Regulation of triglyceride metabolism in medaka (Oryzias latipes) hepatocytes by Neu3a sialidase

Oishi, Kazuki; Miyazaki, Mina; Takase, Ryo; Chigwechokha, Petros Kingstone; Komatsu, Masaharu; Shiozaki, Kazuhiro

doi:10.1007/s10695-019-00730-6

Cited by 9 publications

(3 citation statements)

References 45 publications

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“…In general, E. tarda infection is promoted by high stress environments such as poor water quality, high‐water temperature, and high‐organic content (Park et al, 2012). Our previous study shows that fish Neu3 sialidase gene expression is induced by fasting (Oishi et al, 2020). Since edwardsiellosis is an opportunistic infection, the accumulation of LacCer due to high stressful environments such as fasting and high‐water temperature might facilitate infection.…”

Section: Discussionmentioning

confidence: 98%

Host lactosylceramide enhances Edwardsiella tarda infection

Oishi

Morise

et al. 2021

Cellular Microbiology

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Edwardsiella tarda is a Gram‐negative bacterium causing economic damage in aquaculture. The interaction of E. tarda with microdomains is an important step in the invasion, but the target molecules in microdomains remain undefined. Here, we found that intraperitoneal injection of E. tarda altered splenic glycosphingolipid patterns in the model host medaka (Oryzias latipes) accompanied by alteration of glycosphingolipid metabolism‐related gene expressions, suggesting that glycosphingolipid levels are involved in E. tarda infection. To ascertain the significance of glycosphingolipids in the infection, fish cell lines, DIT29 cells with a high amount of lactosylceramide (LacCer) and glucosylceramide (GlcCer), and GAKS cells with a low amount of these lipids, were treated with methyl‐β‐cyclodextrin to disrupt the microdomain. E. tarda infection was suppressed in DIT29 cells, but not in GAKS cells, suggesting the involvement of microdomain LacCer and GlcCer in the infection. DL‐threo‐1‐phenyl‐2‐palmitoylamino‐3‐morpholino‐1‐propanol, an inhibitor of glycosphingolipid‐synthesis, attenuated the infection in DIT29 cells, while Neu3‐overexpressing GAKS cells, which accumulated LacCer, enhanced the infection. E. tarda possessed binding ability towards LacCer, but not GlcCer, and LacCer preincubation declined the infection towards fish cells, possibly due to the masking of binding sites. The present study suggests that LacCer may be a positive regulator of E. tarda invasion.

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Section: Discussionmentioning

confidence: 98%

Host lactosylceramide enhances Edwardsiella tarda infection

Oishi

Morise

et al. 2021

Cellular Microbiology

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“…Furthermore, the weight increase observed after feeding a high-fat diet (HFD) was slower in IL-17A-KO mice than in WT mice 43 , suggesting that IL-17A may be involved in lipid absorption. Like mammals, teleosts consume lipids as a primary energy source and excess triglycerides are stored in the liver, muscles, and adipose tissues 44 . In medaka, feeding on HFD and body weight increase showed positive correlation, as seen in mammals 45 .…”

Section: Discussionmentioning

confidence: 99%

A defective interleukin-17 receptor A1 causes weight loss and intestinal metabolism-related gene downregulation in Japanese medaka, Oryzias latipes

Okamura

Miyanishi

Kinoshita

et al. 2021

Sci Rep

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In the intestine, the host must be able to control the gut microbiota and efficiently absorb transiently supplied metabolites, at the risk of enormous infection. In mammals, the inflammatory cytokine interleukin (IL)-17A/F is one of the key mediators in the intestinal immune system. However, many functions of IL-17 in vertebrate intestines remain unclarified. In this study, we established a gene-knockout (KO) model of IL-17 receptor A1 (IL-17RA1, an IL-17A/F receptor) in Japanese medaka (Oryzias latipes) using genome editing technique, and the phenotypes were compared to wild type (WT) based on transcriptome analyses. Upon hatching, homozygous IL-17RA1-KO medaka mutants showed no significant morphological abnormality. However, after 4 months, significant weight decreases and reduced survival rates were observed in IL-17RA1-KO medaka. Comparison of gene-expression patterns in WT and IL-17RA1-KO medaka revealed that various metabolism- and immune-related genes were significantly down-regulated in IL-17RA1-KO medaka intestine, particularly genes related to mevalonate metabolism (mvda, acat2, hmgcs1, and hmgcra) and genes related to IL-17 signaling (such as il17c, il17a/f1, and rorc) were found to be decreased. Conversely, expression of genes related to cardiovascular system development, including fli1a, sox7, and notch1b in the anterior intestine, and that of genes related to oxidation–reduction processes including ugp2a, aoc1, and nos1 in posterior intestine was up-regulated in IL-17RA1-KO medaka. These findings show that IL-17RA regulated immune- and various metabolism-related genes in the intestine for maintaining the health of Japanese medaka.

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“…Furthermore, the weight increase observed after feeding with a high-fat diet (HFD) was slower in IL-17A-KO mice than in WT mice 37 , suggesting that IL-17A may be involved in lipid absorption. In addition, in teleosts, lipids are consumed as a primary energy source and excess triglycerides are stored in the liver, muscles, and adipose tissues 38 . In medaka, feeding with an HFD caused an increase in body weight, as seen in mammals 39 .…”

Section: Discussionmentioning

confidence: 99%

Interleukin-17 Receptor A1 Gene Knockout Causes Weight Loss and Reduction of Intestinal Metabolism-Related Genes in The Japanese Medaka, Oryzias Latipes

Okamura¹,

Miyanishi²,

Kinoshita³

et al. 2020

Preprint

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In the intestine, the host must be able to control the gut microbiota and efficiently absorb transiently supplied metabolites, at the risk of enormous infection. In mammals, the inflammatory cytokine interleukin (IL)-17A/F is one of the key mediators in the intestinal immune system. However, many functions of IL-17 in vertebrate intestines remain unclarified. In this study, we established a gene-knockout (KO) model of IL-17 receptor A1 (RA1), an IL-17A/F receptor, in Japanese medaka (Oryzias latipes) using genome editing technique and the phenotypes were compared to wild type (WT) based on transcriptome analyses. Upon hatching, homozygous IL-17RA1-KO medaka mutants showed no significant morphological abnormality. However, after 4 months, significant weight decreases and reduced survival rates were observed in IL-17RA1-KO medaka. Comparing gene-expression patterns in WT and IL-17RA1-KO medaka revealed that various metabolism- and immune-related genes were significantly down-regulated in IL-17RA1-KO medaka intestine, particularly genes related to mevalonate metabolism (mvda, acat2, hmgcs1, and hmgcra) and genes related to IL-17 signaling (such as il17c, il17a/f1, and rorc) were found to be decreased. These findings show that IL-17RA regulated immune- and various metabolism-related genes in the intestine for maintaining the health of Japanese medaka.

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Regulation of triglyceride metabolism in medaka (Oryzias latipes) hepatocytes by Neu3a sialidase

Cited by 9 publications

References 45 publications

Host lactosylceramide enhances Edwardsiella tarda infection

Host lactosylceramide enhances Edwardsiella tarda infection

A defective interleukin-17 receptor A1 causes weight loss and intestinal metabolism-related gene downregulation in Japanese medaka, Oryzias latipes

Interleukin-17 Receptor A1 Gene Knockout Causes Weight Loss and Reduction of Intestinal Metabolism-Related Genes in The Japanese Medaka, Oryzias Latipes

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