Inhibition of Neurosphere Formation in Neural Stem/Progenitor Cells by Acrylamide

Chen, Jong-Hang; Lee, Dong Hoon; Chen, Mei‐Shu; Ko, Ying‐Chin; Chiu, Ing‐Ming

doi:10.3727/096368913x676925

Cited by 6 publications

(4 citation statements)

References 58 publications

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“…Previously, the researchers found that ACR-treated neurospheres of KT98/F1B-GFP showed decrease in phosphorylated AKT through analyzing AKT pathway. 33 At the same time, extracellular TAU induces angiogenesis by activating AKT-dependent signal pathways. 10 TAU promotes cognitive function of prenatally stressed juvenile rats by activating the AKT-CREB-PGC1α pathway, 34 proving that the level of phosphorylated AKT when the rats or the cells treated with TAU.…”

Section: Discussionmentioning

confidence: 99%

Taurine attenuates acrylamide-induced apoptosis via a PI3K/AKT-dependent manner

Sun

Wang

et al. 2018

Hum Exp Toxicol

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As a potent neurotoxic agent, acrylamide (ACR) is formed in food processing at higher temperature. Taurine (TAU), a nonessential amino acid, is used to cure neurodegenerative disorders, followed by activation of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway. In this article, we certified that antiapoptotic efficacy of TAU in vivo and vitro. ACR-treated rats received TAU by drinking water 2 weeks after ACR intoxication. The results showed that in treated rats, TAU alleviated ACR-induced neuronal apoptosis, which was associated with the activation of PI3K/AKT signaling pathway. TAU attenuated apoptosis caused by ACR through observing terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-positive cells, measure of protein expression of Bcl-2, Bax, and caspase 3 activity. TAU-induced antiapoptotic effect is PI3K/AKT-dependent, which was proved in ACR-intoxicated ventral spinal cord 4.1 cells in the presence of AKT inhibitor, MK-2206. Therefore, our results demonstrated that TAU-attenuated ACR-induced apoptosis in vivo through a PI3K/AKT-dependent manner provided new sights in the molecular mechanism of TAU protection against ACR-induced neurotoxicity.

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Section: Discussionmentioning

confidence: 99%

Taurine attenuates acrylamide-induced apoptosis via a PI3K/AKT-dependent manner

Sun

Wang

et al. 2018

Hum Exp Toxicol

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“…1F), which indicated that FAM19A1 is expressed in NSCs and may be associated with the functions of NSCs. Neurospheres were induced to proliferate and were able to generate the 3 major phenotypes of the mammalian CNS: neurons, astrocytes, and oligodendrocytes (26,27); thus, the properties of neurospheres are frequently used as a standard by which to evaluate the abilities of NSCs (28). We then separated primary murine neurospheres from the mouse embryonic brain and demonstrated the expression and secretion of FAM19A1 in NSCs via cell immunofluorescence and the cytometric bead system (Fig.…”

Section: Fam19a1 Inhibits the Proliferation And Self-renewal Of Murinmentioning

confidence: 99%

FAM19A1 is a new ligand for GPR1 that modulates neural stem‐cell proliferation and differentiation

et al. 2018

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FAM19A1 is a member of the family with sequence similarity 19 with unknown function. FAM19A1 mRNA expression is restricted to the CNS. Here, we report that FAM19A1 is a classic secretory protein, and expression levels correlate with brain development, increasing from embryonic d 12.5, peaking between postnatal d (P)1 and P7 and decreasing at wk 8. The adult hippocampus is a region of FAM19A1 high expression. Recombinant FAM19A1 suppressed the proliferation and self-renewal of neural stem cells (NSCs) and altered the lineage progression of NSCs with promoted neuron differentiation and suppressed astrocyte differentiation. Although GPCR 1 (GPR1) has been reported to be expressed in the CNS, its functions in the brain remain unclear. We identified GPR1 to be a functional receptor for FAM19A1. FAM19A1 interacted with GPR1 via the N-terminal domain (GPR1-ND), and its NSC modulatory functions required the Rho-associated protein kinase (ROCK) /ERK1/2 and ROCK/signal transducer and activator of transcription 3 signaling pathways. GPR1-ND that selectively bound to FAM19A1 neutralized the effects of FAM19A1 on NSC functions. Taken together, our results show, for the first time to our knowledge, that FAM19A1 is a novel regulatory factor of the proliferation and differentiation of NSCs, and identified a novel mechanism by which GPCR mediates the effects of FAM19A1 on NSC functions that may be important for brain development and neurogenesis. Additional exploration of the functions of FAM19A1 and GPR1 in the CNS may broaden the range of therapeutic options available for major brain disorders.-Zheng, C., Chen, D., Zhang, Y., Bai, Y., Huang, S., Zheng, D., Liang, W., She, S., Peng, X., Wang, P., Mo, X., Song, Q., Lv, P., Huang, J., Ye, R. D., Wang, Y. FAM19A1 is a new ligand for GPR1 that modulates neural stem-cell proliferation and differentiation.

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“…In addition, glycoalkaloids can cause inflammatory bowel disease (IBD) in the mammalian intestine by destroying the intestinal epithelial barrier if excessively fried potatoes or potato skin are consumed [56,57]. Glycoalkaloids have anticarcinogenic and antiproliferative properties that inhibit the proliferation of cancer and normal cells [32,[58][59][60][61][62]. Unfortunately, this function of glycoalkaloids is detrimental to normal cells and organisms that ingest foods containing higher levels of glycoalkaloids.…”

Section: Discussionmentioning

confidence: 99%

Antioxidants Amelioration Is Insufficient to Prevent Acrylamide and Alpha-Solanine Synergistic Toxicity in BEAS-2B Cells

Eltayeb,

Stewart,

Morgem

et al. 2023

IJMS

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Cells produce free radicals and antioxidants when exposed to toxic compounds during cellular metabolism. However, free radicals are deleterious to lipids, proteins, and nucleic acids. Antioxidants neutralize and eliminate free radicals from cells, preventing cell damage. Therefore, the study aims to determine whether the antioxidants butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) will ameliorate the maximum dose of acrylamide and alpha (α)-solanine synergistic toxic effects in exposed BEAS-2B cells. These toxic compounds are consumed worldwide by eating potato products. BEAS-2B cells were simultaneously treated with BHA 10 μM and BHT 20 μM and incubated in a 5% CO2 humidified incubator for 24 h, followed by individual or combined treatment with acrylamide (3.5 mM) and α-solanine (44 mM) for 48 h, including the controls. Cell morphology, DNA, RNA, and protein were analyzed. The antioxidants did not prevent acrylamide and α-solanine synergistic effects in exposed BEAS-2B cells. However, cell morphology was altered; polymerase chain reaction (PCR) showed reduced RNA constituents but not DNA. In addition, the toxic compounds synergistically inhibited AKT/PKB expression and its downstream genes. The study showed BHA and BHT are not protective against the synergetic toxic effects of acrylamide and α-solanine in exposed BEAS-2B cells.

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Inhibition of Neurosphere Formation in Neural Stem/Progenitor Cells by Acrylamide

Cited by 6 publications

References 58 publications

Taurine attenuates acrylamide-induced apoptosis via a PI3K/AKT-dependent manner

Taurine attenuates acrylamide-induced apoptosis via a PI3K/AKT-dependent manner

FAM19A1 is a new ligand for GPR1 that modulates neural stem‐cell proliferation and differentiation

Antioxidants Amelioration Is Insufficient to Prevent Acrylamide and Alpha-Solanine Synergistic Toxicity in BEAS-2B Cells

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