-Muster ab, das während der enchondralen Ossifikation (EO) in verkalkte, steife und stabile Knochenelemente umgewandelt wird. Mutationen in der Knorpel-ECM können zu einer Chondrodysplasie führen, deren typisches Merkmal Skelettfehlbildungen sind, die häufig mit Kleinwuchs einhergehen [1]. Im vorliegenden Beitrag werden präklinische Daten aus Tiermodellen mit genetisch verändertem Kollagen X zusammengefasst, die zeigen, dass Defekte in der Knorpel-ECM sich auch in Veränderungen des HSC-Kompartiments und in Funktionsstörungen des Immunsystems äußern. Enchondrale OssifikationDas Skelett wird größtenteils durch die EO gebildet, für die eine geordnete Differenzierung von Zellen über ein intermediäres Knorpelmodell in das endgül-tige Knochengewebe charakteristisch ist. Im Verlauf der EO verdichten sich Mesenchymzellen und differenzieren in Chondrozyten, die eine Kollagen-II-reiche ECM sezernieren. Sie ändern ihre Gestalt, ordnen sich als parallele Stapel in der Epiphysenfuge an und modulieren abhängig von der Lage ihre Proliferations-und Expressionseigenschaften (. Abb. 1a). Die Chondrozyten werden zuerst prähyper-troph, dann hypertroph. In diesem Stadium sondern sie eine mineralisationsfähige und Kollagen-X-reiche ECM ab, wodurch die Hydroxylapatitbildung eingeleitet wird. Durch die Bildung des "vascular endothelial growth factor" und anderer Mediatoren werden Blutgefäße zur Vaskularisierung der Epiphysenfuge angeregt. Eindringende Osteoklasten und Osteoblasten bauen die verkalkte Matrix an der osteochondralen Schnittstelle um und lagern eine Kollagen-I-reiche ECM ab, wodurch das Trabekelnetzwerk gebildet und der Markhöhle ihre Gestalt gegeben wird. Die Knochenmark-ECM bietet eine geeignete Mikroumgebung für die Häma-topoese (Übersicht in [2]). Welchen Beitrag ihr ECM-Vorläufer in der chondralen Epiphysenfuge leistet, ist jedoch noch ungeklärt.

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The role of novel and known extracellular matrix and adhesion molecules in the homeostatic and regenerative bone marrow microenvironment

Cited by 79 publications

References 230 publications

Periostin supports hematopoietic progenitor cells and niche-dependent myeloblastoma cells in vitro

Periostin supports hematopoietic progenitor cells and niche-dependent myeloblastoma cells in vitro

Challenges and Opportunities to Harnessing the (Hematopoietic) Stem Cell Niche

Bedeutung der extrazellulären Matrix des Knorpels für die Entwicklung und Funktion des Immunsystems

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