Roles of cyclooxygenase-2 in microvascular endothelial cell proliferation induced by basic fibroblast growth factor

Ran, Qian; Fei, Yue; Zhang, Guoping; Hou, Likun; Wang, Xinhong; Jin, Hongyue

doi:10.1097/00029330-200812020-00023

Cited by 7 publications

(7 citation statements)

References 11 publications

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“…COX-2 is known to induce the expression of FGF-2, which is a major cytokine that activates fibroblasts. 1,5,13,18,28 FGF-2 is involved in neovascularization and contributes to granulation tissue formation during ulcer healing. 23 Therefore, COX-2 and FGF-2 expression may play a role in the excessive granulation tissue seen in the IPMD.…”

Section: Discussionmentioning

confidence: 99%

Pathologic Features of Colorectal Inflammatory Polyps in Miniature Dachshunds

et al. 2016

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The histopathologic characteristics of colorectal inflammatory polyps that formed in Miniature Dachshunds were compared with those of other colorectal proliferative lesions, including adenomas and adenocarcinomas. Fifty-three colorectal polypoid lesions were histopathologically classified into inflammatory polyps (26 cases), adenoma (18 cases), and adenocarcinoma (9 cases). All 26 dogs that were diagnosed with inflammatory polyps were Miniature Dachshunds, indicating that colorectal inflammatory polyps exhibit a marked predilection for this breed. The inflammatory polyps had complex histopathologic features and were classified into 3 stages based on their epithelial composition. In early stage (stage 1), the polyps tended to exhibit a thickened mucosa containing hyperplastic goblet cells, dilated crypts filled with a large amount of mucus, and mild lymphocyte and macrophage infiltration. In later stages (stages 2 and 3), more severe neutrophil infiltration, interstitial mucus accumulation, granulation tissue, and occasional osteoid tissue were seen. Also, a few small foci of dysplastic epithelial cells were detected. The hyperplastic goblet cells, which were a major component of the epithelium of the inflammatory polyps, were positive for cytokeratin 20 (CK20), while the dysplastic epithelial cells found in inflammatory polyps (stage 3) and the tumor cells of the adenomas and adenocarcinomas were negative for CK20. These CK20-negative epithelial cells exhibited cytoplasmic and nuclear immunoreactivity for beta-catenin. In addition, the epithelial cells in the inflammatory polyps demonstrated significantly higher cyclooxygenase 2 and fibroblast growth factor 2 expression than did those of the adenomas and adenocarcinomas, suggesting that the arachidonate cascade is involved in the development of colorectal inflammatory polyps in miniature dachshunds.

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Section: Discussionmentioning

confidence: 99%

Pathologic Features of Colorectal Inflammatory Polyps in Miniature Dachshunds

et al. 2016

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“…PGE 2 induces expression of metalloproteinases and inhibits the production of macromolecules of the extracellular matrix [ 5 , 6 ]. It acts as a signalling molecule in response to proangiogenic factors and also induces release of several angiogenic factors in a manner of positive loop [ 7 – 10 ]. Consequently, inhibition or deletion of the enzymes involved in the biosynthetic pathway of PGE 2 interferes in AAA development in animal models [ 11 – 15 ].…”

Section: Introductionmentioning

confidence: 99%

Active Smoking Increases Microsomal PGE₂-Synthase-1/PGE-Receptor-4 Axis in Human Abdominal Aortic Aneurysms

Dilmé¹,

Solà-Villà

Bellmunt³

et al. 2014

Mediators of Inflammation

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Background. The cyclooxygenase- (COX-) 2/microsomal PGE-synthase- (mPGES-) 1/PGE-receptor- (EP-) 4 axis could play a key role in the physiopathology of abdominal aortic aneurysm (AAA) in humans. In this study, we investigated the influence of cardiovascular risk factors on the expression of the PGE2 pathway in human AAA. Methods. Aortic (n = 89) and plasma (n = 79) samples from patients who underwent AAA repair were collected. Patients were grouped according to risk factors. COX-isoenzymes, mPGES-1, EPs, α-actin, and CD45 and CD68 transcripts levels were quantified by QRT-PCR and plasma PGE2 metabolites by EIA. Results. Current smoking (CS) patients compared to no-CS had significantly higher local levels of mPGES-1 (P = 0.009), EP-4 (P = 0.007), and PGE2 metabolites plasma levels (P = 0.008). In the multiple linear regression analysis, these parameters remained significantly enhanced in CS after adding confounding factors. Results from association studies with cell type markers suggested that the increased mPGES-1/EP-4 levels were mainly associated with microvascular endothelial cells. Conclusions. This study shows that elements of the PGE2 pathway, which play an important role in AAA development, are increased in CS. These results provide insight into the relevance of tobacco smoking in AAA development and reinforce the potential of mPGES-1 and EP-4 as targets for therapy in AAA patients.

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“…There are reports suggesting the involvements of NOS and COX pathways in the down stream signal transduction of bFGF receptors and subsequent activation of endothelial cells as well as angiogenesis [Muñoz‐Chápuli et al, 2004; Yue et al, 2006; Qian et al, 2008; Tsai et al, 2010]. Whether NOS and COX participated in the synergistic effect of histamine on bFGF‐induced production of VEGF‐A was therefore examined.…”

Section: Resultsmentioning

confidence: 99%

“…A variety of studies have proven that NOS and COX signal pathways are also involved in the regulation of bFGF‐induced angiogenesis [Muñoz‐Chápuli et al, 2004; Qian et al, 2008]. NO plays a direct role in the mechanisms of action of bFGF [Tsai et al, 2010].…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, COX, a kind of angiogenesis bystander molecules, belongs to a family of enzymes, which can catalyze the oxygenation of arachidonic acid to prostaglandin G2/H2 (PGG2/H2) [Tan et al, 2007]. BFGF can increase VEGF release in an autocrine manner by increasing COX‐2‐generated PGE2 in microvascular endothelial cells (MVECs), and subsequently stimulate the proliferation of MVECs and angiogenesis [Yue et al, 2006; Qian et al, 2008].…”

Section: Discussionmentioning

confidence: 99%

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Histamine synergistically promotes bFGF‐induced angiogenesis by enhancing VEGF production via H1 receptor

Lü

Wang

Pan

et al. 2013

J of Cellular Biochemistry

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Histamine, a major mediator present in mast cells that is released into the extracellular milieu upon degranulation, is well known to possess a wide range of biological activities in several classic physiological and pathological processes. However, whether and how it participates in angiogenesis remains obscure. In the present study, we observed its direct and synergistic action with basic fibroblast growth factor (bFGF), an important inducer of angiogenesis, on in vitro angiogenesis models of endothelial cells. Data showed that histamine (0.1, 1, 10 µM) itself was absent of direct effects on the processes of angiogenesis, including the proliferation, migration, and tube formation of endothelial cells. Nevertheless, it could concentration-dependently enhance bFGF-induced angiogenesis as well as production of vascular endothelial growth factor (VEGF) from endothelial cells. The synergistic effect of histamine on VEGF production could be reversed by pretreatments with diphenhydramine (H1-receptor antagonist), SB203580 (selective p38 mitogen-activated protein kinase (MAPK) inhibitor) and L-NAME (nitric oxide synthase (NOS) inhibitor), but not with cimetidine (H2-receptor antagonist) and indomethacin (cyclooxygenase (COX) inhibitor). Moreover, histamine could augment bFGF-incuced phosphorylation and degradation of IκBα, a key factor accounting for the activation and translocation of nuclear factor κB (NF-κB) in endothelial cells. These findings indicated that histamine was able to synergistically augment bFGF-induced angiogenesis, and this action was linked to VEGF production through H1-receptor and the activation of endothelial nitric oxide synthase (eNOS), p38 MAPK, and IκBα in endothelial cells.

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Roles of cyclooxygenase-2 in microvascular endothelial cell proliferation induced by basic fibroblast growth factor

Cited by 7 publications

References 11 publications

Pathologic Features of Colorectal Inflammatory Polyps in Miniature Dachshunds

Pathologic Features of Colorectal Inflammatory Polyps in Miniature Dachshunds

Active Smoking Increases Microsomal PGE₂-Synthase-1/PGE-Receptor-4 Axis in Human Abdominal Aortic Aneurysms

Histamine synergistically promotes bFGF‐induced angiogenesis by enhancing VEGF production via H1 receptor

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Roles of cyclooxygenase-2 in microvascular endothelial cell proliferation induced by basic fibroblast growth factor

Cited by 7 publications

References 11 publications

Pathologic Features of Colorectal Inflammatory Polyps in Miniature Dachshunds

Pathologic Features of Colorectal Inflammatory Polyps in Miniature Dachshunds

Active Smoking Increases Microsomal PGE2-Synthase-1/PGE-Receptor-4 Axis in Human Abdominal Aortic Aneurysms

Histamine synergistically promotes bFGF‐induced angiogenesis by enhancing VEGF production via H1 receptor

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Active Smoking Increases Microsomal PGE₂-Synthase-1/PGE-Receptor-4 Axis in Human Abdominal Aortic Aneurysms