Complement dependence of antibody-induced mesangial cell injury in the rat.

Yamamoto, Tetsu; Wilson, C B

doi:10.4049/jimmunol.138.11.3758

Cited by 112 publications

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“…The anti-Thy-1.1-induced glomerulonephritis model in rats was created following the previous study 11 . Seven-week-old male Wister rats were purchased from Japan SLC (Shizuoka, Japan).…”

Section: Methodsmentioning

confidence: 99%

C5a–C5AR1 axis as a potential trigger of the rupture of intracranial aneurysms

Okada,

Shimizu,

Kawashima

et al. 2024

Sci Rep

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Recent studies have indicated the involvement of neutrophil-mediated inflammatory responses in the process leading to intracranial aneurysm (IA) rupture. Receptors mediating neutrophil recruitment could thus be therapeutic targets of unruptured IAs. In this study, complement C5a receptor 1 (C5AR1) was picked up as a candidate that may cause neutrophil-dependent inflammation in IA lesions from comprehensive gene expression profile data acquired from rat and human samples. The induction of C5AR1 in IA lesions was confirmed by immunohistochemistry; the up-regulations of C5AR1/C5ar1 stemmed from infiltrated neutrophils, which physiologically express C5AR1/C5ar1, and adventitial fibroblasts that induce C5AR1/C5ar1 in human/rat IA lesions. In in vitro experiments using NIH/3T3, a mouse fibroblast-like cell line, induction of C5ar1 was demonstrated by starvation or pharmacological inhibition of mTOR signaling by Torin1. Immunohistochemistry and an experiment in a cell-free system using recombinant C5 protein and recombinant Plasmin indicated that the ligand of C5AR1, C5a, could be produced through the enzymatic digestion by Plasmin in IA lesions. In conclusion, we have identified a potential contribution of the C5a–C5AR1 axis to neutrophil infiltration as well as inflammatory responses in inflammatory cells and fibroblasts of IA lesions. This cascade may become a therapeutic target to prevent the rupture of IAs.

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“…The anti-Thy-1.1-induced glomerulonephritis model in rats was created following the previous study 11 . Seven-week-old male Wister rats were purchased from Japan SLC (Shizuoka, Japan).…”

Section: Methodsmentioning

confidence: 99%

C5a–C5AR1 axis as a potential trigger of the rupture of intracranial aneurysms

Okada,

Shimizu,

Kawashima

et al. 2024

Sci Rep

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Immune Aspects of Renal Diseases

Wilson¹

1987

JAMA

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Collagen-binding heat shock protein (HSP) 47 expression in anti-thymocyte serum (ATS)-induced glomerulonephritis

Razzaque

Taguchi

1997

J. Pathol.

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An increased accumulation of extracellular matrix (ECM), predominantly collagens, is the main component of the expanded mesangial matrix in anti‐thymocyte serum (ATS)‐induced glomerulonephritis (GN). Heat shock protein (HSP) 47 is a collagen‐binding stress protein and has been shown to have a specific role in the intracellular processing of procollagen molecules. It is a collagen‐specific molecular chaperone in various organs, but its role in the kidney in relation to matrix expansion is not yet known. This study was designed to assess whether increased ECM accumulation in ATS‐induced GN is associated with HSP47. The expression of type I, type III and type IV collagens, with their molecular chaperone HSP47, was investigated in ATS‐induced GN rat kidneys. Fifteen male Wistar rats were divided into two groups: ATS‐induced GN rats (group I) and age‐matched controls (group II). GN was induced by injecting a single dose of ATS (0·8 ml/100 g body weight). All the rats were killed on the third and tenth day of the experiment. In group I, 3 days after ATS injection, histological examination revealed a reduction in glomerular cell number with mesangiolysis. However, 10 days after ATS injection, histologically severe mesangial cell proliferation with expansion of the mesangial matrix was noted in group I rats. By semiquantitative analysis, compared with controls, increased type I, type III, and type IV collagen immunostaining was observed in the expanded mesangial matrix in ATS‐induced GN (group I) rats on day 10. Immunoreactive HSP47 expression was weak in the intraglomerular cells and was occasionally seen in the interstitial cells in control kidneys. In contrast, strong immunostaining for HSP47 was noted in the glomeruli of the ATS‐treated rat kidneys on day 10. In this study, there was a parallel increase of various collagens and their molecular chaperone HSP47 in the ATS‐treated rat kidneys. Compared with controls, no significant difference in HSP47 expression was found in the ATS‐treated rat kidneys without mesangial matrix expansion (3 days after ATS injection). It is concluded that overexpression of HSP47 might play a significant role in the excessive assembly of collagens and could subsequently contribute to the expansion of mesangial matrix found in ATS‐treated rat kidneys. © 1997 by John Wiley & Sons, Ltd.

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Complement dependence of antibody-induced mesangial cell injury in the rat.

Cited by 112 publications

References 0 publications

C5a–C5AR1 axis as a potential trigger of the rupture of intracranial aneurysms

C5a–C5AR1 axis as a potential trigger of the rupture of intracranial aneurysms

Immune Aspects of Renal Diseases

Collagen-binding heat shock protein (HSP) 47 expression in anti-thymocyte serum (ATS)-induced glomerulonephritis

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