Activation of mesangial cells with TNF-α stimulates M-CSF gene expression and monocyte proliferation: evidence for involvement of protein kinase C and protein tyrosine kinase

Kamanna, Vaijinath S.; Pai, Rama; Bassa, Babu V.; Kirschenbaum, Michael A.

doi:10.1016/0167-4889(96)00064-x

Cited by 18 publications

(12 citation statements)

References 46 publications

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“…CSF-1 is an important chemoattractant, survival, and proliferating factor for M produced by a variety of cell types, including endothelial, mesangial, and tubular epithelial cells and fibroblasts (2)(3)(4). The actions of this homodimeric factor are mediated entirely through a high affinity tyrosine kinase receptor encoded by the c-fms proto-oncogene (5,6).…”

Section: R Enal Tubular Epithelial Cells (Tec)mentioning

confidence: 99%

Reduced Macrophage Recruitment, Proliferation, and Activation in Colony-Stimulating Factor-1-Deficient Mice Results in Decreased Tubular Apoptosis During Renal Inflammation

Lenda

Kikawada

Stanley

et al. 2003

The Journal of Immunology

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Kidney tubular epithelial cell (TEC) death may be dependent on the number and activation state of macrophages (Mφ) during inflammation. Our prior studies indicate that activated Mφ release soluble mediators that incite TEC death, and reducing intrarenal Mφ during kidney disease diminishes TEC apoptosis. CSF-1 is required for Mφ proliferation and survival. We hypothesized that in the absence of CSF-1, Mφ-mediated TEC apoptosis would be prevented during renal inflammation. To test this hypothesis, we evaluated renal inflammation during unilateral ureter obstruction in CSF-1-deficient (Csf1op/Csf1op) mice. We detected fewer Mφ and T cells and less apoptotic TEC in the obstructed kidneys of Csf1op/Csf1op mice compared with wild-type (WT) mice. The decrease in intrarenal Mφ resulted from diminished recruitment and proliferation, not enhanced apoptosis. CSF-1 enhanced Mφ activation. There were far fewer activated (CD69, CD23, Ia, surface expression) Mφ in obstructed CSF-1-deficient compared with WT obstructed kidneys. Similarly, bone marrow Mφ preincubated with anti-CSF-1 receptor Ab or anti-CSF-1 neutralizing Ab were resistant to LPS- and IFN-γ-induced activation. We detected fewer apoptotic-inducing molecules (reactive oxygen species, TNF-α, inducible NO synthase) in 1) Mφ propagated from obstructed Csf1op/Csf1op compared with WT kidneys, and 2) WT bone marrow Mφ blocked with anti-CSF-1 receptor or anti-CSF-1 Ab compared with the isotype control. Furthermore, blocking CSF-1 or the CSF-1 receptor induced less TEC apoptosis than the isotype control. We suggest that during renal inflammation, CSF-1 mediates Mφ recruitment, proliferation, activation, and, in turn, TEC apoptosis.

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Section: R Enal Tubular Epithelial Cells (Tec)mentioning

confidence: 99%

Reduced Macrophage Recruitment, Proliferation, and Activation in Colony-Stimulating Factor-1-Deficient Mice Results in Decreased Tubular Apoptosis During Renal Inflammation

Lenda

Kikawada

Stanley

et al. 2003

The Journal of Immunology

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“…TNF stimulates a variety of proinflammatory responses by intrinsic renal cells. In mesangial cells, TNF stimulates proliferation (18) and increases production of monocyte-colony stimulating factor (M-CSF) (19), monocyte chemoattractant protein (MCP-1) (20), reactive oxygen metabolites (21), and tissue factor expression (22). TNF also induces intercellular adhesion molecule-1 (ICAM-1) expression and enhances monocyte adhesion (23).…”

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confidence: 99%

Intrinsic Renal Cells Are the Major Source of Tumor Necrosis Factor Contributing to Renal Injury in Murine Crescentic Glomerulonephritis

Timoshanko¹,

Sedgwick²,

Holdsworth³

et al. 2003

Journal of the American Society of Nephrology

106

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Abstract. Macrophages are prominent participants in crescentic glomerulonephritis (GN) and have been suggested to be the major source of TNF in this cell-mediated form of glomerular inflammation. Intrinsic renal cells also have the capacity to produce TNF. For dissecting the contribution of local versus bone marrow (BM)-derived TNF in inflammatory renal injury, TNF chimeric mice were created by transplanting normal wildtype (WT) BM into irradiated TNF-deficient recipients (WT3 TNF Ϫ/Ϫ chimeras) and vice versa (TNF Ϫ/Ϫ 3 WT chimeras). A model of crescentic GN induced by an intravenous injection of sheep anti-murine glomerular basement membrane antibody was studied in WT mice, mice with complete TNF deficiency (TNFϪ/Ϫ), and chimeric mice. Crescentic GN was attenuated in TNFϪ/Ϫ mice with fewer crescents (crescents, 13.7 Ϯ 1.7% of glomeruli) and reduced functional indices of renal injury (serum creatinine, 15.2 Ϯ 0.8 mol/L). Similar protection (crescents, 14.3 Ϯ 1.9% of glomeruli; serum creatinine, 18.9 Ϯ 1.1 mol/L) was observed in chimeric mice with intact BM but absent renal-derived TNF (WT3 TNF Ϫ/Ϫ chimeras), suggesting a minor contribution of infiltrating leukocytes to TNF-mediated renal injury. Chimeric mice with TNFdeficient leukocytes but intact intrinsic renal cell-derived TNF (crescents, 20.5 Ϯ 2.0% of glomeruli; serum creatinine, 21.6 Ϯ 1.4 mol/L) developed similar crescentic GN to WT mice (crescents, 22.3 Ϯ 1.4% of glomeruli; serum creatinine, 24.8 Ϯ 1.9 mol/L). Cutaneous delayed-type hypersensitivity after subdermal challenge with the nephritogenic antigen was attenuated in the absence of BM cell-derived TNF but unaffected in WT3 TNF Ϫ/Ϫ chimeric mice. These studies suggest that intrinsic renal cells are the major cellular source of TNF contributing to inflammatory injury in crescentic GN.

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“…Mesenchyme-and epithelium-derived cell types, including osteoblasts, endothelial cells, fibroblasts, T-cells, thymic, and uterine epithelial cells have been shown to synthesize CSF-1 Abboud and Pinzani 1991;Pinzani et al 1992;Rappolee and Werb 1992;Zisman et al 1993;Hofstetter et al 1995;Felix et al 1996;Kamanna et al 1996;Harrington et al 1997;Pollard 1997). Cells synthesize several biologically active forms of CSF-1, including a cell surface glycoprotein, a secreted glycoprotein, and a secreted chondroitin sulfate-containing proteoglycan that is capable of binding to extracellular matrix proteins (Price et al 1992;Ohtsuki et al 1993;Stanley et al 1997;Rettenmier and Roussel 1998).…”

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confidence: 99%

Analysis of the Mouse CSF-1 Gene Promoter in a Transgenic Mouse Model¹

Abboud

Bunegin

Ghosh‐Choudhury

et al. 2003

J Histochem Cytochem.

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S U M M A R Y CSF-1 stimulates monocyte and osteoclast populations. However, the molecular mechanisms involved in regulating CSF-1 gene expression are unclear. To identify regulatory regions that control normal CSF-1 gene expression, a Ϫ 774/ ϩ 183-bp fragment of the murine CSF-1 promoter was analyzed in vitro and in vivo. Transcriptional activity was high in cultured osteoblasts that express CSF-1 mRNA compared to ARH-77 B cells that lack CSF-1 gene expression. Transient transfection of osteoblasts with promoter deletion constructs showed that the Ϫ 774-bp fragment conferred the highest transcriptional activity and contained activator and repressor sequences. To assess the ability of the CSF-1 promoter to confer normal tissue expression of CSF-1, transgenic mice containing the Ϫ 774/ ϩ 183-bp region driving the E. coli ␤ -galactosidase (lacZ) reporter gene were generated. ␤ -Gal analysis of whole tissue extracts showed transgene expression in all tissues tested except liver and kidney. At the cellular level, the pattern of ␤ -gal expression in the spleen, thymus, bone, lung, and testes of adult transgenic mice mimicked normal endogenous CSF-1 mRNA expression in non-transgenic littermates detected by in situ hybridization. This region also directed appropriate transgene expression to sites in other tissues known to synthesize CSF-1, with the exception of the liver and kidney. These findings indicate that the Ϫ 774-bp fragment contains cis -acting elements sufficient to direct CSF-1 gene expression in many tissues. CSF-1 promoter/lacZ mice may be useful for studying the transcriptional mechanisms involved in regulating CSF-1 gene expression in tissues throughout development.

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Activation of mesangial cells with TNF-α stimulates M-CSF gene expression and monocyte proliferation: evidence for involvement of protein kinase C and protein tyrosine kinase

Cited by 18 publications

References 46 publications

Reduced Macrophage Recruitment, Proliferation, and Activation in Colony-Stimulating Factor-1-Deficient Mice Results in Decreased Tubular Apoptosis During Renal Inflammation

Reduced Macrophage Recruitment, Proliferation, and Activation in Colony-Stimulating Factor-1-Deficient Mice Results in Decreased Tubular Apoptosis During Renal Inflammation

Intrinsic Renal Cells Are the Major Source of Tumor Necrosis Factor Contributing to Renal Injury in Murine Crescentic Glomerulonephritis

Analysis of the Mouse CSF-1 Gene Promoter in a Transgenic Mouse Model¹

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Activation of mesangial cells with TNF-α stimulates M-CSF gene expression and monocyte proliferation: evidence for involvement of protein kinase C and protein tyrosine kinase

Cited by 18 publications

References 46 publications

Reduced Macrophage Recruitment, Proliferation, and Activation in Colony-Stimulating Factor-1-Deficient Mice Results in Decreased Tubular Apoptosis During Renal Inflammation

Reduced Macrophage Recruitment, Proliferation, and Activation in Colony-Stimulating Factor-1-Deficient Mice Results in Decreased Tubular Apoptosis During Renal Inflammation

Intrinsic Renal Cells Are the Major Source of Tumor Necrosis Factor Contributing to Renal Injury in Murine Crescentic Glomerulonephritis

Analysis of the Mouse CSF-1 Gene Promoter in a Transgenic Mouse Model1

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Analysis of the Mouse CSF-1 Gene Promoter in a Transgenic Mouse Model¹