Hyaluronan Depolymerization by Megakaryocyte Hyaluronidase-2 Is Required for Thrombopoiesis

Petrey, Aaron C.; Obery, Dana R.; Kessler, Sean P.; Flamion, Bruno; Motte, Carol A. de la

doi:10.1016/j.ajpath.2016.05.004

Cited by 19 publications

(16 citation statements)

References 73 publications

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“…Thus, HA most likely acts as an insulating coat or spatial buffer, permitting lowmolecular-weight molecules such as electrolytes and nutrients to diffuse, but blocking high-molecularweight proteins or even cells from reaching the cell surface, as elegantly demonstrated in the red blood cell exclusion assay [14]. Further, the endothelial HA glycocalyx prevents inflammatory cells from directly interacting with the endothelium by maintaining a nonadhesive surface and, in platelets, HA prevents adherence and degranulation [15]. Degradation of HA, however, reduces its barrier function thus making the HA matrix much more permeable and accessible to cell interactions.…”

Section: Physical Properties Size and Molecular Weight Distributionmentioning

confidence: 99%

“…Hyal2 deficiency leads to high pre-weaning mortality as well as long-term cardiopulmonary dysfunction by 3 months of age. Additionally, Hyal2 is necessary for thrombopoiesis [15]. PH20 (or SPAM1), initially characterized as a hyaluronidase active at neutral and acidic pHs, is critical for fertilization of the oocyte by sperm.…”

Section: Ha Metabolism (Synthesis and Degradation) And Microenvironmementioning

confidence: 99%

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Hyaluronan biology: A complex balancing act of structure, function, location and context

2019

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Cell-matrix interactions are fundamental to many developmental, homeostatic, immune and pathologic processes. Hyaluronan (HA), a critical component of the extracellular matrix (ECM) that regulates normal structural integrity and development, also regulates tissue responses during injury, repair, and regeneration. Though simple in its primary structure, HA regulates biological responses in a highly complex manner with balanced contributions from its molecular size and concentration, synthesis versus enzymatic and/or oxidative-nitrative fragmentation, interactions with key HA binding proteins and cell associated receptors, and its cell context-specific signaling. This review highlights the different, but interrelated factors that dictate the biological activity of HA and introduces the overarching themes that weave throughout this special issue of Matrix Biology on hyaluronan.

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Section: Physical Properties Size and Molecular Weight Distributionmentioning

confidence: 99%

Section: Ha Metabolism (Synthesis and Degradation) And Microenvironmementioning

confidence: 99%

Hyaluronan biology: A complex balancing act of structure, function, location and context

2019

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“…The importance of HA in HSC homing and hematopoiesis was further examined using hyaluronan synthase ( Has1‐3 ) knockout mice [Goncharova et al, ], which confirmed previous reports. More recently, the role of HA has also been revealed in megakaryocyte maturation and proplatelet formation [Petrey et al, ]. Similar to HA, the glycoprotein TNC was shown to affect HSC migration, homing, distribution, adhesion, lineage commitment as well as reconstitution potential [Nakamura‐Ishizu et al, ; Ellis et al, ].…”

Section: Extracellular Matrix Moleculesmentioning

confidence: 99%

Niche Extracellular Matrix Components and Their Influence on HSC

et al. 2017

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Maintenance of hematopoietic stem cells (HSC) takes place in a highly specialized microenvironment within the bone marrow. Technological improvements, especially in the field of in vivo imaging, have helped unravel the complexity of the niche microenvironment and have completely changed the classical concept from what was previously believed to be a static supportive platform, to a dynamic microenvironment tightly regulating HSC homeostasis through the complex interplay between diverse cell types, secreted factors, extracellular matrix molecules, and the expression of different transmembrane receptors. To add to the complexity, non-protein based metabolites have also been recognized as a component of the bone marrow niche. The objective of this review is to discuss the current understanding on how the different extracellular matrix components of the niche regulate HSC fate, both during embryonic development and in adulthood. Special attention will be provided to the description of non-protein metabolites, such as lipids and metal ions, which contribute to the regulation of HSC behavior. J. Cell. Biochem. 118: 1984-1993, 2017. © 2017 Wiley Periodicals, Inc.

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“…Hyal2 -deficient mice exhibit accumulation of extremely large HA molecules in tissues and in circulation, and this contributes to the development of chronic thrombotic microangiopathy (Onclinx et al, 2015) and mild craniofacial and vertebral abnormalities (Bourguignon and Flamion, 2016). Megakaryocyte-derived HYAL-2 causes HA degradation, which is needed for thrombopoiesis (Petrey et al, 2016). HYAL-3 lacks an intrinsic hyaluronidase activity in somatic cells in vivo , whereas it participates in the hyaluronan metabolism by augmenting the activity of HYAL-1 (Hemming et al, 2008).…”

Section: Hyaluronidases and Clinical Relevance And Applicationsmentioning

confidence: 99%

HYAL-2–WWOX–SMAD4 Signaling in Cell Death and Anticancer Response

Hsu

Chiang

Sze

et al. 2016

Front. Cell Dev. Biol.

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Hyaluronidase HYAL-2 is a membrane-anchored protein and also localizes, in part, in the lysosome. Recent study from animal models revealed that both HYAL-1 and HYAL-2 are essential for the metabolism of hyaluronan (HA). Hyal-2 deficiency is associated with chronic thrombotic microangiopathy with hemolytic anemia in mice due to over accumulation of high molecular size HA. HYAL-2 is essential for platelet generation. Membrane HYAL-2 degrades HA bound by co-receptor CD44. Also, in a non-canonical signal pathway, HYAL-2 serves as a receptor for transforming growth factor beta (TGF-β) to signal with downstream tumor suppressors WWOX and SMAD4 to control gene transcription. When SMAD4 responsive element is overly driven by the HYAL-2–WWOX–SMAD4 signaling complex, cell death occurs. When rats are subjected to traumatic brain injury, over accumulation of a HYAL-2–WWOX complex occurs in the nucleus to cause neuronal death. HA induces the signaling of HYAL-2–WWOX–SMAD4 and relocation of the signaling complex to the nucleus. If the signaling complex is overexpressed, bubbling cell death occurs in WWOX-expressing cells. In addition, a small synthetic peptide Zfra (zinc finger-like protein that regulates apoptosis) binds membrane HYAL-2 of non-T/non-B spleen HYAL-2+ CD3− CD19− Z lymphocytes and activates the cells to generate memory anticancer response against many types of cancer cells in vivo. Whether the HYAL-2–WWOX–SMAD4 signaling complex is involved is discussed. In this review and opinion article, we have updated the current knowledge of HA, HYAL-2 and WWOX, HYAL-2–WWOX–SMAD4 signaling, bubbling cell death, and Z cell activation for memory anticancer response.

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Hyaluronan Depolymerization by Megakaryocyte Hyaluronidase-2 Is Required for Thrombopoiesis

Cited by 19 publications

References 73 publications

Hyaluronan biology: A complex balancing act of structure, function, location and context

Hyaluronan biology: A complex balancing act of structure, function, location and context

Niche Extracellular Matrix Components and Their Influence on HSC

HYAL-2–WWOX–SMAD4 Signaling in Cell Death and Anticancer Response

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