Osteopontin: a bridge between bone and blood

Haylock, David N.; Nilsson, Susan K.

doi:10.1111/j.1365-2141.2006.06218.x

Cited by 129 publications

(90 citation statements)

References 90 publications

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“…Osteopontin (OPN), a secreted matrix glycoprotein, is produced in BM stroma by pre‐osteoblasts, osteoblasts and osteocytes (Nilsson et al , 2005; Grassinger et al , 2009). In young mice, OPN regulates HSC pool size, stem cell homing, trans‐marrow migration and engraftment (Nilsson et al , 2005; Stier et al , 2005; Haylock & Nilsson, 2006; Grassinger et al , 2009). Here, we report that OPN is reduced in aged stroma and that reduced OPN levels confer aging‐associated phenotypes on HSCs.…”

Section: Introductionmentioning

confidence: 99%

Osteopontin attenuates aging‐associated phenotypes of hematopoietic stem cells

et al. 2017

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Upon aging, hematopoietic stem cells (HSCs) undergo changes in function and structure, including skewing to myeloid lineages, lower reconstitution potential and loss of protein polarity. While stem cell intrinsic mechanisms are known to contribute to HSC aging, little is known on whether age‐related changes in the bone marrow niche regulate HSC aging. Upon aging, the expression of osteopontin (OPN) in the murine bone marrow stroma is reduced. Exposure of young HSCs to an OPN knockout niche results in a decrease in engraftment, an increase in long‐term HSC frequency and loss of stem cell polarity. Exposure of aged HSCs to thrombin‐cleaved OPN attenuates aging of old HSCs, resulting in increased engraftment, decreased HSC frequency, increased stem cell polarity and a restored balance of lymphoid and myeloid cells in peripheral blood. Thus, our data suggest a critical role for reduced stroma‐derived OPN for HSC aging and identify thrombin‐cleaved OPN as a novel niche informed therapeutic approach for ameliorating HSC phenotypes associated with aging.

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Section: Introductionmentioning

confidence: 99%

Osteopontin attenuates aging‐associated phenotypes of hematopoietic stem cells

et al. 2017

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“…OPN has long attracted the interest of immunologists because of its many functions in inflammation, immunopathology, and hematopoiesis (73)(74)(75)(76)(77)(78). Its expression is increased in response to cell injury or infections and is induced by a variety of proinflammatory mediators and growth factors such as IL-1, TNF-a, and plateletderived growth factor (79).…”

Section: Discussionmentioning

confidence: 99%

Tumor-Conditioned Macrophages Secrete Migration-Stimulating Factor: A New Marker for M2-Polarization, Influencing Tumor Cell Motility

Solinas

Schiarea

Liguori

et al. 2010

The Journal of Immunology

343

292

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Tumor-associated macrophages (TAMs) are key orchestrators of the tumor microenvironment directly affecting neoplastic cell growth, neoangiogenesis, and extracellular matrix remodeling. In turn, the tumor milieu strongly influences maturation of TAMs and shapes several of their features. To address the early macrophage (Mϕ) differentiation phase in a malignant context, we mimicked a tumor microenvironment by in vitro coculturing human blood monocytes with conditioned media from different cancer cell lines. Only 2 out of 16 tumor cell lines induced Mϕ differentiation due to secreted M-CSF isoforms, including high molecular mass species. A global gene profiling of tumor-conditioned Mϕ was performed. Comparison with other datasets (polarized M1-Mϕ, M2-Mϕ, and TAMs isolated from human tumors) highlighted the upregulation of several genes also shared by TAM and M2-polarized Mϕ. The most expressed genes were selenoprotein 1, osteoactivin, osteopontin, and, interestingly, migration-stimulating factor (MSF), a poorly studied oncofoetal isoform of fibronectin. MSF (present in fetal/cancer epithelial and stromal cells but not in healthy tissues) was never identified in Mϕ. MSF production was confirmed by immunohistochemistry in human TAMs. MSF was induced by M-CSF, IL-4, and TGFβ but not by proinflammatory stimuli. RNA and protein analysis clearly demonstrated that it is specifically associated with the M2 polarization of Mϕ. Tumor-conditioned Mϕ-derived MSFs strongly stimulated tumor cell migration, thus contributing to the motile phenotype of neoplastic cells. In conclusion, MSF is a new molecule associated with the M2 polarization of Mϕ and expressed by TAMs. Its biological function may contribute to Mϕ-mediated promotion of cancer cell invasion and metastasis.

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“…Having much more extensively characterized the temporospatial gene expression profile of the developing and adult kidney, the time is ripe for a more an extension of such analyses into distinct renal disease states. For example, osteopontin (Spp1), a key gene in the hematopoietic niche, 50 marks the S3 segment of the proximal tubules of the developing and adult kidney at rest (Fig. 4).…”

confidence: 99%

Renal organogenesis

Little

2011

Organogenesis

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Osteopontin: a bridge between bone and blood

Cited by 129 publications

References 90 publications

Osteopontin attenuates aging‐associated phenotypes of hematopoietic stem cells

Osteopontin attenuates aging‐associated phenotypes of hematopoietic stem cells

Tumor-Conditioned Macrophages Secrete Migration-Stimulating Factor: A New Marker for M2-Polarization, Influencing Tumor Cell Motility

Renal organogenesis

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