ArticleClinical and experimental immunology2002
Intravenous immunoglobulin (IVIG) preparations induce apoptosis in TNF-alpha-stimulated endothelial cells via a mitochondria-dependent pathway.
Article in Clinical and experimental immunology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 18 citations in OpenAlex.
- Successful combined intravenous and subcutaneous immunoglobulin treatment for intractable protein-losing enteropathy in a patient long after Fontan-type operation.Journal of cardiology cases · 2018Article
- Should development of Alzheimer's disease-specific intravenous immunoglobulin be considered?Journal of neuroinflammation · 2014Review
- Amiloride attenuates lipopolysaccharide-accelerated atherosclerosis via inhibition of NHE1-dependent endothelial cell apoptosis.Acta pharmacologica Sinica · 2013Article
- Bench-to-bedside review: Immunoglobulin therapy for sepsis - biological plausibility from a critical care perspective.Critical care (London, England) · 2012Review
- Normal human IgG prevents endothelial cell activation induced by TNFalpha and oxidized low-density lipoprotein atherogenic stimuli.Clinical and experimental immunology · 2003Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial cells (ECs) are a target in inflammation, and the death of EC is regulated by various factors. Although intravenous immunoglobulin (IVIG) preparations are known to be beneficial therapeutic agents for the treatment of autoimmune diseases and systemic inflammatory disorders, their mechanism of action have not yet been completely elucidated. The aim of the present study is to investigate the possible role of IVIG in EC apoptosis. We demonstrate herein that IVIG induced the apoptosis of human umbilical vein ECs (HUVECs) prestimulated by TNF-alpha in vitro, but not in unstimulated HUVECs, in a dose- and time-dependent manner, using a proportion of cells with hypodiploid DNA, DNA ladder formation and morphological changes. Anti-Fas MoAbs had no effect on the IVIG-induced apoptosis in the TNF-alpha-stimulated HUVECs. IVIG decreased the intracellular expression of anti-apoptotic proteins of the Bcl-2 family (A1 and Bcl-XL) while IVIG increased the intracellular expression of pro-apoptotic proteins (Bax and Bcl-XS) in the TNF-alpha-stimulated HUVECs. Furthermore, IVIG increased the intracellular production of reactive oxygen species and decreased the mitochondrial membrane potential (Delta(psi)m). Caspase-inhibitors inhibited the IVIG-induced apoptosis of the TNF-alpha-stimulated HUVECs. The present results show a novel action in which IVIG can induce the apoptosis of TNF-alpha-stimulated HUVECs through a mitochondrial apoptotic signalling pathway. These observations suggest that the clinical use of IVIG preparations may thereby regulate the cell death of activated ECs in inflammation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.