ArticleJournal of inflammation (London, England)2018
Histone deacetylase 2 (HDAC2) attenuates lipopolysaccharide (LPS)-induced inflammation by regulating PAI-1 expression.
Article in Journal of inflammation (London, England), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 48 citations in OpenAlex.
- HDAC2 enhances the antimicrobial activity of neutrophils by promoting the formation of neutrophil extracellular traps (NETs) in sepsis.Journal of advanced research · 2026Article
- Article
- HDAC2 mediates the activation of macrophage in sepsis induced lung injury via regulating the acetylation of SOX2 and the transcription of STAMP2.European journal of medical research · 2025Article
- Advances in Understanding Lipopolysaccharide-Mediated Hepatitis: Mechanisms and Pathological Features.Current issues in molecular biology · 2025Review
- Microglial histone deacetylase 2 is dispensable for functional and histological outcomes in a mouse model of traumatic brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- Variation in presepsin and thrombomodulin levels for predicting COVID-19 mortality.Scientific reports · 2023Article
- Epigenetic perspectives associated with COVID-19 infection and related cytokine storm: an updated review.Infection · 2023Review
- Enhancing HCC Treatment: innovatively combining HDAC2 inhibitor with PD-1/PD-L1 inhibition.Cancer cell international · 2023Review
- Theophylline-based hybrids as acetylcholinesterase inhibitors endowed with anti-inflammatory activity: synthesis, bioevaluation,RSC advances · 2023Article
- The deciphering of the immune cells and marker signature in COVID-19 pathogenesis: An update.Journal of medical virology · 2022Review
- Dynamic monitoring of kidney injury status over 3 days in the intensive care unit as a sepsis phenotype associated with hospital mortality and hyperinflammation.Biomedical journal · 2022Article
- The role of antigen-presenting cells in the pathogenesis of COVID-19.Pathology, research and practice · 2022Review
- TMT-based proteomics analysis of the cerebral cortex of TauT knockout rats.Proteome science · 2022Article
- The Survival of Septic Patients with Compensated Liver Cirrhosis Is Not Inferior to That of Septic Patients without Liver Cirrhosis: A Propensity Score Matching Analysis.Journal of clinical medicine · 2022Article
- Metformin alleviates chronic obstructive pulmonary disease and cigarette smoke extract-induced glucocorticoid resistance by activating the nuclear factor E2-related factor 2/heme oxygenase-1 signaling pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022Article
- Epigenomic and transcriptomic analyses reveal differences between low-grade inflammation and severe exhaustion in LPS-challenged murine monocytes.Communications biology · 2022Article
- Role of Epigenetics in the Regulation of Immune Functions of the Skin.The Journal of investigative dermatology · 2021Review
- Could Antigen Presenting Cells Represent a Protective Element during SARS-CoV-2 Infection in Children?Pathogens (Basel, Switzerland) · 2021Review
- Review
- Acetylation in Tumor Immune Evasion Regulation.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSepsis is a life-threatening organ dysfunction caused by dysregulated host response to infection, and is primarily characterized by an uncontrolled systemic inflammatory response. In the present study, we developed an effective adjunct therapy mediated by a novel mechanism, to attenuate overt inflammation. LPS-treated macrophages were adopted as an in vitro model of endotoxin-induced inflammation during sepsis. Experiments were carried out using primary mouse peritoneal macrophages and the murine macrophage cell line RAW264.7, to elucidate the mechanisms by which HDAC2 modulates endotoxin-induced inflammation.
resultsResults revealed that PAI-1, TNF, and MIP-2 expression were inhibited by theophylline, an HDAC2 enhancer, in a RAW macrophage cell line, following LPS-induced inflammation. Thus, HDAC2 plays an important role in immune defense by regulating the expression of inflammatory genes via the c-Jun/PAI-1 pathway. During LPS-induced inflammation, overexpression of HDAC2 was found to inhibit PAI-1, TNF, and MIP-2 expression. Following LPS stimulation, HDAC2 knockdown increased nuclear translocation and DNA binding of c-Jun to the PAI-1 gene promoter, thereby activating PAI-1 gene transcription. Furthermore, inhibition of PAI-1 by TM5275 alone or in combination with theophylline notably suppressed TNF and MIP-2 expression.
conclusionHDAC2 can attenuate lipopolysaccharide-induced inflammation by regulating c-Jun and PAI-1 expression in macrophages.
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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.