Treatment with sulfasalazine or sulfapyridine, but not 5-aminosalicylic acid, inhibits basic fibroblast growth factor-induced endothelial cell chemotaxis

Volin, Michael V.; Harlow, Lisa A.; Woods, James M.; Campbell, Phillip L.; Amin, M. Asif; Tokuhira, Michihide; Koch, Alisa E.

doi:10.1002/1529-0131(199909)42:9<1927::aid-anr19>3.0.co;2-x

Cited by 45 publications

(24 citation statements)

References 40 publications

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“…In our recent study, sulfasalazine and sulfapyridine inhibited endothelial chemotaxis and tube formation on the laminin-containing matrix Matrigel [113].…”

Section: Possibilities Of Anti-angiogenesis and Anti-chemokine Targetsupporting

confidence: 53%

Angiogenesis and chemokines in rheumatoid arthritis and other systemic inflammatory rheumatic diseases

Bodolay

Koch

Kim

et al. 2002

J Cellular Molecular Medi

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100

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Angiogenesis, the formation of new vessels, is important in the pathogenesis of rheumatoid arthritis (RA) and other inflammatory diseases. Chemotactic cytokines termed chemokines mediate the ingress of leukocytes, including neutrophils and monocytes into the inflamed synovium. In this review, authors discuss the role of the most important angiogenic factors and angiogenesis inhibitors, as well as relevant chemokines and chemokine receptors involved in chronic inflammatory rheumatic diseases. RA was chosen as a prototype to discuss these issues, as the majority of studies on the role of angiogenesis and chemokines in inflammatory diseases were carried out in arthritis. However, other systemic inflammatory (autoimmune) diseases including systemic lupus erythematosus (SLE), systemic sclerosis (SSc), Sjögren's syndrome (SS), mixed connective tissue disease (MCTD), polymyositis/dermatomyositis (PM/DM) and systemic vasculites are also discussed in this context. As a number of chemokines may also play a role in neovascularizaton, this issue is also described here. Apart from discussing the pathogenic role of angiogenesis and chemokines, authors also review the regulation of angiogenesis and chemokine production by other inflammatory meditors, as well as the important relevance of neovascularization and chemokines for antirheumatic intervention.

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“…In our recent study, sulfasalazine and sulfapyridine inhibited endothelial chemotaxis and tube formation on the laminin-containing matrix Matrigel [113].…”

Section: Possibilities Of Anti-angiogenesis and Anti-chemokine Targetsupporting

confidence: 53%

Angiogenesis and chemokines in rheumatoid arthritis and other systemic inflammatory rheumatic diseases

Bodolay

Koch

Kim

et al. 2002

J Cellular Molecular Medi

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100

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“…Pindolol markedly inhibits the development of hypoxic pulmonary vasoconstriction (Takashio et al, 1992). Sulfapyridine, a constituent of sulfasalazine, has been demonstrated to have anti-inflammatory role and can inhibit the production of IL-8/CXCL8 by pro-inflammatory cytokine-stimulated endothelial cells (Volin et al, 1999). Ciclopirox olamine is a synthetic antifungal agent for topical dermatologic treatment of superficial mycoses.…”

Section: Discussionmentioning

confidence: 99%

Expression profiling analysis of hypoxic pulmonary disease

Zhou

Wang²,

Song³

et al. 2013

Genet. Mol. Res.

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ABSTRACT. Exposure of humans to low levels of environmental oxygen results in alveolar hypoxia and normally causes chronic pulmonary hypertension and morphological alterations of precapillary pulmonary vessels. In this study, the microarray dataset GSE11341 was used to identify potential differentially expressed genes related with human lung microvascular endothelial cell hypoxia. In addition, gene ontology term enrichment analysis was performed to explore their underlying functions. In addition, we also investigated the small molecules by comparing with the Connectivity Map. We found that hypoxia samples of 3, 24, and 48 h relative to 0 h displayed 22, 21, and 29 differentially expressed genes, respectively. Among them, six genes (ADM, HMOX1, VEGFA, EGLN3, APOLD1, and ANGPTL4) were closely related to pulmonary microvascular endothelial cell hypoxia response. Three drugs (pindolol, sulfapyridine, and ciclopirox) were selected as candidates to treat hypoxia-related pulmonary diseases. In conclusion, our results provide some underlying drug targets for treatment of hypoxic pulmonary patients.

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“…HMVEC proliferation in response to rhIL-18 was determined using a modified method from previously described procedures (14,36). Briefly, HMVECs fed 1 day before use (with a fresh media exchange to obtain optimal growth conditions) were trypsinized and resuspended at 5 ϫ 10 4 cells/ml in EBM (Clonetics) ϩ 2% FBS ϩ gentamicin.…”

Section: Il-18 Induced Hmvec Proliferationmentioning

confidence: 99%

“…Each chamber was photographed using Polaroid Microcam camera at ϫ22 magnification. The number of tubes formed was quantitated blindly, as previously described (36). Briefly, a connecting branch between two discrete endothelial cells was counted as one tube and required a consistent intensity, thickness, and minimum length (Ͼ1 mm on a 4ϫ enlarged copy of the photomicrograph) to be counted.…”

Section: Matrigel In Vitro Hmvec Tube Formation Assay For In Vitro Anmentioning

confidence: 99%

Evidence of IL-18 as a Novel Angiogenic Mediator

Park

Morel

Amin

et al. 2001

The Journal of Immunology

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244

187

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Angiogenesis, or new blood vessel growth, is a key process in the development of synovial inflammation in rheumatoid arthritis (RA). Integral to this pathologic proliferation are proinflammatory cytokines. We hypothesized a role for IL-18 as an angiogenic mediator in RA. We examined the effect of human IL-18 on human microvascular endothelial cell (HMVEC) migration. IL-18 induced HMVEC migration at 1 nM (p < 0.05). RA synovial fluids potently induced endothelial cell migration, but IL-18 immunodepletion resulted in a 68 ± 5% decrease in HMVEC migration (p < 0.05). IL-18 appears to act on HMVECs via αvβ3 integrin. To test whether IL-18 induced endothelial cell tube formation in vitro, we quantitated the degree of tube formation on Matrigel matrix. IL-18, 1 or 10 nM, resulted in a 77% or 87% increase in tube formation compared with control (p < 0.05). To determine whether IL-18 may be angiogenic in vivo, we implanted IL-18 in Matrigel plugs in mice, and IL-18 at 1 and 10 nM induced angiogenesis (p < 0.05). The angiogenesis observed appears to be independent of the contribution of local TNF-α, as evidenced by adding neutralizing anti-TNF-α Ab to the Matrigel plugs. In an alternative in vivo model, sponges embedded with IL-18 or control were implanted into mice. IL-18 (10 nM) induced a 4-fold increase in angiogenesis vs the control (p < 0.05). These findings support a novel function for IL-18 as an angiogenic factor in RA and may elucidate a potential therapeutic target for angiogenesis-directed diseases.

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Treatment with sulfasalazine or sulfapyridine, but not 5-aminosalicylic acid, inhibits basic fibroblast growth factor-induced endothelial cell chemotaxis

Abstract: These results demonstrate that SSZ and its metabolite SP may affect the pathogenesis of RA by inhibiting EC chemotaxis, proliferation, tube formation, and expression of sICAM-1, IL-8, and MCP-1.

Cited by 45 publications

References 40 publications

Angiogenesis and chemokines in rheumatoid arthritis and other systemic inflammatory rheumatic diseases

Angiogenesis and chemokines in rheumatoid arthritis and other systemic inflammatory rheumatic diseases

Expression profiling analysis of hypoxic pulmonary disease

Evidence of IL-18 as a Novel Angiogenic Mediator

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