Kinetics of chemokines and their receptors in mercuric chloride-induced tubulointerstitial lesions in brown Norway rats

Noninvasive detection of renal allograft inflammation by measurements of mRNA for IP-10 and CXCR3 in urine

“…Alhough absent in normal kidneys, IP-10 hyperexpression within the kidneys of patients with proliferative glomerulonephritis [33], and IP-10 production by both human glomerular mesangial cells [33,34] and renal proximal tubular cells [35], following their activation with interferon gamma (IFN-c) and tumor necrosis factor-a (TNF-a), has been communicated. Experimental data are consistent with these reports, with IP-10 expression detected in vivo during glomerulonephritis [34,36,37] and tubulointerstitial nephritis [38,39], and production of IP-10 by mesangial [40][41][42], tubular [41, A and B). IP-10 was expressed by occasional interstitial cells (arrows) during stable renal function (C), but was strongly up-regulated within tubules and infiltrating mononuclear cells during acute rejection (D); inset shows IP-10+ leukocytes crossing tubules.…”

Chemokines in proliferative diabetic retinopathy and proliferative vitreoretinopathy

“…These findings indicate that VEGF-induced augmentation of IP-10 expression is a major mechanism underlying its proinflammatory function in immunity. Increased expression of IP-10 has also been shown in other fibrotic disorders [48][49][50]. Suzuki et al [49] examined the expression pattern of IP-10 in a rat model of renal tubulointerstitial fibrosis.…”

“…Increased expression of IP-10 has also been shown in other fibrotic disorders [48][49][50]. Suzuki et al [49] examined the expression pattern of IP-10 in a rat model of renal tubulointerstitial fibrosis. They demonstrated that the expression of IP-10 mRNA showed an early increase, which coincided with the onset of infiltration of lymphocytes, followed by a gradual decrease to the control level.…”

Dimethyl fumarate ameliorates cisplatin-induced renal tubulointerstitial lesions

“…Therefore, these results suggested that DMF might ameliorate tubulointerstitial fibrosis by suppressing macrophage infiltration and the increase in myofibroblasts. However, because previous reports suggested that the regenerated proximal tubule may produce chemokines (MCP-1 and RANTES) and a fibrotic cytokine (TGF-β1) in the mercuric chloride-induced renal tubulointerstitial model, it is possible that the inhibitory effect of DMF against tubular injury decreased production of these factors, which would ameliorates the consequent macrophage infiltration and increase in myofibroblasts following tubulointerstitial fibrosis 8 , 30 .…”