2010
DOI: 10.1016/j.atherosclerosis.2009.08.030
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Cellular factors involved in CXCL8 expression induced by glycated serum albumin in vascular smooth muscle cells

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Cited by 22 publications
(15 citation statements)
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“…The decrease in the amount of CXCR1 and CXCR2 present on the cell membrane was not only due to degradation but also curcumin may affect the ligand-promoted trafficking pathway of the CXCR1 and CXCR2. Curcumin delayed the trafficking pathway in the cytosol, and this resulted in the blockage of the recycling pathway to the cell surface [71][72][73].…”
Section: Curcumin Inhibit Proinflammatory Cytokines Chemokines and Omentioning
confidence: 99%
“…The decrease in the amount of CXCR1 and CXCR2 present on the cell membrane was not only due to degradation but also curcumin may affect the ligand-promoted trafficking pathway of the CXCR1 and CXCR2. Curcumin delayed the trafficking pathway in the cytosol, and this resulted in the blockage of the recycling pathway to the cell surface [71][72][73].…”
Section: Curcumin Inhibit Proinflammatory Cytokines Chemokines and Omentioning
confidence: 99%
“…Sixth, curcumin prevented accumulation of AGEs [113] by trapping methylglyoxal [114] in human umbilical vein endothelial cells. Seventh, curcumin suppressed glycated-serum-albumin-(GSA-)induced IL-8 upregulation [115] via promoter activation and enhanced CXCL8 release in vascular smooth muscle cells. Eighth, curcumin attenuated diabetes-induced vascular dysfunction through inhibition of cyclooxygenase-2 (COX-2) activity, NF- κ B, and PKC and by improving the ratio of prostanoid products PGI(2)/TXA(2) in STZ rats [116].…”
Section: Curcumin and Diabetic Vascular Diseasementioning
confidence: 99%
“…On the other hand, although in vivo E. coli-induced vascular dysfunction was TLR4 dependent, the functional change showed only an incomplete necessity of both MyD88 and TRIF signaling (10). In addition, studies by Choi et al (11) employing a glycated serum albumin induced inflammatory response in vascular muscle demonstrated a requirement for TLR4 and signaling through both MyD88 and TRIF adaptor proteins. Therefore, the literature would suggest that intestinal smooth muscle cells could potentially participate as nonprofessional immunocytes in the early MyD88-dependent development of ileus and the generation of various inflammatory mediators but that, additionally, smooth muscle cell TRIF signaling might also contribute.…”
Section: Discussionmentioning
confidence: 95%