2017
DOI: 10.1111/aji.12642
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Palmitic acid stimulates interleukin‐8 via the TLR4/NF‐κB/ROS pathway and induces mitochondrial dysfunction in bovine oviduct epithelial cells

Abstract: We suggest that bovine OECs recognize an excessive increase in endogenous and sterile danger signals, such as PA, which may contribute to chronic oviductal inflammation, resulting in infertility associated with oviductal dysfunction.

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Cited by 22 publications
(13 citation statements)
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“…It may influence physiological functions of OECs, resulting in reduced OECs-sperm binding [9]. It was also hypothesized that raised fatty acid levels can lead to dysfunction and inflammation of OECs, causing infertility in bovine specimen [10].…”
Section: Introductionmentioning
confidence: 99%
“…It may influence physiological functions of OECs, resulting in reduced OECs-sperm binding [9]. It was also hypothesized that raised fatty acid levels can lead to dysfunction and inflammation of OECs, causing infertility in bovine specimen [10].…”
Section: Introductionmentioning
confidence: 99%
“…For example, elemol (Yang et al, 2015b) and thujopsene (Kim et al, 2013) decreased mast cell infiltration and IL-4 production. Palmitic acid has been shown to induce dendritic cell secretion of IL-1b (Nicholas et al, 2017) and activated production of IL-6, TNF-a (Zhou et al, 2013), and IL-8 (Ohtsu et al, 2017) by epithelial cells; 9-octadecenamide was suggested to have anti-inflammatory activities (Chen et al, 2011). It was also reported that terpenoid compounds may cause contact dermatitis (Mobacken and Fregert, 1975;Picman and Picman, 1990).…”
Section: Discussionmentioning
confidence: 99%
“…When the increased intracellular PA level exceeds its βoxidation in mitochondria, it is converted to harmful complex lipids such as diacylglycerin (DAG) and ceramide (5,27). These harmful FA-derived intermediates and excessive PA provoke increased reactive oxygen species (ROS) production, damage the function of mitochondria-related ER membrane (MAM), and induce mitochondrial fragmentation, resulting in mitochondrial dysfunction and loss of ATP production (28)(29)(30)(31). Recently, Rambold et al reported that fragmented mitochondria failed to efficiently take up FA, causing a reduction in β-oxidation rates and further exacerbating the accumulation of FA in Mitofusin1 KO cells (15).…”
Section: Discussionmentioning
confidence: 99%