Similarities in the Phenotypic Expression of Pericytes and Bone Cells

Reilly, Thomas M.; Seldes, Richard M.; Luchetti, Wayne; Brighton, Carl T.

doi:10.1097/00003086-199801000-00014

Cited by 84 publications

(66 citation statements)

References 43 publications

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“…29 Pericytes are cells in physical contact with capillary endothelial cells, with the ability to differentiate into numerous cell types, including osteoblasts. 14,101,133 These cells may serve as a supplementary source of osteoprogenitor cells 32 and may be more important in periosteal bone formation due to their greater abundance in periosteum 20 than in endosteal bone surface apposition. 14 Cultured pericytes mineralize in vitro and synthesize the osteoblast marker, alkaline phosphatase, as well as bone matrix proteins, including osteocalcin, 20 osteonectin, osteopontin, and bone sialoprotein.…”

Section: Microscopic Featuresmentioning

confidence: 99%

“…These cells form an osteogenic tissue that mimics bone-derived tissue, both spatially and temporally, 38 and responds to osteogenic stimuli, such as BMP and parathyroid hormone. 101 Sympathetic nervous fibers in this layer are much denser than in the bone. 74 Extracellular matrix and fibroblasts are less susceptible to histologic staining and this layer of the periosteum is less salient and is brighter, and together with zone I is called cambium (from Latin, meaning to exchange).…”

Section: Microscopic Featuresmentioning

confidence: 99%

See 1 more Smart Citation

RETRACTED: The periosteum

Augustin¹,

Antabak²,

Davila³

2007

Injury

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Section: Microscopic Featuresmentioning

confidence: 99%

Section: Microscopic Featuresmentioning

confidence: 99%

RETRACTED: The periosteum

Augustin¹,

Antabak²,

Davila³

2007

Injury

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“…A dye coupling assay demonstrated a functional coupling between the ECs and stromal cells. Some authors (39,40) have suggested that either vascular ECs or pericytes differentiate into osteoblasts or precursor cells, which means that vessels could directly participate in bone formation. Wound trauma causes mobilization of hematopoietic cells, including pluripotent stem or progenitor cells in spleen, bone marrow, and peripheral blood.…”

Section: Coupling Between Angiogenesis and Mineralizationmentioning

confidence: 99%

Angiogenesis and Mineralization During Distraction Osteogenesis

et al. 2002

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Distraction osteogenesis is currently a standard method of bone lengthening. It is a viable method for the treatment of short extremities as well as extensive bone defects, because large amounts of bone can be regenerated in the distraction gap. Mechanical stimulation by distraction induces biological responses of skeletal regeneration that is accomplished by a cascade of biologic processes that may include differentiation of pluripotential tissue, angiogenesis, mineralization, and remodeling. There are complex interactions between bone-forming osteoblasts and other cells present within the bone microenvironment, particularly vascular endothelial cells that may be pivotal members of a complex interactive communication network in bone. Regenerate bone forms by three modes of ossification, which include intramembranous, enchondral, and transchondroid ossifications, although intramembraneous bone formation is the predominant mechanism of ossification. In this review we discussed the coupling between angiogenesis and mineralization, the biological and mechanical factors affecting them, the cellular and molecular events occurring during distraction osteogenesis, and the emerging modalities to accelerate regenerate bone healing and remodeling.

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“…8,9 Moreover, these studies reconcile contradictory reports demonstrating the presence of MSCs in cortical bone, trabecular bone, periosteum, and the marrow/periosteal perivascular space. [10][11][12][13][14][15][16] Endochondral bone formation, homeostasis, and repair are highly orchestrated processes involving cellular proliferation, migration, differentiation, and apoptosis, as well as cross-talk between the growth plate, perichondrium/periosteum, cortical and trabecular bone, marrow stroma, and invading vasculature and hematopoietic cells. [17][18][19] In addition to mechanical, nervous, and endocrine stimulation, these events are largely mediated by soluble factors such as PDGF, TGF-␤, BMPs, Wnts, parathyroid hormonerelated protein (PTHrP), Indian hedgehog (Ihh), and FGFs, and their associated receptors.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of cellular senescence by developmentally regulated FGF receptors in mesenchymal stem cells

Coutu

François

Galipeau

2011

Blood

111

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IntroductionMesenchymal stem cells (MSCs) are stem/progenitor cells for bone, cartilage, and hematopoietic-supporting marrow stroma (including bone-lining cells, fibroblasts, reticulocytes, adipocytes, and pericytes). However, the fundamental study of these intriguing cells is currently limited by uncertainties regarding their ontology, in vivo identity, and developmental potential. This is complicated by the lack of molecular markers and standard isolation procedures and by difficulties in studying MSCs in mouse models. [1][2][3] Recently, 2 different studies provided evidence that undifferentiated mesenchymal cells are present in murine embryonic perichondrium during endochondral bone formation. [4][5][6][7] These cells were shown to adopt a pericyte identity while migrating from the perichondrium to colonize both the bone collar (cortical bone) and the primary spongiosa (trabecular bone). Moreover, these cells were shown to participate in fracture repair in postnatal bones. These observations are significant because they are the first to unambiguously demonstrate that perichondrium-derived cells participate in both cortical bone and trabecular bone formation and give rise to osteostromal progenitors that have a marrow perivascular niche, which was previously proposed for human MSCs. 8,9 Moreover, these studies reconcile contradictory reports demonstrating the presence of MSCs in cortical bone, trabecular bone, periosteum, and the marrow/periosteal perivascular space. [10][11][12][13][14][15][16] Endochondral bone formation, homeostasis, and repair are highly orchestrated processes involving cellular proliferation, migration, differentiation, and apoptosis, as well as cross-talk between the growth plate, perichondrium/periosteum, cortical and trabecular bone, marrow stroma, and invading vasculature and hematopoietic cells. [17][18][19] In addition to mechanical, nervous, and endocrine stimulation, these events are largely mediated by soluble factors such as PDGF, TGF-␤, BMPs, Wnts, parathyroid hormonerelated protein (PTHrP), Indian hedgehog (Ihh), and FGFs, and their associated receptors. The FGF family comprises 22 ligands displaying high levels of homology, redundancy, and promiscuity. There are 4 known FGF receptors (FGFRs) expressed as multiple splice variants, and 3 of them are involved in bone formation: FGFR1, FGFR2, and FGFR3. FGFs/FGFRs are expressed in a tissue-specific manner, are developmentally regulated, and are crucial for bone formation, maintenance, and repair. 20 However, the large number of ligands and receptor isoforms, as well as their redundancy and promiscuity, makes the study of their roles in endochondral bone formation a particular challenge. The mitogenic effect of FGF-2 on MSCs in vitro has long been observed, and studies have also shown that FGF-2 promotes undifferentiated proliferation of MSCs in vitro. [21][22][23][24][25] However, given the importance of FGFs/FGFRs in bone, it is surprising that this system has not yet been described in more detail in MSCs.In the present study, ...

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Similarities in the Phenotypic Expression of Pericytes and Bone Cells

Cited by 84 publications

References 43 publications

RETRACTED: The periosteum

RETRACTED: The periosteum

Angiogenesis and Mineralization During Distraction Osteogenesis

Inhibition of cellular senescence by developmentally regulated FGF receptors in mesenchymal stem cells

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