Eicosanoids and Cytokines in Glomerular Injury

Williams, Julie; Davies, Malcolm

doi:10.1007/978-94-011-3902-1_7

Cited by 3 publications

(1 citation statement)

References 168 publications

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“…Further functional or antigenic differentiation may then be determined by signals from locally derived factors, as shown for the modulation for smooth muscle cells ( Thyberg et al 1990). In support of this, the biosynthetic profile of fibroblasts, smooth muscle cells and mesangial cells is very similar (Thyberg et al 1990;Williams & Davies 1991). Interestingly, in this study a subpopulation of morphologically typical stellate "mesangial" cells positive for antibodies to smooth muscle actin was found and, likewise, a subpopulation of desmin-positive mesangial cells.…”

Section: Epitopes Shared With Mesangial Cells and Jibroblastssupporting

confidence: 79%

The glomerular mesangium: studies of its developmental origin and markers in vivo and in vitro

Holthöfer

Sainio

Miettinen

1995

APMIS

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Cultured mesangial cells are widely used to explore their role in kidney glomerular functions, but methods to reliably identify these cells in vivo and in vitro are lacking. Furthermore, the proposed relationship of mesangial cells to e.g. fibroblasts and smooth muscle cells has not been systematically studied. Here we wanted to search for markers of practical use also in identifying cultured mesangial cells, and to apply these markers in a study of the origin of glomerular mesangium. No epitopes specific for only mesangial cells could be identified, and no evidence of their true relationship with neural or lymphocytic lineages could be found. Findings with the variety of markers used suggest that mesangial cells may be indistinguishable from smooth muscle cells and fibroblasts. A panel of antibodies, including those against Thy 1.1, smooth muscle actin, desmin, cellular fibronectin and pi integrin al and a5 chains, and Wistaria floribunda (WFA) and Ricinus communis (RCA I) lectins, were found useful for mesangial cell detection in vivo and in vitro. The origin of glomerular mesangial cells could not be conclusively determined, although the results indirectly suggest that mesangial cells together with endothelial cells migrate to the glomerulus from the outside.

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Section: Epitopes Shared With Mesangial Cells and Jibroblastssupporting

confidence: 79%

The glomerular mesangium: studies of its developmental origin and markers in vivo and in vitro

Holthöfer

Sainio

Miettinen

1995

APMIS

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Renal Parenchymal Hypertension: current concepts of pathogenesis and management

Preston¹,

Singer²,

Epstein³

1996

Archives of Internal Medicine

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Renal parenchymal disease is a common but often unrecognized cause of hypertension. Chronic renal disease and systemic hypertension may coexist in two distinct settings. First, essential hypertension is an important cause of chronic renal disease. Second, renal parenchymal disease is a well-established cause of secondary hypertension. Renal parenchymal disease is the most common cause of secondary hypertension, accounting for 2.5% to 5.0% of all cases of systemic hypertension. Secondary hypertension may also accelerate the decline in renal function if inadequately controlled. Therefore, hypertension is both a cause and a consequence of renal disease, and it may be difficult to distinguish them clinically.

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Glomerular antigens in severe hereditary nephrosis

Holthöfer

Haltia

Jalanko

et al. 1995

APMIS

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L. Glomerular antigens in severe hereditary nephrosis. APMIS 103: 823-83 I, 1995. In search of the basic defect and cell type responsible for the massive treatment-resistant proteinuria of congenital nephrotic syndrome of the Finnish type (CNF), we examined tissue samples of CNF kidneys using established antibody and lectin markers of various glomerular cell types. Markers of vascular endothelium (antibodies to factor VIII and a human homologue of podocalyxin (anti-PHM5) and UEA I lectin) showed no qualitative changes in the endothelial cells of glomeruli or peritubular areas in CNF as compared with controls. Markers of glomerular mesangial cells (antibodies to desmin, smooth muscle actin, RCA 1 lectin) revealed a secondary increase in mesangial reactivity reflecting the sclerosis and expansion of the mesangial areas in CNE Markers of visceral epithelial cells (antibodies to a human homologue of podocalyxin, C3b receptor, vimentin, common lymphocytic leukemia antigen, gp44, and the WGA, LFA and, after neuraminidase treatment, PNA lectin) failed to show appreciable qualitative changes in CNF kidney samples. Interestingly, the a2pl integrins appeared greatly reduced in all CNF samples studied, possibly explaining the mechanisms of CNF-associated proteinuria.

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Eicosanoids and Cytokines in Glomerular Injury

Cited by 3 publications

References 168 publications

The glomerular mesangium: studies of its developmental origin and markers in vivo and in vitro

The glomerular mesangium: studies of its developmental origin and markers in vivo and in vitro

Renal Parenchymal Hypertension: current concepts of pathogenesis and management

Glomerular antigens in severe hereditary nephrosis

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