ArticlePloS one2011
Extracellular administration of BCL2 protein reduces apoptosis and improves survival in a murine model of sepsis.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 31 citations in OpenAlex.
- Pathogenesis of ELANE-mutant severe neutropenia revealed by induced pluripotent stem cells.The Journal of clinical investigation · 2015Trial
- Dexmedetomidine regulates the SIRT3-mediated JAK2/STAT3 signaling pathway to protect against sepsis-induced intestinal injury.Scientific reports · 2025Article
- Neutrophil heterogeneity and plasticity: unveiling the multifaceted roles in health and disease.MedComm · 2025Review
- Underestimated Subsequent Sensorineural Hearing Loss after Septicemia.Medicina (Kaunas, Lithuania) · 2023Article
- Molecular characterization and expression analysis of B-cell lymphoma-2 inFrontiers in immunology · 2023Article
- PINK1 contained in huMSC-derived exosomes prevents cardiomyocyte mitochondrial calcium overload in sepsis via recovery of mitochondrial CaStem cell research & therapy · 2021Article
- Adenoviral TMBIM6 vector attenuates ER-stress-induced apoptosis in a neonatal hypoxic-ischemic rat model.Disease models & mechanisms · 2019Article
- Role of microRNAs in sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017Review
- PPAR-Oxidative medicine and cellular longevity · 2017Article
- Inhibition of MicroRNA 195 Prevents Apoptosis and Multiple-Organ Injury in Mouse Models of Sepsis.The Journal of infectious diseases · 2016Article
- Nonhematopoietic β-Arrestin-1 inhibits inflammation in a murine model of polymicrobial sepsis.The American journal of pathology · 2014Article
- IRAK1-dependent signaling mediates mortality in polymicrobial sepsis.Inflammation · 2013Article
- Neuraminidase reprograms lung tissue and potentiates lipopolysaccharide-induced acute lung injury in mice.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Sepsis: multiple abnormalities, heterogeneous responses, and evolving understanding.Physiological reviews · 2013Article
- Sepsis otopathy: experimental sepsis leads to significant hearing impairment due to apoptosis and glutamate excitotoxicity in murine cochlea.Disease models & mechanisms · 2013Article
- BRCA1 gene therapy reduces systemic inflammatory response and multiple organ failure and improves survival in experimental sepsis.Gene therapy · 2013Article
- Hepatitis C virus activates Bcl-2 and MMP-2 expression through multiple cellular signaling pathways.Journal of virology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundSevere sepsis and septic shock are major causes of morbidity and mortality worldwide. In experimental sepsis there is prominent apoptosis of various cell types, and genetic manipulation of death and survival pathways has been shown to modulate organ injury and survival. METHODOLOGY/PRINCIPAL
findingsWe investigated the effect of extracellular administration of two anti-apoptotic members of the BCL2 (B-cell lymphoma 2) family of intracellular regulators of cell death in a murine model of sepsis induced by cecal ligation and puncture (CLP). We show that intraperitoneal injection of picomole range doses of recombinant human (rh) BCL2 or rhBCL2A1 protein markedly improved survival as assessed by surrogate markers of death. Treatment with rhBCL2 or rhBCL2A1 protein significantly reduced the number of apoptotic cells in the intestine and heart following CLP, and this was accompanied by increased expression of endogenous mouse BCL2 protein. Further, mice treated with rhBCL2A1 protein showed an increase in the total number of neutrophils in the peritoneum following CLP with reduced neutrophil apoptosis. Finally, although neither BCL2 nor BCL2A1 are a direct TLR2 ligand, TLR2-null mice were not protected by rhBCL2A1 protein, indicating that TLR2 signaling was required for the protective activity of extracellularly adminsitered BCL2A1 protein in vivo. CONCLUSIONS/SIGNIFICANCE: Treatment with rhBCL2A1 or rhBCL2 protein protects mice from sepsis by reducing apoptosis in multiple target tissues, demonstrating an unexpected, potent activity of extracellularly administered BCL2 BH4-domain proteins.
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.