Taurine Promotes Milk Synthesis via the GPR87-PI3K-SETD1A Signaling in BMECs

Yu, Mengmeng; Wang, Yang; Wang, Zhe; Liu, Yanxu; Yu, Yang; Gao, Xuejun

doi:10.1021/acs.jafc.8b06532

Cited by 35 publications

(32 citation statements)

References 57 publications

(102 reference statements)

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“…Previous reports have validated that Tau can promote cell proliferation and inhibit cell apoptosis in a PI3K dependent manner (15,49,50) , in agreement with our data. It is still largely unclear the molecular mechanism via which Tau can activate PI3K.…”

Section: Discussionsupporting

confidence: 93%

“…For experimental assays, cells were starved with OPTI-MEM I (Gibco) for 24 h before treatments. To examine the dose-dependent effects of Tau, C2C12 myoblast cells reached 60-70 % confluence were treated with Tau (0, 60, 120, 180, and 240 μM) for 24 h. These concentrations were selected by multiple rounds of screening based on our previous report (15) . Morphological images of C2C12 myoblast cells were observed by an inverted microscope (AE31E, Motic, Xiamen, China).…”

Section: Cell Culture and Treatmentsmentioning

confidence: 99%

“…Morphological images of C2C12 myoblast cells were observed by an inverted microscope (AE31E, Motic, Xiamen, China). A specific inhibitor of the phosphoinositide 3-kinase (PI3K), LY 294002 (15 μM) (S1737, Beyotime, Beijing, China), was used to inhibit PI3K activation (15) . The product package of LY 294002 was 30 mM × 0.1 mL, dissolved in dimethylsulfoxide (DMSO) and stored at -20 ℃.…”

Section: Cell Culture and Treatmentsmentioning

confidence: 99%

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Taurine stimulates protein synthesis and proliferation of C2C12 myoblast cells through the PI3K-ARID4B-mTOR pathway

Wang

Zhang

et al. 2021

Br J Nutr

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Taurine (Tau) has many profound physiological functions, but its role and molecular mechanism in muscle cells are still not fully understood. In this study, we investigated the role and underlying molecular mechanism of Tau on protein synthesis and proliferation of C2C12 myoblast cells. Cells were treated with Tau (0, 60, 120, 180 and 240 μM) for 24 h. Tau dose-dependently promoted protein synthesis, cell proliferation, mTOR phosphorylation, and also AT-rich interaction domain 4B (ARID4B) expression, with the best stimulatory effects at 120 μM. LY 294002 treatment showed that Tau promoted ARID4B expression in a PI3K-dependent manner. ARID4B knockdown (by siRNA transfection for 24 h) prevented Tau from stimulating protein synthesis and cell proliferation, whereas ARID4B gene activation (using the CRISPR/dCas9 technology) had stimulatory effects. ARID4B knockdown abolished Tau signaling to mRNA expression and protein phosphorylation of mTOR, whereas ARID4B gene activation had stimulatory effects. ChIP-PCR identified that all of ARID4B, H3K27ac and H3K27me3 bound to the -4368∼-4591 bp site in the mTOR promoter, and ChIP-qPCR further detected that Tau stimulated ARID4B binding to this site. ARID4B knockdown or gene activation did not affect H3K27me3 binding to the mTOR promoter, but decreased or increased H3K27ac binding, respectively. Furthermore, ARID4B knockdown abolished the stimulation of Tau on H3K27ac binding to the mTOR promoter. In summary, these data uncover that Tau promotes protein synthesis and proliferation of C2C12 myoblast cells through the PI3K-ARID4B-mTOR pathway, providing a deep understanding how Tau regulates anabolism in muscle cells.

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Section: Discussionsupporting

confidence: 93%

Section: Cell Culture and Treatmentsmentioning

confidence: 99%

Section: Cell Culture and Treatmentsmentioning

confidence: 99%

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Taurine stimulates protein synthesis and proliferation of C2C12 myoblast cells through the PI3K-ARID4B-mTOR pathway

Wang

Zhang

et al. 2021

Br J Nutr

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“…The biosynthesis of taurine varies according to the developmental stage. In this way, human infants, unlike adults, cannot synthesize taurine from methionine and cysteine precursors [95,96,99,100]. Infants depend on taurine delivered from their mothers via either the placenta or human milk so that the plasma level remains significant [99].…”

Section: Taurinementioning

confidence: 99%

Bioactive Compounds in Infant Formula and Their Effects on Infant Nutrition and Health: A Systematic Literature Review

Almeida

Pereira

Leandro

et al. 2021

International Journal of Food Science

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Infant formulas are an alternative to replace or supplement human milk when breastfeeding is not possible. The knowledge of human milk’s bioactive compounds and their beneficial effects has attracted the interest of researchers in the field of infant nutrition, as well as researchers of technology and food sciences that seek to improve the nutritional characteristics of infant formulas. Several scientific studies evaluate the optimization of infant formula composition. The bioactive compound inclusion has been used to upgrade the quality and nutrition of infant formulas. In this context, the purpose of this systematic literature review is to assess the scientific evidence of bioactive compounds present in infant formulas (α-lactalbumin, lactoferrin, taurine, milk fat globule membrane, folates, polyamines, long-chain polyunsaturated fatty acids, prebiotics, and probiotics) and their effects on infant nutrition and health. Through previously determined criteria, studies published in the last fifteen years from five different databases were included to identify the advances in the optimization of infant formula composition. Over the last few years, there has been optimization of the infant formula composition, not only to increase the similarities in their content of macro and micronutrients but also to include novel bioactive ingredients with potential health benefits for infants. Although the infant food industry has advanced in the last years, there is no consensus on whether novel bioactive ingredients added to infant formulas have the same functional effects as the compounds found in human milk. Thus, further studies about the impact of bioactive compounds in infant nutrition are fundamental to infant health.

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“…Taurine (Tau), the major natural free amino acid in mammals, is widely available and less expensive. Tau has been reported to regulate the inflammatory response in mammary epithelial cells infected by Streptococcus uberis [ 24 , 25 ]. However, it is not clear whether it can achieve the same effects as Se or combination with Se to produce a better effect in the prevention of mastitis or lower feed costs.…”

Section: Introductionmentioning

confidence: 99%

Selenium and Taurine Combination Is Better Than Alone in Protecting Lipopolysaccharide-Induced Mammary Inflammatory Lesions via Activating PI3K/Akt/mTOR Signaling Pathway by Scavenging Intracellular ROS

Liu

Lin

et al. 2021

Oxidative Medicine and Cellular Longevity

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Mastitis is mainly induced by gram-negative bacterial infections, causing devastating economic losses to the global cattle industry. Both selenium (Se) and taurine (Tau) exhibit multiple biological effects, including reducing inflammation. However, no studies have reported the protective effect of the combined use of Se and Tau against mastitis, and the underlying mechanisms remain unclear. In this study, lipopolysaccharide (LPS), the vital virulence factor of gram-negative bacteria, was used to construct the in vivo and vitro mastitis models. The results of in vivo model showed that Se and Tau combination was more effective than either substance alone in reducing tissue hyperemia, edema, and neutrophil infiltration in the mammary acinar cavity, improving the blood-milk barrier in LPS-induced mice mastitis, and decreasing the expression of proinflammatory factors and the activity of MPO. Moreover, Se and Tau combination significantly increased the levels of LPS-induced reduction in PI3K/Akt/mTOR, but the expressions of TLRs and NLRP3 were not significantly changed in the mammary tissue. In the in vitro experiments, the effects of Se and Tau combination or alone on inflammatory factors, inflammatory mediators, MPO activity, and blood-milk barrier were consistent with those in vivo. The Se and Tau combination has also been found to increase the survival rate of BMECs compared with each substance alone via promoting cellular proliferation and inhibiting apoptosis. Also, it has been confirmed that this combination could restore the LPS-induced inhibition in the PI3K/Akt/mTOR signaling pathway. Inhibition of mTOR by Rapamycin counteracted the combined protection of SeMet and Tau against LPS-induced inflammatory damage, the inhibition of PI3K by LY294002 blocked the activation of mTOR, and the accumulation of ROS by the ROS agonist blocked the activation of PI3K. In conclusion, these findings suggested that Se and Tau combination was better than either substance alone in protecting LPS-induced mammary inflammatory lesions by upregulating the PI3K/Akt/mTOR signaling pathway.

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Taurine Promotes Milk Synthesis via the GPR87-PI3K-SETD1A Signaling in BMECs

Cited by 35 publications

References 57 publications

Taurine stimulates protein synthesis and proliferation of C2C12 myoblast cells through the PI3K-ARID4B-mTOR pathway

Taurine stimulates protein synthesis and proliferation of C2C12 myoblast cells through the PI3K-ARID4B-mTOR pathway

Bioactive Compounds in Infant Formula and Their Effects on Infant Nutrition and Health: A Systematic Literature Review

Selenium and Taurine Combination Is Better Than Alone in Protecting Lipopolysaccharide-Induced Mammary Inflammatory Lesions via Activating PI3K/Akt/mTOR Signaling Pathway by Scavenging Intracellular ROS

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