ArticleLung2011
Effects of downregulation of aquaporin1 by peptidoglycan and lipopolysaccharide via MAPK pathways in MeT-5A cells.
Article in Lung, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The trial behind it
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Qi Sui Zhu Shui Plaster Inhibits AQP1 and MAPK Signaling Reduces Liver Damage Induced by Cirrhotic Ascites.Journal of healthcare engineering · 2022Article
- Aquaporin-1 attenuates macrophage-mediated inflammatory responses by inhibiting p38 mitogen-activated protein kinase activation in lipopolysaccharide-induced acute kidney injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019Article
- MicroRNA-495 downregulates AQP1 and facilitates proliferation and differentiation of osteoblasts in mice with tibial fracture through activation of p38 MAPK signaling pathway.Scientific reports · 2019Article
- Function of aquaporins in sepsis: a systematic review.Cell & bioscience · 2018Review
- The Effects of Aquaporin-1 in Pulmonary Edema Induced by Fat Embolism Syndrome.International journal of molecular sciences · 2016Article
- Down-regulation of aquaporin3 expression by lipopolysaccharide via p38/c-Jun N-terminal kinase signalling pathway in HT-29 human colon epithelial cells.World journal of gastroenterology · 2015Article
- Induced expression and functional effects of aquaporin-1 in human leukocytes in sepsis.Critical care (London, England) · 2013Article
- Aquaporin-1 translocation and degradation mediates the water transportation mechanism of acetazolamide.PloS one · 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study was designed to investigate the signaling pathway involved in aquaporin1 (AQP1) expression caused by peptidoglycan (PGN) from Staphylococcus aureus and lipopolysaccharide (LPS) in human pleural mesothelial cell lines (MeT-5A) in vitro. RT-PCR, immunoblot analysis, and immunofluorescence assay were used to determine the relative mRNA and protein levels of AQP1 caused by PGN and LPS in MeT-5A cells. Activation of MAPKs by PGN and LPS was reflected by detecting the phosphorylation constituents of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), and p38 using immunoblot. MAPKs inhibitors were used to determine the effects of PGN- and LPS-induced AQP1 expression by immunoblot. AQP1 transcription and protein expression were decreased by PGN and LPS in dose- and time-dependent manners in MeT-5A cells. Both PGN and LPS activated p38/ERK/JNK pathways in MeT-5A cells. Furthermore, downregulation of AQP1 expression by LPS was blocked by SB203580, SP600125, and PD98059, which are inhibitors of p38, JNK, and ERK1/2, respectively. In contrast, downregulation of AQP1 expression by PGN was blocked only by SB203580, not by SP600125 or PD98059, underlying the importance of p38 MAPK in the downregulation of AQP1 expression by PGN in MeT-5A cells. AQP1 expression was decreased by both PGN and LPS in dose- and time-dependent manners in MeT-5A cells. AQP1 expression was down-regulated by PGN via p38 MAPK pathway, while AQP1 expression was down-regulated by LPS via p38/JNK/ERK pathways.
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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.