All-trans retinoic acid reduces the transcriptional regulation of intestinal sodium-dependent phosphate co-transporter gene (<i>Npt2b</i>)

Masuda, Masashi; Yamamoto, Hironori; Takei, Yuichiro; Nakahashi, Otoki; Adachi, Yuichiro; Ohnishi, Kohta; Ohminami, Hirokazu; Yamanaka-Okumura, Hisami; Sakaue, Hiroshi; Miyazaki, Masaru; Takeda, Eiji; Taketani, Yutaka

doi:10.1042/bcj20190716

Cited by 7 publications

(4 citation statements)

References 51 publications

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“…The organs involved in phosphate regulation include intestine, bone, kidney, and parathyroid gland. The daily intake of dietary phosphate is about 1.0–1.5 g, which is absorbed by the intestinal epithelial cell type II sodium-dependent phosphate co-transporter (Npt)-2a, 2b, and 2c ( Masuda et al, 2020 ). The phosphate absorbed from the intestine is mainly excreted through the kidney.…”

Section: Metabolic Regulation Of Phosphatementioning

confidence: 99%

Hyperphosphatemia and Cardiovascular Disease

Zhou

Shi

Ouyang

et al. 2021

Front. Cell Dev. Biol.

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Hyperphosphatemia or even serum phosphate levels within the “normal laboratory range” are highly associated with increased cardiovascular disease risk and mortality in the general population and patients suffering from chronic kidney disease (CKD). As the kidney function declines, serum phosphate levels rise and subsequently induce the development of hypertension, vascular calcification, cardiac valvular calcification, atherosclerosis, left ventricular hypertrophy and myocardial fibrosis by distinct mechanisms. Therefore, phosphate is considered as a promising therapeutic target to improve the cardiovascular outcome in CKD patients. The current therapeutic strategies are based on dietary and pharmacological reduction of serum phosphate levels to prevent hyperphosphatemia in CKD patients. Large randomized clinical trials with hard endpoints are urgently needed to establish a causal relationship between phosphate excess and cardiovascular disease (CVD) and to determine if lowering serum phosphate constitutes an effective intervention for the prevention and treatment of CVD.

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Section: Metabolic Regulation Of Phosphatementioning

confidence: 99%

Hyperphosphatemia and Cardiovascular Disease

Zhou

Shi

Ouyang

et al. 2021

Front. Cell Dev. Biol.

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“…KEGG enrichment analysis in mice faeces showed that the differential metabolites were signi cantly enriched in the mineral absorption pathway before and after A. muciniphila treatment, and the level of hydrogen phosphate increased in the DSS group, while A. muciniphila treatment could signi cantly decrease the level of hydrogen phosphate (P < 0.05). It has reported that high levels of hydrogen phosphate promote the occurrence of ER stress [37]. Through 16sRNA sequencing, we found that the application of A. muciniphila could reduce the F/B ratio in the model group and adjust the intestinal ora homeostasis, in which Parasutterella was signi cantly reduced after administration.…”

Section: Discussionmentioning

confidence: 70%

Akkermansia muciniphila alleviates colonic epithelial endoplasmic reticulum stress through activation of farnesoid X receptors in murine experimental colitis

Zhou

Dong

et al. 2022

Preprint

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Background Endoplasmic reticulum (ER) stress-related mucin depletion could be involved in the pathogenesis of inflammatory bowel disease (IBD). Akkermansia muciniphila (A. muciniphila), a symbiotic bacterium of the mucus layer, uses mucin as its sole energy source and shows potential in the treatment of colitis. However, the effects and underlying mechanisms of A. muciniphila on colonic epithelial ER stress in colitis are largely unknown. Methods Colitis was induced by adding 2.5% DSS in drinking water. Mice were orally administered A. muciniphila (3*10^7, 3*10^8 cfu/day) once daily for 10 days during DSS intervention. UHPLC high-resolution orbitrap mass spectrometry-based metabolomic analyses were performed on faeces. 16S rRNA sequencing were used to quantify and characterize the gut microbiota of mice and human. Colons were collected from mice and analyzed by histopathology, quantitative PCR and immunofluorescence. Colon biopsies from the patients with ulcerative colitis (UC) and controls were collected and analyzed by immunohistochemistry. Results Metabolite pathway enrichment analysis demonstrated that colitis-affected metabolites after A. muciniphila supplementation were mainly enriched in mineral absorption, bile secretion and protein digestion and absorption. P-hydroxyphenyl acetic acid, which showed the highest VIP scores, was significantly increased by A. muciniphila, and could cause ER stress. A. muciniphila supplementation changed the relative abundance and composition of intestinal microbiotaespecially a decrease inParasutterella, which showed the potential role in bile acid maintenance. A. muciniphila supplementation protected colon shortening, histological injury, intestinal inflammation and barrier damage in wild-type (WT) mice but not in farnesoid X receptor-null (FXR−/−) mice. Mechanistically, A. muciniphila supplementation activated FXR/SHP signaling, which directly increased X-box binding protein-1 splicing (XBP1s) and phosphorylated inositol requiring enzyme 1α (p-IRE1α) expression, and in turn formed XBP1s-SHP regulatory loop in response to ER stress. We further showed that the abundance of A. muciniphila in faeces from UC patients positively correlates with p-IRE1α expression. Conclusions Our results suggest that A. muciniphila supplementation alleviates DSS-induced colitis involvement of the IRE1α/XBP1 ER stress pathway via FXR/SHP axis activation.

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“…EMSA was performed as described previously ( Masuda et al, 2020 ). Double-stranded nucleotides for GADD34-MEF3 and GADD34-MEF3-2-Mutant (GADD34-Mut-M2) were synthesized (Table S3).…”

Section: Methodsmentioning

confidence: 99%

All-trans retinoic acid changes muscle fiber type via increasing GADD34 dependent on MAPK signal

et al. 2022

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All-trans retinoic acid (ATRA) increases the sensitivity to unfolded protein response in differentiating leukemic blasts. The downstream transcriptional factor of PERK, a major arm of unfolded protein response, regulates muscle differentiation. However, the role of growth arrest and DNA damage-inducible protein 34 (GADD34), one of the downstream factors of PERK, and the effects of ATRA on GADD34 expression in muscle remain unclear. In this study, we identified ATRA increased the GADD34 expression independent of the PERK signal in the gastrocnemius muscle of mice. ATRA up-regulated GADD34 expression through the transcriptional activation of GADD34 gene via inhibiting the interaction of homeobox Six1 and transcription co-repressor TLE3 with the MEF3-binding site on the GADD34 gene promoter in skeletal muscle. ATRA also inhibited the interaction of TTP, which induces mRNA degradation, with AU-rich element on GADD34 mRNA via p-38 MAPK, resulting in the instability of GADD34 mRNA. Overexpressed GADD34 in C2C12 cells changes the type of myosin heavy chain in myotubes. These results suggest ATRA increases GADD34 expression via transcriptional and post-transcriptional regulation, which changes muscle fiber type.

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All-trans retinoic acid reduces the transcriptional regulation of intestinal sodium-dependent phosphate co-transporter gene (Npt2b)

Cited by 7 publications

References 51 publications

Hyperphosphatemia and Cardiovascular Disease

Hyperphosphatemia and Cardiovascular Disease

Akkermansia muciniphila alleviates colonic epithelial endoplasmic reticulum stress through activation of farnesoid X receptors in murine experimental colitis

All-trans retinoic acid changes muscle fiber type via increasing GADD34 dependent on MAPK signal

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