Monocytes and Macrophages in Focal Glomerulosclerosis in Zucker Rats

Magil, Alex B.; Fröhlich, Jiří

doi:10.1159/000186532

Cited by 40 publications

(39 citation statements)

References 16 publications

(26 reference statements)

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“…Cholesterol crystals were seen in tubular epithelial lumina. Magil and Fröhlich [28] have shown mesangial matrix expansion with capillary loop collapse and adhesion between Bowman's capsule layers in hypercholesterolemic rats. Guijarro and Keane [1] identified lipid deposits with sclerosis and foam cells in the mesangial matrix of the renal cortex of Sprague-Dawley rats with hypercholesterolemia.…”

Section: Discussionmentioning

confidence: 99%

“…Trapping of LDL in the extracellular matrix causes oxidative modification, especially of mesangial and endothelial cells. Histopathological examination has also shown that oxidated LDL (O-LDL) could be taken up by mesangial cells and macrophages, resulting in foam cell formation [1,6,7]. Foam cells, in turn, produce growth factors that might stimulate growth and proliferation of glomerular mesangial matrix and mesangial cells.…”

Section: Introductionmentioning

confidence: 99%

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Protective Effects of Vitamin E and Selenium on the Renal Morphology in Rats Fed High-Cholesterol Diets

Gonca¹,

Ceylan²,

Yardımoğlu³

et al. 2000

Pathobiology

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The histopathological effects of cholesterol and the protective effects of vitamin E and selenium (Se) on renal histology were examined in Sprague-Dawley rats. Light-microscopic evaluation of the renal cortex revealed: glomerular fibrosis, cellular and mesangial proliferation, capillary obliteration and cholesterol crystals in the tubular lumina of the cholesterol-fed group. These results suggest that oxidated LDL (O-LDL) is a cytotoxic factor which stimulates mesangial cell and matrix proliferation. Ultrastructurally, small and large lipid vacuolization in intracapillary lumina, adhesion of epithelial foot processes, mesangial foam cells and polymorphonuclear leukocytes were seen in the cholesterol-fed group. In the groups fed cholesterol + vitamin E, cholesterol + Se and cholesterol + vitamin E + Se, morphological improvements were observed. It appeared that an excess in O-LDL, reactive oxygen species and growth factors might play an important role in the pathogenesis of glomerulosclerosis. In addition, it was concluded that antioxidant therapy may prevent LDL oxidation and generation of free radicals.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Protective Effects of Vitamin E and Selenium on the Renal Morphology in Rats Fed High-Cholesterol Diets

Gonca¹,

Ceylan²,

Yardımoğlu³

et al. 2000

Pathobiology

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“…Because glomerular macrophage infiltration plays a direct role in the progression to glomerulosclerosis (27,28) and is mediated by MCP-1 (1-4), BMP-7 may have therapeutic potential in the treatment of inflammatory glomerular diseases.…”

Section: Discussionmentioning

confidence: 99%

Bone Morphogenetic Protein-7 Inhibits Constitutive and Interleukin-1β-Induced Monocyte Chemoattractant Protein-1 Expression in Human Mesangial Cells: Role for JNK/AP-1 Pathway

Lee

Yang

Jin

et al. 2003

The Journal of Immunology

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Bone morphogenetic protein-7 (BMP-7), which belongs to the TGF-β superfamily, has been shown to reduce macrophage infiltration and tissue injury in animal models of inflammatory renal disease. To explore the mechanism involved in the anti-inflammatory effect, we investigated the effect of BMP-7 on monocyte chemoattractant protein-1 (MCP-1) expression in cultured human mesangial cells. BMP- 7 significantly inhibited constitutive and IL-1β-induced MCP-1 protein production and MCP-1 mRNA expression by mesangial cells in a time- and concentration-dependent manner. BMP-7 also inhibited IL-1β-induced monocyte chemotactic activity released from the mesangial cells. We examined the role of transcription factors NF-κB and AP-1 in BMP-7 inhibition of IL-1β-induced MCP-1 expression. IL-1β increased NF-κB and AP-1 activity and both transcription factors mediated IL-1β-induced MCP-1 expression in mesangial cells. BMP-7 inhibited IL-1β-induced AP-1 activity in a concentration-dependent manner. In contrast, IL-1β-induced NF-κB activity and IκBα degradation were not affected by BMP-7. Furthermore, IL-1β-induced phosphorylation of c-Jun N-terminal kinase was inhibited by BMP-7. These data suggest that BMP-7 inhibits constitutive and IL-1β-induced MCP-1 expression in human mesangial cells partly by inhibiting c-Jun N-terminal kinase activity and subsequent AP-1 activity, and provide new insight into the therapeutic potential of BMP-7 in the inflammatory renal diseases.

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“…TSP1 appears to have several biological effects that involve migration, proliferation, and cell-matrix interaction [2][3][4]. These biological activities are significantly altered in renal disease and suggest an important role for TSP1 in the progression of chronic renal disease [5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Age-Related Expression of Renal Thrombospondin 1 mRNA in F344 Rats: Resemblance to Diabetes-Induced Expression in Obese Zucker Rats

1999

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Age-related increases occurred in renal thrombospondin 1 (TSP1) mRNA in F344 rats, resembling diabetes-induced TSP1 mRNA in the obese Zucker rat. TSP1 mRNA was 3.5-fold higher in 24-month-old than in 3-month-old F344 rats. TSP1 mRNA increased similarly in 5-month-old obese Zucker rats as compard with lean littermates and correlated positively with the extent of proteinuria (r = 0.71). In situ hybridization identified elevated TSP1 mRNA levels in epithelial cells of distended tubules as well as in interstitium near dilated tubules of both 24-month-old F344 rats and 5-month-old obese Zucker rats. Furthermore, thrombin increased TSP1 mRNA in mesangial and epithelial cells in culture, indicating that thrombin may contribute to elevated TSP1 expression in renal disease. Thrombin increased TSP1 mRNA within 30 min after treatment which required de novo synthesis of protein. The thrombin receptor tethered ligand peptide, SFLLRN, increased TSP1 mRNA, indicating that the thrombin-induced increase in TSP1 mRNA was due to direct thrombin receptor (PAR1) stimulation. These results show that increased TSP1 mRNA levels are a component of interstitial fibrosis seen in aged and diabetic kidneys and suggest that similar pathological changes occur in kidneys of aging and diabetic rats.

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Monocytes and Macrophages in Focal Glomerulosclerosis in Zucker Rats

Cited by 40 publications

References 16 publications

Protective Effects of Vitamin E and Selenium on the Renal Morphology in Rats Fed High-Cholesterol Diets

Protective Effects of Vitamin E and Selenium on the Renal Morphology in Rats Fed High-Cholesterol Diets

Bone Morphogenetic Protein-7 Inhibits Constitutive and Interleukin-1β-Induced Monocyte Chemoattractant Protein-1 Expression in Human Mesangial Cells: Role for JNK/AP-1 Pathway

Age-Related Expression of Renal Thrombospondin 1 mRNA in F344 Rats: Resemblance to Diabetes-Induced Expression in Obese Zucker Rats

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