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Comparative transcriptomics reveals the role of the Toll-like receptor signaling pathway in fluoride-induced cardiotoxicity.

08:00 EDT 9th April 2019 | BioPortfolio

Summary of "Comparative transcriptomics reveals the role of the Toll-like receptor signaling pathway in fluoride-induced cardiotoxicity."

Many studies have shown that fluorosis due to long-term fluoride intake, has damaging effects on the heart. However, the mechanisms underlying cardiac fluorosis have not been illuminated in detail. We performed High-throughput transcriptome sequencing (RNA-Seq) on rat cardiac tissue to explore the molecular effects of NaF exposure. In total, 372 and 254 differentially expressed genes (DEGs) were identified between a group given 30 mg/L NaF and control, and between a group given 90 mg/L NaF and control, respectively. The transcript levels of most of these genes were significantly downregulated and many were distributed in the Toll-like receptor signaling pathway. Transcriptome analysis revealed that herpes simplex infection, ECM-receptor interaction, influenza A, cytokine-cytokine receptor interaction, Apoptosis and Toll-like receptor signaling pathway were significantly affected. IL-6 and IL-10 may play a crucial role in the cardiac damage caused by NaF as external stimuli according to protein-protein interaction (PPI) network analysis. The results of qRT-PCR and western blotting showed markedly decreased mRNA and protein levels of IL-1, IL-6, and IL-10 in the low concentration fluoride (LF) and high concentration fluoride (HF) groups, which was in agreement with RNA-Seq results. This is the first study to investigate NaF-induced cardiotoxicity at a transcriptome level. Key words: fluoride; cardiac injury; inflammatory injury; RNA-seq; Toll-like pathway.

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This article was published in the following journal.

Name: Journal of agricultural and food chemistry
ISSN: 1520-5118
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A pattern recognition receptor that forms heterodimers with TOLL-LIKE RECEPTOR 2.

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A family of pattern recognition receptors characterized by an extracellular leucine-rich domain and a cytoplasmic domain that share homology with the INTERLEUKIN 1 RECEPTOR and the DROSOPHILA toll protein. Following pathogen recognition, toll-like receptors recruit and activate a variety of SIGNAL TRANSDUCING ADAPTOR PROTEINS.

A receptor tyrosine kinase that transduces signals from EXTRACELLULAR MATRIX to the CYTOPLASM by binding ligands such as GALECTIN 3. It regulates many physiologic processes that include cell survival, migration, differentiation, and PHAGOCYTOSIS of apoptotic cells and ROD PHOTORECEPTORS in the RETINAL PIGMENT EPITHELIUM. Mutations in the MERTK gene are associated with type 38 RETINITIS PIGMENTOSA; it also plays a critical role as an inhibitor of TOLL-LIKE RECEPTORS signaling.

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