ArticleExperimental and therapeutic medicine2021
LMTK2 regulates inflammation in lipopolysaccharide-stimulated BV2 cells.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Novel involvement of LMTK2 and EML6 in rheumatoid arthritis: potential biomarkers for disease activity and seronegative patients.Frontiers in immunology · 2026Article
- Genome-wide association study identifies genetic variants associated with single-parity reproductive loss in three commercial pig breeds.BMC genomics · 2025Article
- The lemur tail kinase family in neuronal function and disfunction in neurodegenerative diseases.Cellular and molecular life sciences : CMLS · 2024Review
- Remifentanil inhibits the inflammatory response of BV2 microglia and protects PC12 cells from damage caused by microglia activation.Bioengineered · 2022Article
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9 authors.
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Abstract
Microglia activation plays vital roles in neuroinflammatory pathologys. Lemurs tyrosine kinase 2 (LMTK2) was reported to regulate NF-κB signals. In the present study, the roles of LMTK2 were investigated in lipopolysaccharide (LPS)-treated BV-2 cells. Reverse transcription-quantitative (RT-q)PCR and western blotting (WB) were utilized to analyze LMTK2 levels in LPS-treated BV2 cells. MTT assay determined cell viabilities. Nitric oxide (NO) and prostaglandin E2 (PGE2) levels were assessed through Griess and enzyme-linked immunosorbent assay (ELISA), respectively. The expression level of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) were detected through RT-qPCR and WB. The release of inflammatory mediators under LPS stimulation, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6 and IL-10, were analyzed through ELISA. WB was used to analyze the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1)/NAD(P)H dehydrogenase quinone 1 (NQO1) signal pathway. The results showed that the levels of the inflammatory mediators, iNOS, NO, COX-2 and PGE2, along with pro-inflammatory factors, TNF-α, IL-1β and IL-6, were significantly decreased following the induction of exogenous LMTK2 expression by LMTK2 overexpression plasmids in LPS-induced BV2 microglia. In contrast, anti-inflammatory factor IL-10 showed obvious decrease. Additionally, LMTK2 overexpression induced the elevation of Nrf2 in the cytoplasm and nucleus, along with the upregulation of HO-1 and NQO1 expression. In conclusion, LMTK2 is postulated to regulate neuroinflammation possibly through Nrf2 pathway. The present study is essential to reveal the underlying function of LMTK2 and to identify novel therapeutic targets for drug development in treating neuroinflammation.
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