ArticleMolecular and cellular biochemistry2012
Lipopolysaccharide upregulates the expression of corticotropin-releasing hormone via MAP kinase pathway in rat peritoneal macrophages.
Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Progress in the mechanism and targeted drug therapy for COPD.Signal transduction and targeted therapy · 2020Review
- Corticotropin-releasing hormone improves survival in pneumococcal pneumonia by reducing pulmonary inflammation.Physiological reports · 2017Article
- Corticotropin-releasing Factor Changes the Phenotype and Function of Dendritic Cells in Mouse Mesenteric Lymph Nodes.Journal of neurogastroenterology and motility · 2015Article
- Hypothalamic neurohormones and immune responses.Frontiers in integrative neuroscience · 2013Article
- p38 MAPK inhibitors, IKK2 inhibitors, and TNFα inhibitors in COPD.Current opinion in pharmacology · 2012Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The stress neuropeptide, corticotropin-releasing hormone (CRH) is expressed in peripheral tissues and inflammatory sites and is implicated in the modulation of the inflammatory response in a paracrine/ autocrine manner. However, the mechanisms by which CRH expression is regulated in peripheral immune cells are unclear. In this article, we address this question by employing primary rat peritoneal macrophages treated with lipopolysaccharide (LPS). Our results showed that CRH could be detected at the mRNA and protein levels in normal peritoneal macrophages and the levels increased significantly and reached a peak at 4 h after stimulation with 100 ng/ml LPS. Furthermore, LPS-induced CRH expression was inhibited by pretreatment with PD98059, a specific MAP kinase inhibitor, in a dose-dependent fashion in which the mRNA and protein levels of CRH was decreased by 90% and 95%, respectively. In addition, pretreatment with 50 μM SB203580, a p38 MAPK inhibitor, led to the decrease of CRH mRNA level by about 41%. Altogether, these results demonstrate that LPS significantly upregulates CRH expression through MAP kinase signaling pathway in rat peritoneal macrophages.
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