IFN-Inducible Protein 10 (CXCL10) Regulates Tubular Cell Proliferation in Renal Ischemia-Reperfusion Injury

Furuichi, Kengo; Wada, Takashi; Kitajikma, Shinji; Toyama, Tadasi; Okumura, Tomoko; Hara, Akinori; Kawachi, Hiroshi; Shimizu, Fujio; Sugaya, Takeshi; Mukaida, Naofumi; Narumi, Shosaku; Matsushima, Kouji; Kaneko, Shuichi

doi:10.1159/000135675

Cited by 14 publications

(12 citation statements)

References 63 publications

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“…Therefore, renal disease could be affected by the stimulation of TLRs in leucocytes or renal cells. Zhai et al reported that TLR4-IRF3 activation triggers CXCL10 expression in ischemia reperfusion injury (IRI) mouse liver [22], and Furuichi et al found that CXCL10 was expressed in the kidney after IRI [34]. Thus, we investigated the expression of TLR4 and phosphorylated (activated) IRF3 in both Mxi1 −/− and Mxi1 +/+ mice.…”

Section: Discussionmentioning

confidence: 96%

CXCL10 expression induced by Mxi1 inactivation induces mesangial cell apoptosis in mouse Habu nephritis

Chen

Mei

et al. 2015

Cellular Signalling

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Section: Discussionmentioning

confidence: 96%

CXCL10 expression induced by Mxi1 inactivation induces mesangial cell apoptosis in mouse Habu nephritis

Chen

Mei

et al. 2015

Cellular Signalling

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“…In addition to Cxcl1/KC, Cxcl2/MIP-2α has also been shown to stimulate proliferation of epithelial cells (43). Conversely, Furuichi et al (44) showed that the induction of Cxcl10/IP-10 in ischemic kidney inhibits tubular cell proliferation. This controversy can be explained by the presence or absence of the ELR motif in CXC chemokines.…”

Section: Discussionmentioning

confidence: 99%

Chemokine expression in renal ischemia/reperfusion injury is most profound during the reparative phase

Stroo

Stokman

Teske

et al. 2010

International Immunology

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Chemokines are important players in the migration of leukocytes to sites of injury and are also involved in angiogenesis, development and wound healing. In this study, we performed microarray analyses to identify chemokines that play a role during the inflammatory and repair phase after renal ischemia/reperfusion (I/R) injury and investigated the temporal relationship between chemokine expression, leukocyte accumulation and renal damage/repair. C57Bl/6 mice were subjected to unilateral ischemia for 45 min and sacrificed 3 h, 1 day and 7 days after reperfusion. From ischemic and contralateral kidney, RNA was isolated and hybridized to a microarray. Microarray results were validated with quantitative real-time reverse transcription–PCR (QRT–PCR) on RNA from an independent experiment. (Immuno)histochemical analyses were performed to determine renal damage/repair and influx of leukocytes. Twenty out of 114 genes were up-regulated at one or more reperfusion periods. All these genes were up-regulated 7 days after I/R. Up-regulated genes included CC chemokines MCP-1 and TARC, CXC chemokines KC and MIP-2α, chemokine receptors Ccr1 and Cx3cr1 and related genes like matrix metalloproteinases. Microarray data of 1 and 7 days were confirmed for 17 up-regulated genes by QRT–PCR. (Immuno)histochemical analysis showed that the inflammatory and repair phase after renal I/R injury take place after, respectively, 1 and 7 days. Interestingly, chemokine expression was highest during the repair phase. In addition, expression profiles showed a biphasic expression of all up-regulated CXC chemokines coinciding with the early inflammatory and late repair phase. In conclusion, we propose that temporal expression of chemokines is a crucial factor in the regulation of renal I/R injury and repair.

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“…On this topic we reported that IP-10 had an inhibitory effect on tubular cell proliferation in vivo and in vitro. The interstitial infiltrated F4/80-positive cells were main source of IP-10 [39]. Further studies are needed to investigate whether regeneration from tubular necrosis is a very important part of recovery of the injured kidney.…”

Section: Regenerationmentioning

confidence: 99%

Chemokine/chemokine receptor-mediated inflammation regulates pathologic changes from acute kidney injury to chronic kidney disease

2009

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Ischemia-reperfusion injury is a main cause of acute kidney injury. Tubular necrosis and interstitial inflammatory cell infiltration are characteristic pathologic changes of acute kidney injury. The main necrotic area should be repaired with new tubular epithelial cells after the injury. On the other hand, some parts of the injured kidney progress to interstitial fibrosis, a characteristic pathologic change in chronic kidney disease. We hypothesized that interstitial infiltrating leukocytes, that are attracted and activated by chemokines, are key mediators in the pathogenesis of tubular necrosis, regeneration of the necrotic area, or interstitial fibrosis. A large number of chemokines were upregulated after ischemic injury, and chemokine receptor-expressing inflammatory cells were attracted by these chemokines. Genetic or molecular modulating experiments in the mouse model have begun to reveal the key participants and their specific roles at the levels of inflammation, regeneration, and fibrosis. Among these chemokines/chemokine receptors, our data indicated CCR2-mediated macrophage infiltration mainly affected tubular necrosis after ischemic acute kidney injury, interferon-gamma-inducible protein (IP)-10-producing macrophages participate in regeneration of tubular epithelial cells, and CX3CR1-mediated macrophages and platelet infiltration and aggregation play roles in interstitial fibrosis in chronic kidney disease. These chemokines and chemokine receptors on infiltrating inflammatory cells would be novel clinical markers or targets for therapeutic intervention.

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IFN-Inducible Protein 10 (CXCL10) Regulates Tubular Cell Proliferation in Renal Ischemia-Reperfusion Injury

Cited by 14 publications

References 63 publications

CXCL10 expression induced by Mxi1 inactivation induces mesangial cell apoptosis in mouse Habu nephritis

CXCL10 expression induced by Mxi1 inactivation induces mesangial cell apoptosis in mouse Habu nephritis

Chemokine expression in renal ischemia/reperfusion injury is most profound during the reparative phase

Chemokine/chemokine receptor-mediated inflammation regulates pathologic changes from acute kidney injury to chronic kidney disease

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