ArticleNucleic acids research2006
Kruppel-like factor 5 is an important mediator for lipopolysaccharide-induced proinflammatory response in intestinal epithelial cells.
Article in Nucleic acids research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 95 citations in OpenAlex.
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- LncRNA/CircRNA-miRNA-mRNA Axis in Atherosclerotic Inflammation: Research Progress.Current pharmaceutical biotechnology · 2024Review
- Krüppel-like Factor 5 Plays an Important Role in the Pathogenesis of Chronic Pancreatitis.Cancers · 2023Article
- Participation of Krüppel-like Factors in Atherogenesis.Metabolites · 2023Review
- Targeting the KLF5-EphA2 axis can restrain cancer stemness and overcome chemoresistance in basal-like breast cancer.International journal of biological sciences · 2023Article
- Prevention of LPS-Induced Acute Kidney Injury in Mice by Bavachin and Its Potential Mechanisms.Antioxidants (Basel, Switzerland) · 2022Article
- YB-1 is a positive regulator of KLF5 transcription factor in basal-like breast cancer.Cell death and differentiation · 2022Article
- The roles and regulation of the KLF5 transcription factor in cancers.Cancer science · 2021Review
- Roles of Krüppel-like factor 5 in kidney disease.Journal of cellular and molecular medicine · 2021Review
- KLF5 Is Crucial for Androgen-AR Signaling to Transactivate Genes and Promote Cell Proliferation in Prostate Cancer Cells.Cancers · 2020Article
- miR-145 improves metabolic inflammatory disease through multiple pathways.Journal of molecular cell biology · 2020Article
- The Novel Small-Molecule SR18662 Efficiently Inhibits the Growth of Colorectal CancerMolecular cancer therapeutics · 2019Article
- The roles of TNFAIP2 in cancers and infectious diseases.Journal of cellular and molecular medicine · 2018Review
- Downregulation of Krüppel‑like factor 1 inhibits the metastasis and invasion of cervical cancer cells.Molecular medicine reports · 2018Article
- The transcription factor Klf5 is essential for intrahepatic biliary epithelial tissue remodeling after cholestatic liver injury.The Journal of biological chemistry · 2018Article
- KLF5 promotes cervical cancer proliferation, migration and invasion in a manner partly dependent on TNFRSF11a expression.Scientific reports · 2017Article
- miR-5195-3p Inhibits Proliferation and Invasion of Human Bladder Cancer Cells by Directly Targeting Oncogene KLF5.Oncology research · 2017Article
- KLF5 promotes breast cancer proliferation, migration and invasion in part by upregulating the transcription of TNFAIP2.Oncogene · 2016Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Lipopolysaccharide (LPS) is a bacterially-derived endotoxin that elicits a strong proinflammatory response in intestinal epithelial cells. It is well established that LPS activates this response through NF-kappaB. In addition, LPS signals through the mitogen-activated protein kinase (MAPK) pathway. We previously demonstrated that the Krüppel-like factor 5 [KLF5; also known as intestine-enriched Krüppel-like factor (IKLF)] is activated by the MAPK. In the current study, we examined whether KLF5 mediates the signaling cascade elicited by LPS. Treatment of the intestinal epithelial cell line, IEC6, with LPS resulted in a dose- and time-dependent increase in KLF5 messenger RNA (mRNA) and protein levels. Concurrently, mRNA levels of the p50 and p65 subunits of NF-kappaB were increased by LPS treatment. Pretreatment with the MAPK inhibitor, U0126, or the LPS antagonist, polymyxin B, resulted in an attenuation of KLF5, p50 and p65 NF-kappaB subunit mRNA levels from LPS treatment. Importantly, suppression of KLF5 by small interfering RNA (siRNA) resulted in a reduction in p50 and p65 subunit mRNA levels and NF-kappaB DNA binding activity in response to LPS. LPS treatment also led to an increase in secretion of TNF-alpha and IL-6 from IEC6, both of which were reduced by siRNA inhibition of KLF5. In addition, intercellular adhesion molecule-1 (ICAM-1) levels were increased in LPS-treated IEC6 cells and this increase was associated with increased adhesion of Jurkat lymphocytes to IEC6. The induction of ICAM-1 expression and T cell adhesion to IEC6 by LPS were both abrogated by siRNA inhibition of KLF5. These results indicate that KLF5 is an important mediator for the proinflammatory response elicited by LPS in intestinal epithelial cells.
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