ArticleJournal of cellular physiology2010
Regulation of lipopolysaccharide-induced inflammatory response and endotoxemia by beta-arrestins.
Article in Journal of cellular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 53 citations in OpenAlex.
- Article
- Anti-inflammatory potential of Piper betleoides C. DC., a promising Piper species of Northeast India: in vitro and in vivo evidence and mechanistic insight.Inflammopharmacology · 2024Article
- CMTM 6 promotes the development of thyroid cancer by inhibiting NIS activity through activating the MAPK signaling pathway.Functional & integrative genomics · 2024Article
- Characterization of lncRNA-Based ceRNA Network and Potential Prognostic Hub Genes for Sepsis.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- The Link between Gut Dysbiosis Caused by a High-Fat Diet and Hearing Loss.International journal of molecular sciences · 2021Review
- ARRB1 suppresses the activation of hepatic macrophages via modulating endoplasmic reticulum stress in lipopolysaccharide-induced acute liver injury.Cell death discovery · 2021Article
- Betamethasone induces potent immunosuppression and reduces HIV infection in a PBMC in vitro model.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2021Article
- β-arrestin 2 attenuates lipopolysaccharide-induced liver injuryWorld journal of gastroenterology · 2018Article
- Lipopolysaccharide-induced inflammation in monocytes/macrophages is blocked by liposomal delivery of GInternational journal of nanomedicine · 2018Article
- NLRP12 Inflammasome Expression in the Rat Brain in Response to LPS during Morphine Tolerance.Brain sciences · 2017Article
- Non-Hematopoietic β-Arrestin1 Confers Protection Against Experimental Colitis.Journal of cellular physiology · 2016Article
- A Standardized Chemically Modified Curcuma longa Extract Modulates IRAK-MAPK Signaling in Inflammation and Potentiates Cytotoxicity.Frontiers in pharmacology · 2016Article
- Multifaceted role of β-arrestins in inflammation and disease.Genes and immunity · 2015Review
- Protective Role of β-arrestin2 in Colitis Through Modulation of T-cell Activation.Inflammatory bowel diseases · 2015Article
- Activation of N-methyl-d-aspartate receptor downregulates inflammasome activity and liver inflammation via a β-arrestin-2 pathway.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- β-Arrestin 2 negatively regulates Toll-like receptor 4 (TLR4)-triggered inflammatory signaling via targeting p38 MAPK and interleukin 10.The Journal of biological chemistry · 2014Article
- Nonhematopoietic β-Arrestin-1 inhibits inflammation in a murine model of polymicrobial sepsis.The American journal of pathology · 2014Article
- β-Arrestins 1 and 2 are critical regulators of inflammation.Innate immunity · 2014Review
- Lithium chloride induces TNFα in mouse macrophages via MEK-ERK-dependent pathway.Journal of cellular biochemistry · 2014Article
- Arrestins in host-pathogen interactions.Handbook of experimental pharmacology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Beta-arrestins are scaffolding proteins implicated as negative regulators of TLR4 signaling in macrophages and fibroblasts. Unexpectedly, we found that beta-arrestin-1 (beta-arr-1) and -2 knockout (KO) mice are protected from TLR4-mediated endotoxic shock and lethality. To identify the potential mechanisms involved, we examined the plasma levels of inflammatory cytokines/chemokines in the wild-type (WT) and beta-arr-1 and -2 KO mice after lipopolysaccharide (LPS, a TLR4 ligand) injection. Consistent with lethality, LPS-induced inflammatory cytokine levels in the plasma were markedly decreased in both beta-arr-1 and -2 KO, compared to WT mice. To further explore the cellular mechanisms, we obtained splenocytes (separated into CD11(b+) and CD11(b-) populations) from WT, beta-arr-1, and -2 KO mice and examined the effect of LPS on cytokine production. Similar to the in vivo observations, LPS-induced inflammatory cytokines were significantly blocked in both splenocyte populations from the beta-arr-2 KO compared to the WT mice. This effect in the beta-arr-1 KO mice, however, was restricted to the CD11(b-) splenocytes. Our studies further indicate that regulation of cytokine production by beta-arrestins is likely independent of MAPK and IkappaBalpha-NFkappaB pathways. Our results, however, suggest that LPS-induced chromatin modification is dependent on beta-arrestin levels and may be the underlying mechanistic basis for regulation of cytokine levels by beta-arrestins in vivo. Taken together, these results indicate that beta-arr-1 and -2 mediate LPS-induced cytokine secretion in a cell-type specific manner and that both beta-arrestins have overlapping but non-redundant roles in regulating inflammatory cytokine production and endotoxic shock in mice.
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.