scholarly journals Expression of connective tissue growth factor in bone: Its role in osteoblast proliferation and differentiation in vitro and bone formation in vivo

2003 ◽  
Vol 196 (1) ◽  
pp. 51-62 ◽  
Author(s):  
Fayez F. Safadi ◽  
Jie Xu ◽  
Steven L. Smock ◽  
Reem A. Kanaan ◽  
Abdul-Hafez Selim ◽  
...  
Keyword(s):  
Growth Factor ◽  
Connective Tissue ◽  
Bone Formation ◽  
Connective Tissue Growth Factor ◽  
Tissue Growth ◽  
Osteoblast Proliferation ◽  
Proliferation And Differentiation

scholarly journals Acceleration of Osteogenesis via Stimulation of Angiogenesis by Combination with Scaffold and Connective Tissue Growth Factor

Materials ◽  
2019 ◽  
Vol 12 (13) ◽  
pp. 2068 ◽  
Author(s):  
Michiyo Honda ◽  
Ryo Hariya ◽  
Morio Matsumoto ◽  
Mamoru Aizawa
Keyword(s):  
Growth Factor ◽  
Connective Tissue ◽  
Connective Tissue Growth Factor ◽  
Cell Interaction ◽  
Tissue Growth ◽  
Matrix Remodeling ◽  
Bioactive Materials ◽  
Stimulation Of

In bone regeneration, there are some important cellular biological processes, such as mineralization, cell organization, and differentiation. In particular, vascularization into regenerative tissues is a key step for the survival of cells and tissues. In this study, to fabricate biomimetic-engineered bone, including vascular networks, we focused on connective tissue growth factor (CTGF), a multifunctional protein which could regulate the extracellular matrix remodeling. By combination with CTGF and hydroxyapatite (HAp) ceramics (2D) or apatite-fiber scaffold (AFS, 3D), we have fabricated bioactive materials. The CTGF-loaded HAp ceramics could enhance the cellular attachment through interaction with integrin and promote actin cytoskeletal reorganization. CTGF-loaded HAp also enhanced the differentiation of osteoblasts by integrin-mediated activation of the signaling pathway. Under co-culture conditions, both osteoblasts and endothelial cells in the CTGF-loaded AFS were stimulated by CTGF, and each cell could penetrate the central region of the scaffold in vitro and in vivo. Direct cell-cell interaction would also improve the functionality of cells in bone formation. These results suggest that coupling between effective optimized scaffold and CTGF with multifunction could provide better mimicking natural bone by stimulation of angiogenesis.

scholarly journals Connective tissue growth factor causes EMT-like cell fate changes in vivo and in vitro

2013 ◽  
Vol 126 (10) ◽  
pp. 2164-2175 ◽  
Author(s):  
S. Sonnylal ◽  
S. Xu ◽  
H. Jones ◽  
A. Tam ◽  
V. R. Sreeram ◽  
...  
Keyword(s):  
Growth Factor ◽  
Connective Tissue ◽  
Cell Fate ◽  
Connective Tissue Growth Factor ◽  
Tissue Growth

scholarly journals Connective tissue growth factor promotes chemotaxis of preosteoblasts through integrin α5 and Ras during tensile force-induced intramembranous osteogenesis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Wei Jiang ◽  
Nobuo Takeshita ◽  
Toshihiro Maeda ◽  
Chisumi Sogi ◽  
Toshihito Oyanagi ◽  
...  
Keyword(s):  
Growth Factor ◽  
Connective Tissue ◽  
Bone Formation ◽  
Connective Tissue Growth Factor ◽  
Tensile Force ◽  
Tissue Growth ◽  
New Bone Formation ◽  
Integrin Α5 ◽  
Osteoblast Lineage

AbstractIn vertebrates, new bone formation via intramembranous osteogenesis is a critical biological event for development, remodeling, and fracture healing of bones. Chemotaxis of osteoblast lineage cells is an essential cellular process in new bone formation. Connective tissue growth factor (CTGF) is known to exert chemotactic properties on various cells; however, details of CTGF function in the chemotaxis of osteoblast lineage cells and underlying molecular biological mechanisms have not been clarified. The aim of the present study was to evaluate the chemotactic properties of CTGF and its underlying mechanisms during active bone formation through intramembranous osteogenesis. In our mouse tensile force-induced bone formation model, preosteoblasts were aggregated at the osteogenic front of calvarial bones. CTGF was expressed at the osteogenic front, and functional inhibition of CTGF using a neutralizing antibody suppressed the aggregation of preosteoblasts. In vitro experiments using μ-slide chemotaxis chambers showed that a gradient of CTGF induced chemotaxis of preosteoblastic MC3T3-E1 cells, while a neutralizing integrin α5 antibody and a Ras inhibitor inhibited the CTGF-induced chemotaxis of MC3T3-E1 cells. These findings suggest that the CTGF-integrin α5-Ras axis is an essential molecular mechanism to promote chemotaxis of preosteoblasts during new bone formation through intramembranous osteogenesis.

Connective tissue growth factor/CCN-2 is upregulated in epididymal and subcutaneous fat depots in a dietary-induced obesity model

2013 ◽  
Vol 304 (12) ◽  
pp. E1291-E1302 ◽  
Author(s):  
Joanne T. M. Tan ◽  
Susan V. McLennan ◽  
Paul F. Williams ◽  
Alireza Rezaeizadeh ◽  
Lisa W.-Y. Lo ◽  
...  
Keyword(s):  
Growth Factor ◽  
Connective Tissue ◽  
Connective Tissue Growth Factor ◽  
Adipocyte Differentiation ◽  
Subcutaneous Fat ◽  
Tissue Growth ◽  
Mrna Levels ◽  
Fat Depots

Connective tissue growth factor (CTGF), also known as CCN-2, is a cysteine-rich secreted protein that is involved in a range of biological processes, including regulation of cell growth and differentiation. Our previous in vitro studies have shown that CCN-2 inhibits adipocyte differentiation, although whether CCN-2 is regulated in vivo in adipogenesis is undetermined and was investigated in this study. C57BL/6 male mice were fed either standard laboratory chow (ND) or a diet high in fat (HFD; 45% fat) for 15 or 24 wk. HFD animals that gained >5 g in weight (termed HFD-fat) were insulin resistant and were compared with HFD-fed animals, which failed to gain weight (termed HFD-lean). HFD-fat mice had significantly increased CCN-2 mRNA levels in both the subcutaneous and epididymal fat pads, whereas CCN-2 mRNA was not induced in the epididymal site in HFD-lean mice. Also in HFD-fed animals, epididymal CCN-2 mRNA correlated positively with key genes involved in adipocyte differentiation, adiponectin and PPARγ ( P < 0.001 and P < 0.002, respectively). Additionally, epididymal CCN-2 mRNA correlated positively with two markers of tissue turnover, PAI-1 in HFD-fat mice only and TIMP-1, but only in the HFD-lean mice. Collectively, these findings suggest that CCN-2 plays a role in adipocyte differentiation in vivo and thus in the pathogenesis of obesity linked with insulin resistance.

scholarly journals Connective-Tissue Growth Factor (CTGF/CCN2) Induces Astrogenesis and Fibronectin Expression of Embryonic Neural Cells In Vitro

PLoS ONE ◽  
2015 ◽  
Vol 10 (8) ◽  
pp. e0133689 ◽  
Author(s):  
Fabio A. Mendes ◽  
Juliana M. Coelho Aguiar ◽  
Suzana A. Kahn ◽  
Alice H. Reis ◽  
Luiz Gustavo Dubois ◽  
...  
Keyword(s):  
Growth Factor ◽  
Connective Tissue ◽  
Connective Tissue Growth Factor ◽  
Tissue Growth ◽  
Neural Cells ◽  
Fibronectin Expression

scholarly journals CCN2 (Connective Tissue Growth Factor) Promotes Fibroblast Adhesion to Fibronectin

2004 ◽  
Vol 15 (12) ◽  
pp. 5635-5646 ◽  
Author(s):  
Yunliang Chen ◽  
David J. Abraham ◽  
Xu Shi-wen ◽  
Jeremy D. Pearson ◽  
Carol M. Black ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Growth Factor ◽  
Protein Kinase ◽  
Connective Tissue ◽  
Connective Tissue Growth Factor ◽  
Tissue Growth ◽  
Mitogen Activated Protein Kinase ◽  
Mitogen Activated Protein ◽  
Fibroblast Adhesion

In vivo, CCN2 (connective tissue growth factor) promotes angiogenesis, osteogenesis, tissue repair, and fibrosis, through largely unknown mechanisms. In vitro, CCN2 promotes cell adhesion in a variety of systems via integrins and heparin sulfate proteoglycans (HSPGs). However, the physiological relevance of CCN2-mediated cell adhesion is unknown. Here, we find that HSPGs and the mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase cascade are required for adult human dermal fibroblasts to adhere to CCN2. Endogenous CCN2 directly binds fibronectin and the fibronectin receptors integrins α4 β1 and α5 and syndecan 4. Using Ccn2-/- mouse embryonic fibroblasts, we show that loss of endogenous CCN2 results in impaired spreading on fibronectin, delayed α-smooth muscle actin stress fiber formation, and reduced ERK and focal adhesion kinase phosphorylation. These results suggest that a physiological role of CCN2 is to potentiate the ability of fibroblasts to spread on fibronectin, which may be important in modulating fibroblast adhesion to the provisional matrix during tissue development and wound healing. These results are consistent with the notion that a principal function of CCN2 is to modulate receptor/ligand interactions in vivo.

scholarly journals Keratinocytes Inhibit Expression of Connective Tissue Growth Factor in Fibroblasts In Vitro by an Interleukin-1α-Dependent Mechanism

2002 ◽  
Vol 119 (2) ◽  
pp. 449-455 ◽  
Author(s):  
Daniel Nowinski ◽  
Patrik Höijer ◽  
Thomas Engstrand ◽  
Bengt Gerdin ◽  
Mikael Ivarsson ◽  
...  
Keyword(s):  
Growth Factor ◽  
Connective Tissue ◽  
Connective Tissue Growth Factor ◽  
Tissue Growth ◽  
Interleukin 1Α ◽  
Dependent Mechanism
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