Expression Of Taurine Transporter Research Articles

Observation of Acupuncture Effects on the Expression of Taurine Transporter and Taurine in the Senescence-Accelerated Mouse Brain: A Pilot Study.

In living organisms, taurine is important for homeostasis and is known to have preventive and inhibitory effects on various diseases. Taurine has been reported to play an important role in the development of the brain in newborns and in reducing the damage caused by cerebral ischemia. Previous studies indicated that acupuncture on a pair of acupoints of "DU16" and "DU20" can increase brain taurine transporter (TauT) expression in mice with penicillin-induced epilepsy and enhanced taurine anti-epilepsy effects. Our previous study reported that manual acupuncture stimulation of the head acupuncture points "Bai-Hui" (GV 20) and "Yintang" (Ex-HN3) could produce antidepressant effects. In this study, we investigated whether acupuncture stimulation of the head acupuncture points GV 20 and Ex-HN3 affects the expression of TauT and taurine in the cerebellum and hippocampus in senescence-accelerated mice. Acupuncture stimulation significantly increased the mRNA expression of TauT in the cerebellum and hippocampus. Immunohistochemical staining confirmed that the expression of TauT and taurine in the cerebellum and hippocampus increased. These results indicate that acupuncture stimulation might improve cognitive and behavioral abilities by increasing the expression of TauT and taurine.

Caloric restriction increases levels of taurine in the intestine and stimulates taurine uptake by conjugation to glutathione

Our previous study indicated increased levels of taurine-conjugated bile acids (BA) in the intestine content of mice submitted to caloric restriction (CR). In the current project, we found increased levels of free taurine and taurine conjugates, including glutathione (GSH)-taurine, in CR compared to ad libitum fed animals in the mucosa along the intestine but not in the liver. The levels of free GSH were decreased in the intestine of CR compared to ad libitum fed mice. However, the levels of oxidized GSH were not affected and were complemented by the lack of changes in the antioxidative parameters. Glutathione-S transferases (GST) enzymatic activity was increased as was the expression of GST genes along the gastrointestinal tract of CR mice. In the CR intestine, addition of GSH to taurine solution enhanced taurine uptake. Accordingly, the expression of taurine transporter (TauT) was increased in the ileum of CR animals and the levels of free and BA-conjugated taurine were lower in the feces of CR compared to ad libitum fed mice. Fittingly, BA- and GSH-conjugated taurine levels were increased in the plasma of CR mice, however, free taurine remained unaffected. We conclude that CR-triggered production and release of taurine-conjugated BA in the intestine results in increased levels of free taurine what stimulates GST to conjugate and enhance uptake of taurine from the intestine.

Taurine requirement and metabolism response of tiger puffer Takifugu rubripes to graded taurine supplementation

An eight week feeding trial was conducted to investigate the effect of taurine supplementation on growth performance, sulfur amino acid concentrations, the activity and gene expression of enzymes related to taurine synthesis, and gene expression of taurine transporter (TAUT) in tiger puffer (Takifugu rubripes). Test diets were respectively supplemented with 0, 3, 6, 9, 12 and 20 g kg−1 taurine (the T0, T3, T6, T9, T12 and T20 diets) and a control diet was supplemented with 12 g kg−1 cysteine (the Cys diet). All experimental diets were fed to triplicate groups of 25 fish (initial weight 20.05 ± 0.06 g). Dose responses were observed in terms of specific growth rate and feed efficiency ratio. Dietary taurine requirement was estimated at 5.25 and 8.23 g kg−1 of dry matter of the diet based on regression analysis for specific growth rate and feed efficiency ratio, respectively. Free taurine concentrations of muscle and liver tissues increased with the increase of dietary taurine concentration. However, there was no significant difference in free taurine concentrations in muscle or liver between the Cys and T0 groups (p > .05). Free methionine concentration of liver tissue gradually increased with the increase of dietary taurine, which implied that exogenous taurine appeared to spare hepatic methionine. Cysteine sulfinic acid decarboxylase (CSD) activity and mRNA level in liver were down-regulated in the T9, T12 and T20 groups compared with the T0 group (p < .05), while no statistical difference was observed in cysteine dioxygenase (CDO) activity and expression between the T0 group and the taurine supplementation groups (the T3, T6, T9, T12 and T20 groups (p > .05). TAUT mRNA levels in muscle had a decrease trend in fish fed diets containing 1.7 to 8.2 g kg−1 taurine (the T0, T3 and T6 groups), while there was no significant difference when dietary taurine concentrations increased from 8.2 to 21.9 g kg−1 (the T6, T9, T12 and T20 groups). In conclusion, tiger puffer cannot synthesize taurine in the liver at the level of cysteine used in this study, whereas a sparing effect on the methionine demand may be observed in liver by dietary taurine supplementation. Our data indicates that taurine is a conditionally essential amino acid for tiger puffer, and the taurine requirement was estimated ranged from 5.25 to 8.23 g kg−1 of dry matter of the diet.

The Effect of Drug Pre-treatment on Taurine Transport at the Inner Blood-Retinal Barrier Under Variable Conditions.

Taurine is essential for the development and function of the central nervous system, retina, and cardiovascular system. It is a naturally occurring amino acid, abundantly found in the retina. It has been shown to exhibit antioxidant, neuroprotective, and osmoregulatory functions in the retina. We used conditionally immortalized rat retinal capillary endothelial cells (TR-iBRB), in vitro, to investigate the effects of oxidative stress, high glucose (HG) and hypertonic conditions on taurine transport. TR-iBRB cells pre-treated with tumor necrosis factor alpha (TNF-α) showed a significant increase in [3H]taurine uptake rate, which, however, decreased when treated with taurine (50mM). Addition of paeonol and propranolol to TNF-α pre-treated cells had no significant effect on [3H]taurine uptake, but the addition of 10mM taurine caused a reduction. The uptake rate decreased under HG conditions, in contrast to that under hypertonic conditions. [3H]Taurine uptake increased with pre-incubation time. Additionally, uptake of [3H]taurine and mRNA expression of taurine transporter (TauT) decreased significantly under hypertonic and HG conditions, following pre-incubation with 10mM taurine, 1mM paeonol, and 0.1mM propranolol. [3H]Taurine uptake was significantly inhibited in the presence of taurine transporters such as taurine and β-alanine. Results indicate that oxidative stress and hypertonic conditions increased taurine uptake in iBRB cell lines, whereas HG conditions reduced the uptake rate. Taurine may be useful in stabilizing the microenvironment in cells affected by oxidative stress as well as hypertonic and HG conditions. Moreover, taurine may play a key role in maintaining taurine concentrations in the taurine transporter system of retinal cells.

Anti-obesity effect of taurine through inhibition of adipogenesis in white fat tissue but not in brown fat tissue in a high-fat diet-induced obese mouse model.

This study was conducted to evaluate the anti-obesity effects of long-term taurine supplementation in a mild obese ICR mouse model and to study the mechanism by which taurine induces weight loss. Three groups of male ICR mice were fed a normal chow diet, a high-fat diet (HFD), or an HFD supplemented with 2% taurine in drinking water for 28weeks. Body weight was measured every week. Metabolic, behavioral, and physiological monitoring were carried out using PhenoMaster at 28weeks. Interscapular brown fat (BAT), inguinal white fat tissue (WAT), and quadriceps muscle were analyzed and compared to assess the change of gene expression related to adipogenesis. Taurine supplementation showed the trend of anti-obesity effect in ICR mice fed an HFD for 28weeks. HFD-fed mice did not show significant difference of oxygen consumption (VO2), energy expenditure (EE), respiratory exchange rate (RER), and locomotive activity compared with those of normal chow diet fed mice. The expression of adipogenesis-related genes such as PPAR-α, PPAR-γ, C/EBP-α, C/EBP-β, and AP2 increased in BAT and WAT, but not in muscle tissue. Taurine supplementation showed the downregulation of these genes in WAT but not in BAT or muscle. Consistently, the expression of taurine transporter (TauT) and adipocyte-specific genes such as adiponectin, leptin, and IL-6 was regulated in a similar pattern by taurine supplementation. Long-term taurine supplementation causes weight loss, most likely by inhibiting adipogenesis in WAT. TauT expression may be involved in the expression of various genes regulated by taurine supplementation.

Protein malnutrition blunts the increment of taurine transporter expression by a high-fat diet and impairs taurine reestablishment of insulin secretion.

Taurine (Tau) restores β-cell function in obesity; however, its action is lost in malnourished obese rodents. Here, we investigated the mechanisms involved in the lack of effects of Tau in this model. C57BL/6 mice were fed a control diet (CD) (14% protein) or a protein-restricted diet (RD) (6% protein) for 6 wk. Afterward, mice received a high-fat diet (HFD) for 8 wk [CD + HFD (CH) and RD + HFD (RH)] with or without 5% Tau supplementation after weaning on their drinking water [CH + Tau (CHT) and RH + Tau (RHT)]. The HFD increased insulin secretion through mitochondrial metabolism in CH and RH. Tau prevented all those alterations in CHT only. The expression of the taurine transporter (Tau-T), as well as Tau content in pancreatic islets, was increased in CH but had no effect on RH. Protein malnutrition programs β cells and impairs Tau-induced restoration of mitochondrial metabolism and biogenesis. This may be associated with modulation of the expression of Tau-T in pancreatic islets, which may be responsible for the absence of effect of Tau in protein-malnourished obese mice.-Branco, R. C. S., Camargo, R. L., Batista, T. M., Vettorazzi, J. F., Borck, P. C., dos Santos-Silva, J. C. R., Boschero, A. C., Zoppi, C. C., Carneiro, E. M. Protein malnutrition blunts the increment of taurine transporter expression by a high-fat diet and impairs taurine reestablishment of insulin secretion.

Effect of Radiation on the Expression of Taurine Transporter in the Intestine of Mouse.

There has been a growing interest on the effects of radiation since the Fukushima nuclear power plant accident of 2011. Taurine has been reported to have a radioprotective effect in irradiated mice. However, the detailed mechanism of this radioprotective effect is still awaiting clarification. The aim of this study was to investigation how radiation affects the expression of taurine and to shed light on the mechanism accounting for radioprotective and radiation mitigating effect. Six-week-old male mice were randomly divided into two groups: IR group (7 Gy irradiation) and IR + Tau group (7 Gy irradiation + taurine 3000 mg/kg/day). We examined the survival rate, the expression of taurine and taurine transporter in the small intestine and the urinary taurine concentration. In this study, no statistically significant difference was found in the survival rate between IR Group and IR + Tau Group. Three days and 7 days after irradiation, the urinary taurine concentration of IR + Tau group increased more than that of IR group. Three days and 10 days after irradiation, the expression of taurine and taurine transporter in the small intestine of IR group and IR + Tau group decreased more than that of normal small intestine. It is reported that radiation exposure increases the urinary taurine concentration. We found that the radiation exposure decreases the expression of the taurine transporter in the small intestine of mouse. This finding suggests that a decrease in the expression of the taurine transporter promotes the release of taurine from the tissue into the urine.

A Novel Cysteine Sulfinic Acid Decarboxylase Knock-Out Mouse: Taurine Distribution in Various Tissues With and Without Taurine Supplementation.

Taurine, a sulfur containing amino acid, has various physiological functions including development of the eye and brain, immune function, reproduction, osmo-regulatory function as well as anti-oxidant and anti-inflammatory activities. In order to understand the physiological role, we developed taurine deficient mice deleting a rate-liming enzyme, cysteine sulfinic acid decarboxylase (CSAD) for biosynthesis of taurine. Taurine was measured in various tissues including the liver, brain, lung, spleen, thymus, pancreas, heart, muscle and kidney as well as plasma from CSAD knock-out mice (CSAD KO) with and without treatment of taurine in the drinking water at the age of 2 months (2 M). Taurine was determined using HPLC as a phenylisothiocyanate derivative of taurine at 254 nm. Taurine concentrations in the liver and kidney from homozygotes of CSAD KO (HO), in which CSAD level is high, were 90% and 70% lower than WT, respectively. Taurine concentrations in the brain, spleen and lung, where CSAD level is low, were 21%, 20% and 28% lower than WT, respectively. At 2 M, 1% taurine treatment of HO restored taurine concentrations in all tissues compared to that of WT. To select an appropriate taurine treatment, HO were treated with various concentrations (0.05, 0.2, 1%) of taurine for 4 months (4 M). Restoration of taurine in all tissues except the liver, kidney and lung requires 0.05% taurine to be restored to that of WT. The liver and kidney restore taurine back to WT with 0.2% taurine. To examine which enzymes influence taurine concentrations in various tissues from WT and HO at 2 M, expression of five taurine-related enzymes, two antioxidant enzymes as well as lactoferrin (Lft) and prolactin receptor (Prlr) was determined using RT2 qPCR. The expression of taurine transporter in the liver, brain, muscle and kidney from HO was increased except in the lung. Our data showed expression of glutamate decarboxylase-like 1(Gadl-1) was increased in the brain and muscle in HO, compared to WT, indicating taurine in the brain and muscle from HO was replenished through taurine transporter and increased biosynthesis of taurine by up-regulated Gadl-1. The expression of glutathione peroxidase 3 was increased in the brain and peroxireductase 2 was increased in the liver and lung, suggesting taurine has anti-oxidant activity. In contrast to newborn and 1 month CSAD KO, Ltf and Prlr in the liver from CSAD KO at 2 M were increased more than two times and 52%, respectively, indicating these two proteins may be required for pregnancy of CSAD KO. Ltf in HOT1.0 was restored to WT, while Prlr in HOT1.0 was increased more than HO, explaining improvement of neonatal survival with taurine supplementation.These data are essential for investigating the role of taurine in development of the brain and eye, immune function, reproduction and glucose tolerance.

Ionic and Amino Acid Regulation in Hard Clam (Meretrix lusoria) in Response to Salinity Challenges.

Most marine mollusks are osmoconformers, in that, their body fluid osmolality changes in the direction of the change in environmental salinity. Marine mollusks exhibit a number of osmoregulatory mechanisms to cope with either hypo- or hyperosmotic stress. The effects of changes in salinity on the osmoregulatory mechanisms of the hard clam (Meretrix lusoria, an economically important species of marine bivalve for Taiwan) have not been determined. In this study, we examined the effect of exposure to hypo (10‰)- and hyper (35‰)-osmotic salinity on hard clams raised at their natural salinity (20‰). The osmolality, [Na+], and [Cl−] of the hard clam hemolymph were changed in the same direction as the surrounding salinity. Further, the contents of total free amino acids including taurine in the gills and mantles were significantly upregulated in hard clam with increasing salinity. The gill Na+, K+-ATPase (NKA) activity, the important enzyme regulating cellular inorganic ions, was not affected by the changed salinity. Mantle NKA activity, however, was stimulated in the 35‰ SW treatment. The taurine transporter (TAUT) is related to the regulation of intracellular contents of taurine, the dominant osmolyte. Herein, a TAUT gene of hard clam was cloned and a TAUT antibody was derived for the immunoblotting. The TAUT mRNA expression of the mantle in hard clam was significantly stimulated in 35‰ SW, but protein expression was not modulated by the changed salinity. In gills of the hard clam with 10‰ SW, both TAUT mRNA and protein expressions were significantly stimulated, and it may reflect a feedback regulation from the decreased gills taurine content under long-term hypoosmotic acclimation. These findings suggest that TAUT expression is regulated differently in gills and mantles following exposure to alterations in environmental salinity. Taken together, this study used the physiological, biochemical and molecular approaches to simultaneously explore the osmoregulation in tissues of hard clam and may further help to understand the osmoregulation in bivalves.

Effect of sulfide, osmotic, and thermal stresses on taurine transporter mRNA levels in the gills of the hydrothermal vent-specific mussel Bathymodiolus septemdierum

Hydrothermal vent environmental conditions are characterized by high sulfide concentrations, fluctuating osmolality, and irregular temperature elevations caused by vent effluents. These parameters represent potential stressors for organisms that inhabit the area around hydrothermal vents. Here, we aimed to obtain a better understanding of the adaptation mechanisms of marine species to hydrothermal vent environments. Specifically, we examined the effect of sulfide, osmolality, and thermal stress on the expression of taurine transporter (TAUT) mRNA in the gill of the deep-sea mussel Bathymodiolus septemdierum, which is a dominant species around hydrothermal vent sites. We analyzed TAUT mRNA levels by quantitative real-time polymerase chain reaction (PCR) in the gill of mussels exposed to sulfide (0.1 or 1mg/L Na2S·9H2O), hyper- (115% seawater) and hypo- (97.5%, 95.5%, and 85% seawater) osmotic conditions, and thermal stresses (12°C and 20°C) for 24 and 48h. The results showed that mussels exposed to relatively low levels of sulfide (0.1mg/L) and moderate heat stress (12°C) exhibited higher TAUT mRNA levels than the control. Although hyper- and hypo-osmotic stress did not significantly change TAUT mRNA levels, slight induction was observed in mussels exposed to low osmolality. Our results indicate that TAUT is involved in the coping mechanism of mussels to various hydrothermal vent stresses.

Down‐regulation of placental mTOR, insulin/IGF‐I signaling, and nutrient transporters in response to maternal nutrient restriction in the baboon

The mechanisms by which maternal nutrient restriction (MNR) causes reduced fetal growth are poorly understood. We hypothesized that MNR inhibits placental mechanistic target of rapamycin (mTOR) and insulin/IGF-I signaling, down-regulates placental nutrient transporters, and decreases fetal amino acid levels. Pregnant baboons were fed control (ad libitum, n=11) or an MNR diet (70% of controls, n=11) from gestational day (GD) 30. Placenta and umbilical blood were collected at GD 165. Western blot was used to determine the phosphorylation of proteins in the mTOR, insulin/IGF-I, ERK1/2, and GSK-3 signaling pathways in placental homogenates and expression of glucose transporter 1 (GLUT-1), taurine transporter (TAUT), sodium-dependent neutral amino acid transporter (SNAT), and large neutral amino acid transporter (LAT) isoforms in syncytiotrophoblast microvillous membranes (MVMs). MNR reduced fetal weights by 13%, lowered fetal plasma concentrations of essential amino acids, and decreased the phosphorylation of placental S6K, S6 ribosomal protein, 4E-BP1, IRS-1, Akt, ERK-1/2, and GSK-3. MVM protein expression of GLUT-1, TAUT, SNAT-2 and LAT-1/2 was reduced in MNR. This is the first study in primates exploring placental responses to maternal undernutrition. Inhibition of placental mTOR and insulin/IGF-I signaling resulting in down-regulation of placental nutrient transporters may link maternal undernutrition to restricted fetal growth.

Exogenous taurine attenuates mitochondrial oxidative stress and endoplasmic reticulum stress in rat cardiomyocytes

Taurine, a conditionally essential amino acid, plays a critical role in cardiovascular function. Here we examined the effect of taurine on mitochondria and endoplasmic reticulum in rat cardiomyocytes during glucose deprivation (GD). Data showed that cell viability, intracellular taurine contents, and taurine transporter expression were decreased during GD. In contrast, an increase in reactive oxygen species and intracellular Ca(2+) contents was observed. GD also caused disrupted mitochondrial membrane potential, apoptotic cell death, and dissociation of unfolded protein response (UPR)-relative proteins in cardiomyocytes. Signal transduction analysis showed that Bcl-2 family protein balance was disturbed, caspase-12 was activated and UPR-relative protein levels were up-regulated. Moreover, pre-treatment with 80 mM exogenous taurine attenuated GD effect in cardiomyocytes. Our results suggest that taurine have beneficial effects on inhibiting mitochondria-dependent cell apoptosis and UPR-associated cell apoptosis and might have clinical implications on acute myocardial infarction in future.

Low-dose taurine upregulates taurine transporter expression in acute myocardial ischemia

Taurine exerts a protective effect on cardiomyocytes. The aim of this study was to determine whether the protective effect of taurine is associated with the upregulation of taurine transporter (TAUT) expression in acute myocardial ischemia (AMI). To this end, we investigated TAUT expression in cultured cardiomyocytes exposed to hypoxia as well as in rats with AMI treated with or not with taurine. The morphology of cardiac tissues, the apoptosis of cardiomyocytes and cardiac function were examined. In addition, the taurine content and the expression of TAUT were measured. Our data demonstrated that taurine reversed the apoptosis induced by hypoxia and AMI, thereby, effectively protecting the myocardium. Taurine content and TAUT expression levels were significantly decreased when cardiomyocytes and cardiac tissues were subjected to hypoxic or ischemic stress, while the expression of cysteine sulfinate decarboxylase was unchanged. Moreover, treatment with taurine (100 mg/kg/day) significantly upregulated TAUT expression and elevated the taurine content in ischemic myocardial tissues. In vitro, the low-dose (40 mM) but not the high-dose (120 mM) administration of taurine significantly induced TAUT expression and elevated the intracellular taurine content in hypoxic cardiomyocytes. In conclusion, our data demonstrate that taurine exerts a protective effect on the ischemic myocardium. Low-dose but not high-dose taurine treatment upregulated TAUT expression and increased the intracellular taurine content in cardiomyocytes subjected to hypoxia as well as in AMI tissues.

Expression of Taurine Transporter (TauT) is Modulated by Heat Shock Factor 1 (HSF1) in Motor Neurons of ALS

Amyotrophic lateral sclerosis (ALS) is a fatal neurological disorder characterized by progressive paralysis caused by the degeneration of motor neurons throughout the central nervous system. Mutations of the free radical scavenging enzyme Cu/Zn superoxide dismutase 1 (SOD1) are a cause of familial ALS. In the present study, we demonstrated an age-dependent increase in taurine transporter (TauT) immunoreactivity in spinal cord motor neurons of ALS transgenic mice (mutant SOD1 (G93A)) and a similar increase in TauT in spinal motor neurons of patients with ALS. Chromatin immunoprecipitation analysis verified that heat shock factor 1 (HSF1) preferentially occupies the HSF1 binding element in the promoter of TauT under oxidative stress conditions. Knockdown of HSF1 by small interfering RNA reduced the transcriptional activity of TauT. Using [(3)H] taurine, we confirmed that an elevated expression of TauT directly contributes to increased taurine uptake in ALS motor neurons. In addition, we showed that taurine plays an antioxidant role and may prevent motor neuron loss due to oxidative stress in ALS. Our findings suggest that HSF1-induced TauT expression partially protects motor neurons by compensating for constitutive oxidative stress, which is thought to be a key mechanism contributing to the pathogenesis of ALS. Taken together, our results suggest that TauT is a novel pathological marker for stressed motor neurons in ALS and that modulation of TauT and taurine may slow neuronal degeneration in ALS.

Taurine and liver diseases: a focus on the heterogeneous protective properties of taurine

Taurine (2-aminoethylsulfonic acid) has many physiological and pharmacological functions in most tissues. It is abundantly maintained in the liver by both endogenous biosynthesis and exogenous transport, but is decreased in liver diseases. In the hepatic lobule, there are heterogeneous differences in metabolism between the pericentral (PC) and periportal regions, and the distributions of the biosynthesis capacity and specific taurine transporter expression are predominantly in the PC region. In cases of depletion of hepatic taurine level, serious liver damages were observed in the PC region. Taurine has protective effects against xenobiotics-induced liver damages in the PC region, but not xenobiotics-induced PP region damages. The xenobiotics that injure the PC region are mainly catabolized by NADPH-dependent cytochrome P450 2E1 that is also predominantly expressed in the PC region. Taurine treatment seems to be a useful agent for CYP2E1-related liver diseases with predominant damages in the PC region.

Taurine inhibits osteoblastic differentiation of aortic valve interstitial cells induced by beta-glycerophosphate, dexamethasone and ascorbic acid via the ERK pathway

PurposeAortic valve calcification (AVC) has been recognised as an active process characterised by osteoblastic differentiation of the aortic valve interstitial cells (AVICs). Taurine is a free β-amino acid and has...

Effects of Taurine on Glial Cells Apoptosis and Taurine Transporter Expression in Retina Under Diabetic Conditions

Taurine, a ß-aminosulfonic acid, has been reported to reduce the risk of a number of diseases, including cardiovascular disease, diabetes, and also perhaps to reduce neurodegeneration in the elderly. The transport of taurine is known to be mediated by taurine transporter (TauT). The purpose of this study is to examine the effects of taurine on glial cells apoptosis and on TauT expression in retina of diabetic rats and retinal glial cells cultured with high glucose. TdT-mediated dUTP-biotin nick-end labeling (TUNEL) staining analysis showed that the number of TUNEL-positive cells in taurine treated diabetic rats was significantly lower than those of untreated diabetic rats over the 8-, and 12-week time courses, respectively (all P<0.001). No TUNEL-positive cells were observed in retina of control groups and taurine treated control groups. In cultured retinal glial cells, the apoptosis in high glucose-treated cells was significantly increased vs the control. When the cells were incubated with high glucose and taurine at 0.1, 1.0 and 10mmol/l, the percentage of apoptosis was significantly decreased to 16.4, 5.7 and 7.6% respectively (all P<0.05). With supplementation of taurine in diet and culture medium, higher expression of TauT in retina of diabetic rats and cultured retinal glial cells under diabetic conditions were detected by western-blotting (P<0.05). Taken together, our data suggest that diabetes or high glucose induced retinal glial cells apoptosis can be inhibited by taurine, and that taurine reverses the diabetes-induced or high glucose-induced decrease in TauT expression.

L-carnitine and taurine synergistically inhibit the proliferation and osteoblastic differentiation of vascular smooth muscle cells

To investigate the synergistic action of L-carnitine (LC) and taurine (TAU) on the proliferation and osteoblastic differentiation of vascular smooth muscle cells (VSMCs). DNA and protein synthesis of VSMCs were assessed using scintillation counting. Alkaline phosphatase (ALP) activity and calcium content were determined to investigate the effects of LC and TAU on the osteoblastic differentiation and mineralization of VSMCs. TAU uptake by VSMCs was assayed. RNA interference was used to down-regulate the expression of the TAU transporter (TAUT) in rat VSMCs. LC and TAU synergistically inhibited the proliferation and beta-glycerophosphate (beta-GP)-induced osteoblastic differentiation of VSMCs as evidenced by the decreased [(3)H]thymidine incorporation, ALP activity and calcium deposition. Furthermore, LC stimulated the TAU uptake and TAUT expression in VSMCs. Suppression of TAUT with short hairpin RNA (shRNA) abolished the synergistic action of LC and TAU in VSMCs. The synergistic inhibitory action of LC and TAU on the proliferation and osteoblastic differentiation of VSMCs is attributable to the up-regulation of TAUT expression and TAU uptake by LC.

Changes in messenger RNA abundance of amino acid transporters in rat mammary gland during pregnancy, lactation, and weaning

During lactation, the mammary gland increases the needs for nutrients to fulfill the milk production requirements. Among these nutrients, amino acids play an important role for the synthesis of milk proteins. Amino acids are supplied to the mammary gland through amino acid transporters, although some are synthesized in situ. The purpose of this study was to establish the pattern of changes in messenger RNA abundance of the amino acid transporters ASC, system L, EAAC1, GLAST, CAT-1, and Tau in the mammary gland of the rat during different stages of pregnancy and lactation. Rats were fed during pregnancy and lactation a 20% casein diet. Food intake increased significantly during the lactation period. Amino acid transporter ASC expression increased during the first days of pregnancy about 2-fold, and it was increased in a lesser extent again during the peak of lactation. The expression of system L (LAT-1) and CAT-1 transporters was increased only during the lactation period. On the other hand, the expression of the transporters for anionic amino acids EAAC1 and GLAST was low during both stages. Finally, taurine transporter expression decreased during pregnancy; and it was significantly lower during lactation. These results showed that amino acid transporters were not expressed similarly in the mammary gland during pregnancy and lactation, indicating that the expression of these transporters did not respond only to the metabolic needs of the gland but depended on the dietary protein supply and possibly the specific hormonal changes that occur during pregnancy and lactation.

The Change of Taurine Transport in Osteocytes by Oxidative Stress, Hypertonicity and Calcium Channel Blockers

Taurine is the most abundant amino acid in many tissues and is found to be enhancing the bone tissue formation or inhibits the bone loss. Although it is reported that taurine reduces the alveolar bone loss through inhibiting the bone resorption, its functions of taurine and expression of taurine transporter (TauT) in bone have not been identified yet. The purpose of this study is to clarify the uptake mechanism of taurine in osteoblast using mouse osteoblast cell lines. In this study, mouse stromal ST2 cells and mouse osteoblast-like MC3T3-E1 cells as osteoblast cell lines were used. The activity of taurine uptake was assessed by measuring the uptake of [<TEX>$^3H$</TEX>]taurine in the presence or absence of inhibitors. TauT mRNA was detected in ST2 and MC3T3-E1 cells. [<TEX>$^3H$</TEX>]Taurine uptake by these cells was dependent on the presence of extracellular calcium ion. The [<TEX>$^3H$</TEX>]taurine uptake in ST2 cells treated with 4 mM calcium was increased by 1.7-fold of the control which was a significant change. In contrast, in <TEX>$Ca^{++}$</TEX>-free condition and L-type calcium channel blockers (CCBs), taurine transport to osteocyte was significantly inhibited. In oxidative stress conditions, [<TEX>$^3H$</TEX>]taurine uptake was decreased by TNF-<TEX>$\alpha$</TEX> and <TEX>$H_2O_2$</TEX>. Under the hyperosmotic conditions, taurine uptake was increased, but inhibited by CCBs in hyperosmotic condition. These results suggest that, in mouse osteoblast cell lines, taurine uptake by TauT was increased by the presence of extracellular calcium, whereas decreased by CCBs and oxidative stresses, such as TNF-<TEX>$\alpha$</TEX> and <TEX>$H_2O_2$</TEX>.