CCN1 Promotes VEGF Production in Osteoblasts and Induces Endothelial Progenitor Cell Angiogenesis by Inhibiting miR-126 Expression in Rheumatoid Arthritis

Chen, Cheng-Yu; Su, Chen-Ming; Hsu, Chin‐Jung; Huang, Chien-Chung; Wang, Shih‐Wei; Liu, Shih‐Chia; Chen, Wei-Cheng; Fuh, Lih‐Jyh; Tang, Chih-Hsin

doi:10.1002/jbmr.2926

Cited by 71 publications

(78 citation statements)

References 44 publications

(59 reference statements)

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“…Mononuclear cells were isolated from blood components by centrifugation on Ficoll-Paque plus (Amersham Biosciences, Uppala, Sweden). EPCs were characterized and maintained using methods described in our previous reports [9,40]. …”

Section: Methodsmentioning

confidence: 99%

“…In vivo angiogenic activity was evaluated by CAM assay, as described in our previous reports [9,38,39]. Data were examined by microscopy and photographed using a digital camera.…”

Section: Methodsmentioning

confidence: 99%

“…The Matrigel plug angiogenesis assay was used, as described in our previous reports [9,38,39]. BALB/c male nude mice (National Laboratory Animal Center, Taipei, Taiwan) were subcutaneously injected with Matrigel containing osteoblast CM.…”

Section: Methodsmentioning

confidence: 99%

“…While the dynamics of synovial inflammation and cartilage destruction are well-documented, increasing evidence suggests that subchondral bone plays a role in pathogenesis of RA [5,6]. Increasing evidence indicates that osteoblasts in subchondral bone are involved in arthritis development, which regulates many pathological cellular processes including monocyte infiltration, inflammatory cytokine release, and angiogenesis [7,8,9]. An understanding of the normal functions that regulate subchondral bone integrity in arthritis is important for more effective therapeutic strategies in arthritis.…”

Section: Introductionmentioning

confidence: 99%

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YKL-40-Induced Inhibition of miR-590-3p Promotes Interleukin-18 Expression and Angiogenesis of Endothelial Progenitor Cells

Liu

Huang

et al. 2017

IJMS

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YKL-40, also known as human cartilage glycoprotein-39 or chitinase-3-like-1, is a pro-inflammatory protein that is highly expressed in rheumatoid arthritis (RA) patients. Angiogenesis is a critical step in the pathogenesis of RA, promoting the infiltration of inflammatory cells into joints and providing oxygen and nutrients to RA pannus. In this study, we examined the effects of YKL-40 in the production of the pro-inflammatory cytokine interleukin-18 (IL-18), and the stimulation of angiogenesis and accumulation of osteoblasts. We observed that YKL-40 induces IL-18 production in osteoblasts and thereby stimulates angiogenesis of endothelial progenitor cells (EPCs). We found that this process occurs through the suppression of miR-590-3p via the focal adhesion kinase (FAK)/PI3K/Akt signaling pathway. YKL-40 inhibition reduced angiogenesis in in vivo models of angiogenesis: the chick embryo chorioallantoic membrane (CAM) and Matrigel plug models. We report that YKL-40 stimulates IL-18 expression in osteoblasts and facilitates EPC angiogenesis.

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Section: Methodsmentioning

confidence: 99%

“…In vivo angiogenic activity was evaluated by CAM assay, as described in our previous reports [9,38,39]. Data were examined by microscopy and photographed using a digital camera.…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

YKL-40-Induced Inhibition of miR-590-3p Promotes Interleukin-18 Expression and Angiogenesis of Endothelial Progenitor Cells

Liu

Huang

et al. 2017

IJMS

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“…Adiponectin induces ostoblast production of mediators that drive synovitis and joint destruction such as matrix metallo-proteinase-1 (MMP-1) and MMP-13, and vascular endothelial growth factor (VEGF) [44,45]. Recently, Chen et al [46] have observed that the pro-inflammatory cytokine Cysteine-rich 61 (Cyr61 or CCN1), a secreted protein from the CCN family, induces VEGF expression in osteoblasts and increases endothelial progenitor cells angiogenesis in RA. Adiponectin is also involved in RA bone remodeling by inhibiting Osx and inducing OPG expression in osteoblasts [44].…”

Section: Osteoblast Role In Ramentioning

confidence: 99%

Osteoblast Role in Rheumatic Diseases

Corrado¹,

Maruotti²,

Cantatore³

2017

IJMS

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Alterations in osteoblast growth, differentiation and activity play a role in the pathogenesis of several rheumatic diseases, such as rheumatoid arthritis, spondyloarthritides, osteoarthritis, and osteoporosis. In fact, in these rheumatic diseases, abnormal activity of Wnt signaling, receptor activator of nuclear factor-κB (RANK)-RANK ligand (RANKL)-osteoprotegerin (OPG) signaling, bone morphogenetic proteins (BMPs) pathway and other mechanisms have been described in osteoblasts. This review article is focused on current knowledge on the role of osteoblast dysregulation occurring in rheumatic diseases.

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DDR2–CYR61–MMP1 Signaling Pathway Promotes Bone Erosion in Rheumatoid Arthritis Through Regulating Migration and Invasion of Fibroblast-Like Synoviocytes

Huang

et al. 2016

Journal of Bone and Mineral Research

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Regulation of matrix metalloproteinases (MMPs) by collagen in the fibroblast-like synoviocytes (FLSs) plays a critical role in joint destruction in rheumatoid arthritis (RA). Our previous study indicated that discoidin receptor 2 (DDR2) mediated collagen upregulation of MMPs. However, the precise underlying mechanism remains unclear. We report here that CYR61, a secreted, extracellular matrix-associated signaling protein which is capable of regulating a broad range of cellular activities, including cell adhesion, migration, proliferation, and apoptosis, is significantly upregulated in collagen II-stimulated RA FLS. Further studies found that collagen II-activated phosphorylated-DDR2 induces CYR61 through activation of transcription factor activator protein 1 (AP-1). The elevated CYR61, in turn, accelerates MMP1 production via ETS1 (ETS proto-oncogene 1). In addition, CYR61 significantly promotes FLS invasion and migration. Blockade of CYR61 by an adenovirus expressing CYR61 shRNA (Ad-shCYR61) in vivo remarkably ameliorated the severity of arthritis, reduced inflammatory cytokine secretion, and attenuated bone erosion as detected by micro-computed tomography (μCT), in collagen-induced arthritis (CIA) rats. Taken together, we uncovered the Collagen II-DDR2-AP-1-CYR61-ETS1-MMP1 loop in RA FLS. In which, CYR61 acts as a hinge to promote cartilage damage through regulating FLS invasion, migration, and MMP1 production and the inflammatory cascade in RA. Thus, CYR61 may be a promising diagnostic and therapeutic target for RA treatment. © 2016 American Society for Bone and Mineral Research.

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CCN1 Promotes VEGF Production in Osteoblasts and Induces Endothelial Progenitor Cell Angiogenesis by Inhibiting miR-126 Expression in Rheumatoid Arthritis

Abstract: Angiogenesis is the formation of new capillaries from preexisting vasculature.

Cited by 71 publications

References 44 publications

YKL-40-Induced Inhibition of miR-590-3p Promotes Interleukin-18 Expression and Angiogenesis of Endothelial Progenitor Cells

YKL-40-Induced Inhibition of miR-590-3p Promotes Interleukin-18 Expression and Angiogenesis of Endothelial Progenitor Cells

Osteoblast Role in Rheumatic Diseases

DDR2–CYR61–MMP1 Signaling Pathway Promotes Bone Erosion in Rheumatoid Arthritis Through Regulating Migration and Invasion of Fibroblast-Like Synoviocytes

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