Induction of Renal Cell Apoptosis by Antibodies and Complement

Roos, Anja; Sato, Toshinobu; Maier, Hans; Kooten, Cees van; Daha, Mohamed R.

doi:10.1159/000052596

Cited by 13 publications

(4 citation statements)

References 22 publications

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“…Proliferation and apoptosis play a pivotal role in a variety of biological processes, such as morphogenesis during the embryonic stage, cell selection during lymphoid development, tissue repair after injury, regression of inflammation, elimination of cells at risk of developing into a tumor and lymphocyte-mediated killing [19]. A balance of proliferation and apoptosis is essential for the tissue homeostasis [20,21].…”

Section: Discussionmentioning

confidence: 99%

“…Probably the most thoroughly characterized death receptor is the cell membrane receptor Fas (CD 95), a member of the TNF receptor family. Cross-linking of Fas, either via specific antibodies or via its specific ligand, activates a cascade reaction of caspases, which are responsible for induction of membrane alterations, breakdown of cellular constituents and DNA, and finally cell death [19]. …”

Section: Discussionmentioning

confidence: 99%

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Effects of chemokines on proliferation and apoptosis of human mesangial cells

et al. 2004

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BackgroundProliferation and apoptosis of mesangial cells (MC) are important mechanisms during nephrogenesis, for the maintenance of glomerular homeostasis as well as in renal disease and glomerular regeneration. Expression of chemokines and chemokine receptors by intrinsic renal cells, e.g. SLC/CCL21 on podocytes and CCR7 on MC is suggested to play a pivotal role during these processes. Therefore the effect of selected chemokines on MC proliferation and apoptosis was studied.MethodsProliferation assays, cell death assays including cell cycle analysis, hoechst stain and measurement of caspase-3 activity were performed.ResultsA dose-dependent, mesangioproliferative effect of the chemokine SLC/CCL21, which is constitutively expressed on human podocytes was seen via activation of the chemokine receptor CCR7, which is constitutively expressed on MC. In addition, in cultured MC SLC/CCL21 had a protective effect on cell survival in Fas-mediated apoptosis. The CXCR3 ligands IP-10/CXCL10 and Mig/CXCL9 revealed a proproliferative effect but did not influence apoptosis of MC. Both the CCR1 ligand RANTES/CCL5 and the amino-terminally modified RANTES analogue Met-RANTES which blocks CCR1 signalling had no effect on proliferation and apoptosis.ConclusionsThe different effects of chemokines and their respective receptors on proliferation and apoptosis of MC suggest highly regulated, novel biological functions of chemokine/chemokine receptor pairs in processes involved in renal inflammation, regeneration and glomerular homeostasis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effects of chemokines on proliferation and apoptosis of human mesangial cells

et al. 2004

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“…Injury in anti-Thy-1.1 nephritis is caused directly by binding of administered antibody to Thy-1.1 on the mesangial cell surface, which results in complement-dependent cell death in which both necrosis and apoptosis are prominent. 29 The earliest phase is accompanied by a marked influx of ED1-positive cells. Substantial numbers of macrophages have already localized 1 hour after injection of OX7 and this is consistent with the very early glomerular expression of MCP-1.…”

Section: Discussionmentioning

confidence: 99%

Heterogeneity of Macrophage Activation in Anti-Thy-1.1 Nephritis

Minto¹,

Erwig²,

Rees³

2003

The American Journal of Pathology

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Macrophages infiltrating glomeruli in telescoped nephrotoxic nephritis are programmed. The purpose of this study was to assess whether macrophages infiltrating glomeruli of rats with passively induced injury become similarly programmed, and to determine whether macrophage commitment is an early event. Glomerular macrophages isolated from rats with resolving and proliferative anti-Thy-1 nephritis were examined for nitric oxide (NO) generation and expression of lysosomal hydrolases. After a single injection of Thy-1 antibody the cells generated large amounts of NO that was attenuated ex vivo by transforming growth factor-beta and other anti-inflammatory cytokines. In contrast macrophages infiltrating glomeruli immediately after a second injection of Thy-1 antibody generated NO spontaneously and were unresponsive to alternative activation. beta-Glucuronidase expression was used as a second independent assay for macrophage activation and the results confirmed the observations made for NO. Furthermore, macrophages infiltrating the glomerulus after the second antibody injection exhibited a striking dichotomy in that 70% of the cells behave as programmed by interferon-gamma and 30% by transforming growth factor-beta. The results show that macrophage commitment occurs very early after monocyte migration and that infiltration itself does not invariably induce macrophage programming. It demonstrates that macrophages infiltrating inflamed glomeruli at the same time do not respond uniformly, but are capable of engaging different activation programs. This emphasizes the critical importance of the underlying disease process for macrophage functional development in an inflamed environment.

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“…In addition, Bcl-2 binds to Bax to form a Bax/Bcl-2 polymer to inhibit the apoptotic process (33). High expression levels of Bcl-2 also maintain cell stability by inducing glutathione aggregation in the cell nucleus to reduce caspase activity (34). The results of the present study suggested that PUMA may inhibit GBC invasion at least partially by regulating the expression of Bax and Bcl-2.…”

Section: Discussionmentioning

confidence: 52%

Expression and inhibitory effects of p53‑upregulated modulator of apoptosis in gallbladder carcinoma

et al. 2021

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The p53-upregulated modulator of apoptosis (PUMA) has been reported to be involved in various types of cancer. However, its potential biological role in gallbladder carcinoma (GBC) has not been fully elucidated. The present study aimed to determine the expression levels of PUMA and its biological effects on GBC. The mRNA and protein expression levels of PUMA in GBC tissues and cell lines were measured using reverse transcription-quantitative PCR and western blotting, respectively. The effects of PUMA overexpression on cell viability, proliferation and invasive ability were determined in vitro using the MTT, colony formation and Transwell invasion assays, respectively. The apoptotic rates were detected using the Annexin V-FITC apoptosis detection kit. Furthermore, follow-up of patients with GBC was performed to identify the association between PUMA expression levels and GBC prognosis. The results of the present study demonstrated that the expression levels of PUMA were significantly lower in the GBC tissues and cell lines compared with those in adjacent normal gallbladder tissues and normal gallbladder cells, respectively. Further experiments indicated that overexpression of PUMA inhibited the viability, proliferation and invasive ability of GBC cells compared with those in the control-transfected GBC cells. In addition, overexpression of PUMA significantly promoted apoptosis in GBC cells. Furthermore, overexpression of PUMA inhibited epithelial-mesenchymal transition, and promoted Bax upregulation and Bcl-2 downregulation compared with those in the control group. Low PUMA expression levels were associated with a short overall survival time in patients with GBC. In conclusions, PUMA may act as a tumor suppressor in GBC and may serve as a potential novel treatment target for human GBC.

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Induction of Renal Cell Apoptosis by Antibodies and Complement

Cited by 13 publications

References 22 publications

Effects of chemokines on proliferation and apoptosis of human mesangial cells

Effects of chemokines on proliferation and apoptosis of human mesangial cells

Heterogeneity of Macrophage Activation in Anti-Thy-1.1 Nephritis

Expression and inhibitory effects of p53‑upregulated modulator of apoptosis in gallbladder carcinoma

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