Basic Fibroblast Growth Factor Induces Cyclooxygenase-2 Expression in Endothelial Cells Derived from Bone

Kage, Kumie; Fujita, Naoya; Oh‐hara, Tomoko; Ogata, Etsuro; Fujita, Toshiro; Tsuruo, Takashi

doi:10.1006/bbrc.1998.9875

Cited by 54 publications

(44 citation statements)

References 31 publications

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“…We previously established bone-derived endothelial cells (BDECs) to study their roles in bone disease (13). We found that they play an important role in bone metabolism by producing IL-11 and PGE 2 (13,14). These facts indicate that endothelial cells in bone play an important role in osteoclastogenesis.…”

mentioning

confidence: 66%

“…COX-1 is constitutively expressed, and COX-2 is inducibly expressed by a variety of mitogen and inflammatory stimuli (25)(26)(27)(28). It is also reported that COX-2 is up-regulated in BDECs by cytokine stimulation such as IL-1␣ and basic fibroblast growth factor (14). Moreover, TGF-␤ was seen to stimulates COX-2 expression and PGE 2 release in a few cell types (29,30).…”

Section: Fig 2 Tgf-␤ Up-regulates Rankl Expression In Huvecsmentioning

confidence: 96%

“…Hence, it is possible that bone endothelial cells participate in the regulation of bone remodeling as osteoblasts. After establishing BDECs, we found that they promoted bone resorption in vitro by secreting IL-11 (13) or PGE 2 (14) in response to several osteotropic factors. Recently, RANKL was cloned from stromal and osteoblasts and has been reported to be essential for osteoclastogenesis (3).…”

Section: Tgf-␤ Induces Rankl Mrna and Protein Expression In Endothelialmentioning

confidence: 99%

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Transforming Growth Factor-β Induces Expression of Receptor Activator of NF-κB Ligand in Vascular Endothelial Cells Derived from Bone

Ishida¹,

Fujita²,

Kitazawa³

et al. 2002

Journal of Biological Chemistry

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Vascular endothelial cells in bone are thought to have significant roles on pathological bone resorption such as bone metastasis and hypercalcemia because this resorption is often seen where blood vessels are abundant. However, the detailed mechanisms have not yet been elucidated. Here, we focused on transforming growth factor-␤ (TGF-␤) and studied its effects on vascular endothelial cells because TGF-␤ is abundantly stored in bone matrix and is released and activated during bone resorption. We found that TGF-␤ up-regulated the expression of receptor activator of NF-B ligand (RANKL) mRNA and protein in bone marrow-derived endothelial cells and in primary vascular endothelial cells but not in osteoblasts. Further analysis revealed that TGF-␤ promoted phosphorylation of cAMP response element-binding protein and p38. Protein kinase A inhibitor KT5720 and p38 inhibitor SB203580 significantly reduced the TGF-␤-induced RANKL expression. Moreover, we found two CRE-like domains in murine RANKL promoter region that were critical for TGF-␤-dependent RANKL expression. Therefore, protein kinase A and p38 signaling pathways are involved in TGF-␤-induced RANKL expression by stimulating transcription factors that bind to the CRE-like domains. Our findings indicate that TGF-␤ stimulates osteoclastogenesis by promoting RANKL expression in endothelial cells under pathological conditions.

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mentioning

confidence: 66%

Section: Fig 2 Tgf-␤ Up-regulates Rankl Expression In Huvecsmentioning

confidence: 96%

Section: Tgf-␤ Induces Rankl Mrna and Protein Expression In Endothelialmentioning

confidence: 99%

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Transforming Growth Factor-β Induces Expression of Receptor Activator of NF-κB Ligand in Vascular Endothelial Cells Derived from Bone

Ishida¹,

Fujita²,

Kitazawa³

et al. 2002

Journal of Biological Chemistry

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“…Transient exposure to FGF1 and FGF2 upregulates the expression of cell adhesion molecules ICAM-1 and VCAM-1 in endothelial cells, increasing polymorphonuclear leukocyte adhesion and transendothelial migration [223]. Also, FGF2-stimulated endothelial cells upregulate the synthesis of various chemoattractants, including VEGF, that may exert a chemotactic activity on monocytes [224], the angiogenic/monocyte chemotactic protein osteopontin [225], monocyte chemoattractant protein-1 [107,226], and the proangiogenic cyclooxygenase-2 [227]. Moreover, FGF2 exerts a direct chemotactic effect on monocytes (Presta, unpublished observations).…”

Section: Fgf-dependent Angiogenesis and Inflammationmentioning

confidence: 99%

Fibroblast growth factor/fibroblast growth factor receptor system in angiogenesis

Presta

Dell’Era

Mitola

et al. 2005

Cytokine & Growth Factor Reviews

1,120

870

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Fibroblast growth factors (FGFs) are a family of heparin-binding growth factors. FGFs exert their pro-angiogenic activity by interacting with various endothelial cell surface receptors, including tyrosine kinase receptors, heparan-sulfate proteoglycans, and integrins. Their activity is modulated by a variety of free and extracellular matrix-associated molecules. Also, the cross-talk among FGFs, vascular endothelial growth factors (VEGFs), and inflammatory cytokines/chemokines may play a role in the modulation of blood vessel growth in different pathological conditions, including cancer. Indeed, several experimental evidences point to a role for FGFs in tumor growth and angiogenesis. This review will focus on the relevance of the FGF/FGF receptor system in adult angiogenesis and its contribution to tumor vascularization. #

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“…57 Interestingly, VEGF and bFGF induce COX-2 and subsequent prostaglandin production in endothelial cells, suggesting that the effects of PGE 2 on regulation of VEGF and bFGF are likely amplified through a positive feedback loop. 58 Since PGE 2 induces VEGF expression and indirectly transactivates PPARδ in CRC cells, 17,59 we postulated that activation of PPARδ may up-regulate VEGF expression. Indeed, our recent study reveals for the first time that activation of PPARδ induced VEGF expression in both epithelial and stromal cells of intestinal polyps in Apc Min/+ mice and colorectal carcinoma cells.…”

Section: Crosstalk Between Pge 2 and Vegf In Crcmentioning

confidence: 99%

Inflammatory Mediators and Nuclear Receptor Signaling in Colorectal Cancer

Wang¹,

DuBois²

2007

Cell Cycle

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Long-term use of cyclooxygenase (COX) inhibitors (NSAIDs) in humans leads to a 50% reduction in risk for colorectal cancer. However, prolonged use of COX-2 selective inhibitors (coxibs) increases cardiovascular toxicity in some individuals, which highlights the importance of identifying all of the molecular targets that drive progression of colorectal cancer. Colorectal cancer offers a unique model to study the synergistic induction of intestinal neoplasia via dysregulation of multiple signaling pathways. Emerging evidence demonstrates that the peroxisome proliferator-activated receptor δ (PPARδ) is a focal point of crosstalk between the signaling cascades involved in the progression of colorectal cancer. More importantly, activation of PPARδ can promote tumor growth by inhibiting epithelial tumor cell apoptosis via a VEGF autocrine signaling loop. These findings may provide a rationale for the development of PPARδ antagonists for cancer prevention and/or treatment.

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Basic Fibroblast Growth Factor Induces Cyclooxygenase-2 Expression in Endothelial Cells Derived from Bone

Cited by 54 publications

References 31 publications

Transforming Growth Factor-β Induces Expression of Receptor Activator of NF-κB Ligand in Vascular Endothelial Cells Derived from Bone

Transforming Growth Factor-β Induces Expression of Receptor Activator of NF-κB Ligand in Vascular Endothelial Cells Derived from Bone

Fibroblast growth factor/fibroblast growth factor receptor system in angiogenesis

Inflammatory Mediators and Nuclear Receptor Signaling in Colorectal Cancer

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