Fibroblast growth factor expression in the postnatal growth plate

Lazarus, Jacob E.; Hegde, Anita; Andrade, Anenisia C.; Nilsson, Ola; Baron, Jeffrey

doi:10.1016/j.bone.2006.10.013

Cited by 104 publications

(90 citation statements)

References 49 publications

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“…Furthermore, FGF2 and its receptor, FGFR2, were also found to be highly induced during chondrogenesis of committed Kp-hMSCs. In accordance with the findings from previous studies, FGF2 and FGFRs cooperatively contribute to growth plate development, and thus are determining factors in the adult skeleton (48).…”

Section: Discussionsupporting

confidence: 92%

In vitro stage‐specific chondrogenesis of mesenchymal stem cells committed to chondrocytes

Chen

Lai

et al. 2009

Arthritis & Rheumatism

110

118

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Objective. Osteoarthritis is characterized by an imbalance in cartilage homeostasis, which could potentially be corrected by mesenchymal stem cell (MSC)-based therapies. However, in vivo implantation of undifferentiated MSCs has led to unexpected results. This study was undertaken to establish a model for preconditioning of MSCs toward chondrogenesis as a more effective clinical tool for cartilage regeneration.Methods. A coculture preconditioning system was used to improve the chondrogenic potential of human MSCs and to study the detailed stages of chondrogenesis of MSCs, using a human MSC line, Kp-hMSC, in commitment cocultures with a human chondrocyte line, hPi (labeled with green fluorescent protein [GFP]). In addition, committed MSCs were seeded into a collagen scaffold and analyzed for their neocartilage-forming ability.Results. Coculture of hPi-GFP chondrocytes with Kp-hMSCs induced chondrogenesis, as indicated by the increased expression of chondrogenic genes and accumulation of chondrogenic matrix, but with no effect on osteogenic markers. The chondrogenic process of committed MSCs was initiated with highly activated chondrogenic adhesion molecules and stimulated cartilage developmental growth factors, including members of the transforming growth factor ␤ superfamily and their downstream regulators, the Smads, as well as endothelial growth factor, fibroblast growth factor, insulin-like growth factor, and vascular endothelial growth factor. Furthermore, committed Kp-hMSCs acquired neocartilageforming potential within the collagen scaffold. Osteoarthritis (OA), one of the most common musculoskeletal diseases, has been ascribed to an imbalance in cartilage homeostasis in the aging process (1,2). Hyaline cartilage has little capacity for self-repair. As a result, continuous mechanical stress can lead to the degradation of articular cartilage, culminating in a vicious cycle of destructive processes (3). Many therapeutic interventions directed at the restoration of the reparative capacity of chondrocytes have been explored (3-5). One of the emerging approaches is cell-based therapy, in which expanded chondrocytes are used for cartilage repair. However, the outcome of this approach has been disappointing, due to the difficulties in maintaining chondrocytic phenotypes and the decrease in proliferative capacity of autologous chondrocytes with increasing age (1,6,7). Conclusion. These findings help define the molecular markers of chondrogenesis and more accuratelyCell therapy based on autologous mesenchymal stem cells (MSCs), which have a vast proliferative ca-

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Section: Discussionsupporting

confidence: 92%

In vitro stage‐specific chondrogenesis of mesenchymal stem cells committed to chondrocytes

Chen

Lai

et al. 2009

Arthritis & Rheumatism

110

118

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“…None of the other identified cell surface markers (Fgfr3, (44) Pthr1, (45) or TrkB) was suitable for cell-sorting experiments. No signals were detected in immunofluorescence or flow cytometric studies.…”

Section: Discussionmentioning

confidence: 99%

Sorting of growth plate chondrocytes allows the isolation and characterization of cells of a defined differentiation status

Belluoccio¹,

Etich²,

Rosenbaum³

et al. 2010

Journal of Bone and Mineral Research

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Axial growth of long bones occurs through a coordinated process of growth plate chondrocyte proliferation and differentiation. This maturation of chondrocytes is reflected in a zonal change in gene expression and cell morphology from resting to proliferative, prehypertrophic, and hypertrophic chondrocytes of the growth plate followed by ossification. A major experimental limitation in understanding growth plate biology and pathophysiology is the lack of a robust technique to isolate cells from the different zones, particularly from small animals. Here, we report on a new strategy for separating distinct chondrocyte populations from mouse growth plates. By transcriptome profiling of microdissected zones of growth plates, we identified novel, zone-specific cell surface markers and used these for flow cytometry and immunomagnetic cell separation to quantify, enrich, and characterize chondrocytes populations with respect to their differentiation status. This approach provides a novel platform to study cartilage development and characterize mouse growth plate chondrocytes to reveal unique cellular phenotypes of the distinct subpopulations within the growth plate. ß

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“…However, FGF9 and FGF18 are good candidates because both are expressed in the adjacent perichondrium (Liu et al 2002;Ohbayashi et al 2002;Hung et al 2007), and FGF18 is also expressed at low levels by growth plate chondrocytes (Lazarus et al 2007). In addition, both ligands are known to activate FGFR3 in vitro (Zhang et al 2006).…”

Section: Fgfmentioning

confidence: 99%

Development of the Endochondral Skeleton

Long

Ornitz

2013

Cold Spring Harbor Perspectives in Biology

491

493

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SUMMARYMuch of the mammalian skeleton is composed of bones that originate from cartilage templates through endochondral ossification. Elucidating the mechanisms that control endochondral bone development is critical for understanding human skeletal diseases, injury response, and aging. Mouse genetic studies in the past 15 years have provided unprecedented insights about molecules regulating chondrocyte formation, chondrocyte maturation, and osteoblast differentiation, all key processes of endochondral bone development. These include the roles of the secreted proteins IHH, PTHrP, BMPs, WNTs, and FGFs, their receptors, and transcription factors such as SOX9, RUNX2, and OSX, in regulating chondrocyte and osteoblast biology. This review aims to integrate the known functions of extracellular signals and transcription factors that regulate development of the endochondral skeleton.

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Fibroblast growth factor expression in the postnatal growth plate

Cited by 104 publications

References 49 publications

In vitro stage‐specific chondrogenesis of mesenchymal stem cells committed to chondrocytes

In vitro stage‐specific chondrogenesis of mesenchymal stem cells committed to chondrocytes

Sorting of growth plate chondrocytes allows the isolation and characterization of cells of a defined differentiation status

Development of the Endochondral Skeleton

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