Abstract:The purpose of this study was to investigate the effect of taurine on human fetal brain neuron cell proliferation and differentiation using a glial-free, pure cerebral neuronal culture grown in a serum-free environment. We found that taurine was necessary for neuronal survival and neurite extension. Taurine, on the other hand, has a trophic effect on the human fetal brain cell, promoting both proliferation and differentiation. Results showed that DNA synthesis of the neurons was increased in a dose-dependent m… Show more
“…2), which agreed with the earlier reports (Chen et al 1997;Shivaraj et al 2012). In their studies, DNA synthesis of human fetal neuron cells was increased in a dose-dependent manner when neurons were cultured in the medium containing taurine at 100 to 6,400 µM (12.515 to 800.96 µg/ml) (Chen et al 1997). And taurine at appropriate concentrations ranging from 100 µM (12.515 µg/ml) to 500 µM (62.575 µg/ml) stimulated the proliferation of P5 NPCs (neural progenitor cell) for 2 days (Shivaraj et al 2012).…”
supporting
confidence: 93%
“…2), which agreed with the earlier reports (Chen et al 1997;Shivaraj et al 2012). In their studies, DNA synthesis of human fetal neuron cells was increased in a dose-dependent manner when neurons were cultured in the medium containing taurine at 100 to 6,400 µM (12.515 to 800.96 µg/ml) (Chen et al 1997).…”
Articular cartilage is characterized by the lack of blood vessels and has a poor self-healing potential. Limited cell numbers and dedifferentiation of chondrocytes when expanded in vitro are the major obstacles of autologous chondrocyte implantation. Autologous chondrocyte implantation is a cell-based treatment that can be used as a second-line measure to regenerate chondral or osteochondral defects in younger, active patients. There is an urgent need to find an effective chondrogenic protection agent alleviating or inhibiting chondrocyte dedifferentiation. In this study, we explored the effect of taurine (2-aminoethane sulfonic acid) on proliferation and phenotype maintenance of human articular chondrocytes by analyzing the cell proliferation, morphology, viability, and expression of cartilage specific mRNAs and proteins. Primary chondrocytes were isolated from human articular cartilage tissues. Results showed that taurine effectively promoted chondrocyte growth and enhanced accumulation of glycosaminoglycans and collagens in the conditioned media of chondrocytes. Moreover, taurine exposure caused significant increases in the relative expression levels of mRNAs for cartilage specific markers, including aggrecan, collagen type II and SOX9. Aggrecan is a cartilage-specific proteoglycan, and SOX9 is a chondrogenic transcription factor. In contrast, the mRNA expression of collagen type I, a marker for chondrocyte dedifferentiation, was significantly decreased in cells treated with taurine, indicating that taurine inhibits the chondrocyte dedifferentiation. This study reveals that taurine is effective in proliferation promotion and phenotype maintenance of chondrocytes. Thus, taurine may be a useful pro-chondrogenic agent for autologous chondrocyte implantation in the treatment of cartilage repair.
“…2), which agreed with the earlier reports (Chen et al 1997;Shivaraj et al 2012). In their studies, DNA synthesis of human fetal neuron cells was increased in a dose-dependent manner when neurons were cultured in the medium containing taurine at 100 to 6,400 µM (12.515 to 800.96 µg/ml) (Chen et al 1997). And taurine at appropriate concentrations ranging from 100 µM (12.515 µg/ml) to 500 µM (62.575 µg/ml) stimulated the proliferation of P5 NPCs (neural progenitor cell) for 2 days (Shivaraj et al 2012).…”
supporting
confidence: 93%
“…2), which agreed with the earlier reports (Chen et al 1997;Shivaraj et al 2012). In their studies, DNA synthesis of human fetal neuron cells was increased in a dose-dependent manner when neurons were cultured in the medium containing taurine at 100 to 6,400 µM (12.515 to 800.96 µg/ml) (Chen et al 1997).…”
Articular cartilage is characterized by the lack of blood vessels and has a poor self-healing potential. Limited cell numbers and dedifferentiation of chondrocytes when expanded in vitro are the major obstacles of autologous chondrocyte implantation. Autologous chondrocyte implantation is a cell-based treatment that can be used as a second-line measure to regenerate chondral or osteochondral defects in younger, active patients. There is an urgent need to find an effective chondrogenic protection agent alleviating or inhibiting chondrocyte dedifferentiation. In this study, we explored the effect of taurine (2-aminoethane sulfonic acid) on proliferation and phenotype maintenance of human articular chondrocytes by analyzing the cell proliferation, morphology, viability, and expression of cartilage specific mRNAs and proteins. Primary chondrocytes were isolated from human articular cartilage tissues. Results showed that taurine effectively promoted chondrocyte growth and enhanced accumulation of glycosaminoglycans and collagens in the conditioned media of chondrocytes. Moreover, taurine exposure caused significant increases in the relative expression levels of mRNAs for cartilage specific markers, including aggrecan, collagen type II and SOX9. Aggrecan is a cartilage-specific proteoglycan, and SOX9 is a chondrogenic transcription factor. In contrast, the mRNA expression of collagen type I, a marker for chondrocyte dedifferentiation, was significantly decreased in cells treated with taurine, indicating that taurine inhibits the chondrocyte dedifferentiation. This study reveals that taurine is effective in proliferation promotion and phenotype maintenance of chondrocytes. Thus, taurine may be a useful pro-chondrogenic agent for autologous chondrocyte implantation in the treatment of cartilage repair.
“…Taurine increases cell proliferation in human fetal neurons [17], in rabbit and human retinal pigment epithelium [18] and in human osteoblasts [19]. Taurine reverses the antiproliferative effect of high glucose and glycosylation end products in the glomerular mesangial and in renal tubule epithelial cells, two cell types which play a central role in the pathogenesis of diabetic nephropathy [20,21].…”
The decline of taurine content during brain maturation as well as the consequences of taurine deficiency disturbing brain development, suggest its involvement in basic processes of developing brain cells. If taurine participates in cell protection, differentiation or proliferation in the developing brain is as yet unclear. Extensive and solid evidence supports taurine cytoprotective actions, directly or indirectly related to an antioxidant effect. Since redox status and oxidative stress are now implicated in signalling processes regulating cell differentiation and proliferation, the question is raised of whether the taurine antioxidant activity is on the basis of its requirement during brain development.
“…Studies in monkeys fed formulas without taurine showed a similar defective maturation of the visual cortex (Neuringer et al, 1990). In vitro, defective migration in taurine-deficient cultured brain cells, and effects of taurine increasing or restoring cell proliferation of human fetal neurons have been documented (Maar et al, 1995;Chen et al, 1998). Altogether, these findings point to a possible effect of taurine in some steps of brain ontogeny, as a trophic factor and/or a protective factor necessary for optimal maturation of brain cells.…”
Taurine is present in high levels in fetal brain which decrease in the adult, suggesting its role in brain development. In some regions of taurine deficient animals cells show defective migration and the presence of numerous mitotic figures, suggesting a delay in cell proliferation. To know more about the role of taurine in the developing brain cells, the present study investigated whether taurine is a factor involved in proliferation or/and viability of neural progenitor cells (NPC). NPC were obtained from 13.5-days mice embryos mesencephalon, and cultured during 4-5 days to form neurospheres in the presence of EGF plus FGFb (EGF/FGF) or EGF alone. Mesencephalon taurine content (349 mmoles/kg protein) was lost in NPC and recovered after addition of 10 mM taurine to the culture. Neurospheres-forming NPC were over 94% nestin-positive. Taurine increased 38.6% and 43.2% the number of NPC formed in EGF/FGF or EGF conditions, respectively. In secondary neurospheres this increase was 24.6% and 62.1%, in EGF/FGF or EGF cultures respectively. Correspondingly neurospheres size was increased by taurine but neurospheres number was not enhanced. Taurine significantly increased the number of BrdU-positive cells, without affecting cell viability, suggesting proliferation as the mechanism responsible for taurine action increasing NPC. Taurine seems unable to increase the number of beta-III-tubulin-positive cells differentiated from neurospheres after serum addition, and rather an increase in astrocytes was observed. These results point to taurine as a trophic factor contributing to optimize NPC proliferation.
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