Downregulation of ICAM-1 and VCAM-1 expression in endothelial cells treated by photodynamic therapy

Volanti, Cédric; Gloire, Geoffrey; Vanderplasschen, Alain; Jacobs, Nathalie; Habraken, Yvette; Piette, Jacques

doi:10.1038/sj.onc.1207871

Cited by 51 publications

(38 citation statements)

References 38 publications

(43 reference statements)

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“…Here we extend these findings to show that bradykinin, through TRPM7, induces expression of proinflammatory molecules VCAM-1 and COX-2, which are known downstream targets of calpain (24,37,45). Previous studies showed that bradykinin influences inflammatory mediators and cellular adhesion molecules (35).…”

Section: Discussionmentioning

confidence: 55%

Bradykinin regulates calpain and proinflammatory signaling through TRPM7-sensitive pathways in vascular smooth muscle cells

Yogi¹,

Callera²,

Tostes³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Yogi A, Callera GE, Tostes R, Touyz RM. Bradykinin regulates calpain and proinflammatory signaling through TRPM7-sensitive pathways in vascular smooth muscle cells. Am J Physiol Regul Integr Comp Physiol 296: R201-R207, 2009. First published September 17, 2008 doi:10.1152/ajpregu.90602.2008.-Transient receptor potential melastatin-7 (TRPM7) channels have recently been identified to be regulated by vasoactive agents acting through G protein-coupled receptors in vascular smooth muscle cells (VSMC). However, downstream targets and functional responses remain unclear. We investigated the subcellular localization of TRPM7 in VSMCs and questioned the role of TRPM7 in proinflammatory signaling by bradykinin. VSMCs from Wistar-Kyoto rats were studied. Cell fractionation by sucrose gradient and differential centrifugation demonstrated that in bradykinin-stimulated cells, TRPM7 localized in fractions corresponding to caveolae. Immunofluorescence confocal microscopy revealed that TRPM7 distributes along the cell membrane, that it has a reticular-type intracellular distribution, and that it colocalizes with flotillin-2, a marker of lipid rafts. Bradykinin increased expression of calpain, a TRPM7 target, and stimulated its cytosol/membrane translocation, an effect blocked by 2-APB (TRPM7 inhibitor) and U-73122 (phospholipase C inhibitor), but not by chelerythrine (PKC inhibitor). Expression of proinflammatory mediators VCAM-1 and cyclooxygenase-2 (COX-2) was time-dependently increased by bradykinin. This effect was blocked by Hoe-140 (B 2 receptor blocker) and 2-APB. Our data demonstrate that in bradykinin-stimulated VSMCs: 1) TRPM7 is upregulated, 2) TRPM7 associates with cholesterol-rich microdomains, and 3) calpain and proinflammatory mediators VCAM-1 and COX2 are regulated, in part, via TRPM7-and phospholipase C-dependent pathways through B 2 receptors. These findings identify a novel signaling pathway for bradykinin, which involves TRPM7. Such phenomena may play a role in bradykinin/B 2 receptor-mediated inflammatory responses in vascular cells.

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Section: Discussionmentioning

confidence: 55%

Bradykinin regulates calpain and proinflammatory signaling through TRPM7-sensitive pathways in vascular smooth muscle cells

Yogi¹,

Callera²,

Tostes³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Moreover, the elevation of VCAM-1 expression only at mRNA level also suggests a potential for synergism. The discrepancy between mRNA and protein levels of VCAM-1 is not unknown [44,45]. MicroRNAs may block translation of VCAM-1 without degradation of mRNA or post-translational degradation can decrease the protein level, however, the exploration of the molecular mechanism is beyond the scope of this study.…”

Section: Discussionmentioning

confidence: 99%

Complement MASP-1 enhances adhesion between endothelial cells and neutrophils by up-regulating E‐selectin expression

Jani

Schwaner

Kajdácsi

et al. 2016

Molecular Immunology

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Abbreviation: HUVEC, human umbilical vein endothelial cell; MBL, mannan-binding lectin; MASP, mannan-binding lectin-associated serine protease; PAR, protease-activated receptor. AbstractThe complement system and neutrophil granulocytes are indispensable in the immune response against extracellular pathogens such as bacteria and fungi. Endothelial cells also participate in antimicrobial immunity largely by regulating the homing of leukocytes through their cytokine production and their pattern of cell surface adhesion molecules. We have previously shown that mannan-binding lectin-associated serine protease-1 (MASP-1), a complement lectin pathway enzyme, is able to activate endothelial cells by cleaving protease activated receptors, which leads to cytokine production and enables neutrophil chemotaxis. Therefore, we aimed to investigate how recombinant MASP-1 (rMASP-1) can modify the pattern of P-selectin, E-selectin, ICAM-1, ICAM-2, and VCAM-1 adhesion molecules in human umbilical vein endothelial cells (HUVEC), and whether these changes can enhance the adherence between endothelial cells and neutrophil granulocyte model cells (differentiated PLB-985). We found that HUVECs activated by rMASP-1 decreased the expression of ICAM-2 and increased that of E-selectin, whereas ICAM-1, VCAM-1 and P-selectin expression remained unchanged. Furthermore, these changes resulted in increased adherence between differentiated PLB-985 cells and endothelial cells. Our finding suggests that complement MASP-1 can increase adhesion between neutrophils and endothelial cells in a direct fashion. This is in agreement with our previous finding that MASP-1 increases the production of pro-inflammatory cytokines (such as IL-6 and IL-8) and chemotaxis, and may thereby boost neutrophil functions. This newly described cooperation between complement lectin pathway and neutrophils via endothelial cells may be an effective tool to enhance the antimicrobial immune response.

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“…Real-time quantitative PCR cDNA was prepared in a 20 ml final volume with 1 mg RNA as described (Volanti et al, 2004). cDNA (2 ml) was mixed with 10 ml SYBR Green Mix (Applied Biosystems, Warrington, UK) and forward and reverse primers for each gene of interest, or with 300 nM forward (5 0 -GAGTATGCCTGCCGTGTG-3 0 ) and 300 nM reverse (5 0 -AATCCAAATGCGGCATCT-3 0 ) b2-microglobulin (B2M) primers in a 20 ml final volume.…”

Section: Analysis Of Microarraysmentioning

confidence: 99%

Molecular effectors and modulators of hypericin-mediated cell death in bladder cancer cells

et al. 2007

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Photodynamic therapy (PDT) is an anticancer approach utilizing a light-absorbing molecule and visible light irradiation to generate, in the presence of O 2 , cytotoxic reactive oxygen species, which cause tumor ablation. Given that the photosensitizer hypericin is under consideration for PDT treatment of bladder cancer we used oligonucleotide microarrays in the T24 bladder cancer cell line to identify differentially expressed genes with therapeutic potential. This study reveals that the expression of several genes involved in various metabolic processes, stress-induced cell death, autophagy, proliferation, inflammation and carcinogenesis is strongly affected by PDT and pinpoints the coordinated induction of a cluster of genes involved in the unfolded protein response pathway after endoplasmic reticulum stress and in antioxidant response. Analysis of PDT-treated cells after p38 MAPK inhibition or silencing unraveled that the induction of an important subset of differentially expressed genes regulating growth and invasion, as well as adaptive mechanisms against oxidative stress, is governed by this stress-activated kinase. Moreover, p38 MAPK inhibition blocked autonomous regrowth and migration of cancer cells escaping PDT-induced cell death. This analysis identifies new molecular effectors of the cancer cell response to PDT opening attractive avenues to improve the therapeutic efficacy of hypericin-based PDT of bladder cancer.

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Downregulation of ICAM-1 and VCAM-1 expression in endothelial cells treated by photodynamic therapy

Cited by 51 publications

References 38 publications

Bradykinin regulates calpain and proinflammatory signaling through TRPM7-sensitive pathways in vascular smooth muscle cells

Bradykinin regulates calpain and proinflammatory signaling through TRPM7-sensitive pathways in vascular smooth muscle cells

Complement MASP-1 enhances adhesion between endothelial cells and neutrophils by up-regulating E‐selectin expression

Molecular effectors and modulators of hypericin-mediated cell death in bladder cancer cells

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