Colchicine attenuates inflammatory cell infiltration and extracellular matrix accumulation in diabetic nephropathy

Li, Jin Ji; Lee, Sun Ha; Kim, Yon Su; Jin, Ri; Jung, Dong-Sub; Kwak, Seung-Jae; Kim, Seung Hye; Han, Seung Hyeok; Lee, Jung Eun; Moon, Sung Jin; Ryu, Dong Ryeol; Yoo, Tae‐Hyun; Han, Dae Suk; Kang, Shin Wook

doi:10.1152/ajprenal.90649.2008

Cited by 59 publications

(57 citation statements)

References 47 publications

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“…51 Lower expression of MCP-1 and intercellular adhesion molecule-1 as pro-inflammatory proteins led to reduced infiltration of inflammatory cells, and an accompanying reduction in ECM accumulation. 52 Moreover, cytokines are known to be sequestered in the ECM and can be released by MMPs. 53 The correlation between ECM and inflammatory proteins may be of importance in thickened BM as observed in both types of AMD.…”

Section: Discussionmentioning

confidence: 99%

Sub-lytic C5b-9 induces functional changes in retinal pigment epithelial cells consistent with age-related macular degeneration

Lueck

Wasmuth

Williams³

et al. 2011

Eye

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Purpose There is evidence for complement dysfunction in age-related macular degeneration (AMD). Complement activation leads to formation of the membrane attack complex (MAC), known to assemble on retinal pigment epithelial (RPE) cells. Therefore, the effect of sub-lytic MAC on RPE cells was examined with regard to pro-inflammatory or pro-angiogenic mediators relevant in AMD. Methods For sub-lytic MAC induction, RPE cells were incubated with an antiserum to complement regulatory protein CD59, followed by normal human serum (NHS) to induce 5% cell death, measured by a viability assay. MAC formation was evaluated by immunofluorescence and FACS analysis. Interleukin (IL)-6, -8, monocytic chemoattractant protein-1 (MCP-1), and vascular endothelial growth factor (VEGF) were quantified by enzyme-linked immunosorbent assay (ELISA). Intracellular MCP-1 was analysed by immunofluorescence, vitronectin by western blotting, and gelatinolytic matrix metalloproteinases (MMPs) by zymography. Results Incubation of RPE cells with the CD59 antiserum followed by 5% NHS induced sub-lytic amounts of MAC, verified by FACS and immunofluorescence. This treatment stimulated the cells to release IL-6, -8, MCP-1, and VEGF. MCP-1 staining, production of vitronectin, and gelatinolytic MMPs were also elevated in response to sub-lytic MAC. Conclusions MAC assembly on RPE cells increases the IL-6, -8, and MCP-1 production.

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Section: Discussionmentioning

confidence: 99%

Sub-lytic C5b-9 induces functional changes in retinal pigment epithelial cells consistent with age-related macular degeneration

Lueck

Wasmuth

Williams³

et al. 2011

Eye

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“…In a recent experimental study, colchicine administration to streptozotocin-induced diabetic rats significantly reduced UAE, inflammatory cell infiltration and extracellular matrix accumulation. These beneficial effects were associated with inhibition of inflammatory molecules expression in the renal tissue, including ICAM-1 [102] .…”

Section: Intercellular Adhesion Molecule-1mentioning

confidence: 98%

Pathophysiological role and therapeutic implications of inflammation in diabetic nephropathy

Luis-Rodríguez¹,

Martínez‐Castelao²,

Górriz³

et al. 2012

WJD

115

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Diabetes mellitus and its complications are becoming one of the most important health problems in the world. Diabetic nephropathy is now the main cause of end-stage renal disease. The mechanisms leading to the development and progression of renal injury are not well known. Therefore, it is very important to find new pathogenic pathways to provide opportunities for early diagnosis and targets for novel treatments. At the present time, we know that activation of innate immunity with development of a chronic low grade inflammatory response is a recognized factor in the pathogenesis of diabetic nephropathy. Numerous experimental and clinical studies have shown the participation of different inflammatory molecules and pathways in the pathophysiology of this complication.

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“…MC proliferation is commonly observed in a variety of pathological changes in glomerular injury. It has been demonstrated that MC dysfunction, including overproliferation and an increase in ECM production [3,4] , is implicated in the development of DN [5,6] . Hyperglycemia has been well documented as an independent risk factor for DM-induced complications.…”

Section: Introductionmentioning

confidence: 99%

Insulin deficiency induces rat renal mesangial cell dysfunction via activation of IGF-1/IGF-1R pathway

Kong

Shen

et al. 2016

Acta Pharmacol Sin

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Aim: Diabetic nephropathy is one of the major complications of diabetes and the major cause of end-stage renal disease. In this study we investigated the insulin deficiency (ID) induced changes in renal mesangial cells (MCs) and in the kidney of STZ-induced diabetic rats. Methods: Cultured rat renal MCs were incubated in ID media. Cell proliferation was analyzed using BrdU incorporation assay. The expression of insulin receptor (IR), insulin-like growth factor-1 receptor (IGF-1R), phosphorylated IGF-1R, fibronectin, and collagen IV was determined with Western blot analysis. STZ-induced diabetic rats were treated with an IGF-1R antagonist picropodophyllin (PPP, 20 mg·kg -1 ·d -1, po) for 8 weeks. After the rats were euthanized, plasma and kidneys were collected. IGF-1 levels in renal cortex were measured with RT-PCR or ELISA. The morphological changes in the kidneys were also examined. Results: Incubation in ID media significantly increased cell proliferation, the synthesis of fibronectin and collagen IV, and the expression of IGF-1 and IGF-1R and phosphorylated IGF-1R in renal MCs. Pretreatment of the cells with PPP (50 nmol/L) blocked ID-induced increases in cell proliferation and the synthesis of fibronectin and collagen IV; knockdown of IGF-1R showed a similar effect as PPP did. In contrast, treatment of the cells with IGF-1 (50 ng/mL) exacerbated ID-induced increases in cell proliferation. In the kidneys of diabetic rats, the expression of IGF-1, IGF-1R and phosphorylated IGF-1R were significantly elevated. Treatment of diabetic rats with PPP did not lower the blood glucose levels, but significantly suppressed the expression of TGF-β, fibronectin and collagen IV in the kidneys, the plasma levels of urinary nitrogen and creatinine, and the urinary protein excretion. Conclusion: Insulin deficiency increases the expression of IGF-1 and IGF-1R in renal MCs and the kidney of diabetic rats, which contributes to the development of diabetic nephropathy.

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Colchicine attenuates inflammatory cell infiltration and extracellular matrix accumulation in diabetic nephropathy

Cited by 59 publications

References 47 publications

Sub-lytic C5b-9 induces functional changes in retinal pigment epithelial cells consistent with age-related macular degeneration

Sub-lytic C5b-9 induces functional changes in retinal pigment epithelial cells consistent with age-related macular degeneration

Pathophysiological role and therapeutic implications of inflammation in diabetic nephropathy

Insulin deficiency induces rat renal mesangial cell dysfunction via activation of IGF-1/IGF-1R pathway

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