Effects of the rotary cell culture system-simulated microgravity on growth features of thyroid follicular epithelial cells in rats / 中华内分泌代谢杂志

The rotary cell culture system(RCCS)was used to simulate the microgravity environment, and FRTL-5 cells were divided into simulated microgravity group(SMG)and normal gravity group(NG). FRTL-5 cells were harvested after treatment for 6, 12, 24, and 36 h, the cell viability was measured by MTT assay, and the cells cycles were detected by flow cytometry. The ultrastructure of FRTL-5 cells was observed under laser confocal microscope with FITC-labeled technique. The MTT assay showed that the proliferation of FRTL-5 cells was significantly inhibited after RCCS treatment for 6, 12, 24, and 36h compared with NG(P<0.05), in which the most obvious effect was observed at 24h. The flow cytometry showed that the proportion of FRTL-5 cells at G1 stage in RCCS group was increased significantly after 6, 12, 24, and 36h compared with NG(P<0.05), while the proportion of FRTL-5 cells at S stage was decreased significantly(P<0.05)except that cultured with RCCS for 6 h. The proportion of FRTL-5 cells at G2/M stage was decreased in early phase(6-12 hours)of RCCS culture, with the lowest at 12h and transient increase at 24h of RCCS culture. The laser confocal microscope revealed that there were local microfilament depolymerization, tension fibers decrease, structure disorder, cellular pseudopodia reduction, and irregular shape among FITC-labeled FRTL-5 cells cultured with RCCS for 36h. (Chin J Endocrinol Metab, 2018, 34: 598-601)

Effects of fluoride on the expression of functional genes related with the metabolism of thyroid hormone in FRTL cells / 中国兽医学报

To investigate the effects of fluoride on the expression of thyroglobulin (TG),thyroid peroxidase(TPO),odium iodide symporter (NIS) genes in FRTL cells,FRTL cells cultured in vitro were treated in logarithmic phase with sodium fluoride at different concentration of 20.0,10.0,5.0,2.5,1.25 mg/L,respectively.After 72 h,the cells were collected and semi-quantitative RT-PCR for TG mRNA,TPO mRNA and NIS mRNA and β-actin was performed.The results showed that compared with the control cells,the expression levels of TG gene in FRTL cells treated with lower concentration of sodium fluoride increased compensatively,but decreased significantly (P<0.05) with higher concentration(>5.0 mg/L);the RT-PCR products of TPO and NIS in FRTL cells treated with all concentration of sodium fluoride reduced,some of them were significant (P<0.05).It is concluded that fluoride can reduce the expression of TG,TPO,NIS genes in thyroid cells,conseguently cause dysfunction" of thyroid in uptaking and unilizing of iodine,and synthesizing,storing,secreting of thyroid hormones.

Overexpression of USF Increases TGF-beta1 Protein Levels, But G1 Phase Arrest was not Induced in FRTL-5 Cells

Transforming growth factor-beta1 (TGF-beta1) is a potent inhibitor of cellular growth and proliferation by G1 phase arrest or apoptosis. We investigated the association of TGF-beta1 with the anti-proliferative effect of upstream stimulatory factor (USF) in Fischer rat thyroid cell line (FRTL-5) cells. [Methyl-(3)H] thymidine uptake was measured after treatment of FRTL-5 cells with TGF-beta1 to identify its anti-proliferative effect. USF-1 and USF-2 proteins were in vitro translated, and an electrophoretic mobility shift assay was performed to identify the interaction between USF and the TGF-beta1 promoter. FRTL-5 cells were transfected with USF cDNA, and then the expression of TGF-beta1 was examined with Northern and Western blotting. The cell cycle-regulating proteins associated with TGF-beta1 were also measured. TGF-beta1 significantly inhibited [methyl-(3)H] thymidine uptake in FRTL-5 cells. Two specific binding sites for USF were found in the TGF-beta1 promoter: -1,846~-1,841 (CACATG) and -621~-616 (CATGTG). Overexpression of USF increased both the mRNA levels and protein levels of TGF-beta1. However, the expression of cyclin D1, CDK4, cyclin E, and CDK2, and the phosphorylation of retinoblastoma protein remained unchanged. Overexpression of USF in FRTL-5 cells increased the expression of TGF-beta10 through specific binding to TGF-beta1 promoter. However, the USF-induced expression of TGF-beta1 did not cause G1 arrest.

STUDY ON THE EFFECT OF IODINE EXCESS ON CATHEPSINS IN RAT THYROID CELLS / 营养学报

Objective: To explore the effect of iodine overdose on cathepsin B and D in thyroidcell line (FRTL). Method: The cells were treated with potassium iodide (0, 1, 5, 10, 50 and 100mmol/L). After treatment 6, 12, 24, 48 and 72 hours, the cells were collected. The activities of cathepsin B (CB) and cathepsin D (CD) were assayed by fluorospectrophotometry and Lowry, respectively. The mRNA levels of CB and CD were determined with real-time PCR. Results: After 12 and 24 hours, the activities of CB and CD, treated by 50mmol/L potassium iodide were decreased significanty. The mRNA levels of CB and CD of 50mmol/L potassium iodide group were decreased significanty after treatment 24 hours. Conclusion: The decreased activities of CB and CD were one of reasons of thyroid colloid retention resulted from iodine excess.

Effect of Estrogen on H2O2 Induced Apoptosis of FRTL-5 Cells / 대한내분비학회지

BACKGROUND: Understanding the pathways and controlling mechanisms of thyrocyte apoptosis is important for the elucidation of the pathogenesis of goiter or thyroid cancer. A system for evaluating apoptosis, in FRTL-5 cells, triggered by hydrogen peroxide (H2O2), a highly likely apoptogenic signal in physiologic condition, was be set up to see the effects of TSH and estrogen on H2O2-induced apoptosis. METHOD: DNA laddering was used in the optimization process or the conditions of the set-up of system for the evaluation of apoptosis in the FRTL-5 cells. To quantify the apoptosis under the optimized conditions, histone-bound DNA fragments in the cytoplasm were measured by ELISA. RESULTS: 1) The optimized conditions for induction of apoptosis in the FRTL-5 cells by H2O2 were; observation of DNA laddering 18~24 hrs after the addition of 0.3 mM H2O2 to cells maintained in TSH-free, low serum containing media (5H1 or 5H0 media) for 48 hrs. 2) Exposure of the FRTL-5 cells to TSH (1 mU/L) for more than 48 hrs (6H0 media). before the addition of H2O2 significantly decreased the degree of apoptosis, compared to cells maintained under TSH-free conditions (0.98+/-0.21 vs. 2.27 0.11 arbitrary unit, p<0.05), whereas exposure for 24 hrs. did not. 3) Exposure of the FRTL-5 cells to high dose 17- estradiol (1-100 M) significantly decreased the degree of H2O2-induced apoptosis in a dose dependent manner. The addition of serum (1%) blunted the effects of estrogen on H2O2-induced apoptosis, and TSH totally abrogated the estrogen effect.Physiologic doses of estrogen (10~100 nM) showed no suppressive effects on H2O2-induced apoptosis in FRTL-5 cells. CONCLUSION: A system for evaluating apoptosis in FRTL-5 cells triggered by hydrogen peroxide (H2O2), a highly likely apoptogenic signal in physiologic condition, was set up, and found for the first time that high dose estrogen suppressed the H2O2-induced apoptosis in FRTL-5 cells

Effect of Estrogen on H2O2 Induced Apoptosis of FRTL-5 Cells / 대한내분비학회지

BACKGROUND: Understanding the pathways and controlling mechanisms of thyrocyte apoptosis is important for the elucidation of the pathogenesis of goiter or thyroid cancer. A system for evaluating apoptosis, in FRTL-5 cells, triggered by hydrogen peroxide (H2O2), a highly likely apoptogenic signal in physiologic condition, was be set up to see the effects of TSH and estrogen on H2O2-induced apoptosis. METHOD: DNA laddering was used in the optimization process or the conditions of the set-up of system for the evaluation of apoptosis in the FRTL-5 cells. To quantify the apoptosis under the optimized conditions, histone-bound DNA fragments in the cytoplasm were measured by ELISA. RESULTS: 1) The optimized conditions for induction of apoptosis in the FRTL-5 cells by H2O2 were; observation of DNA laddering 18~24 hrs after the addition of 0.3 mM H2O2 to cells maintained in TSH-free, low serum containing media (5H1 or 5H0 media) for 48 hrs. 2) Exposure of the FRTL-5 cells to TSH (1 mU/L) for more than 48 hrs (6H0 media). before the addition of H2O2 significantly decreased the degree of apoptosis, compared to cells maintained under TSH-free conditions (0.98+/-0.21 vs. 2.27 0.11 arbitrary unit, p<0.05), whereas exposure for 24 hrs. did not. 3) Exposure of the FRTL-5 cells to high dose 17- estradiol (1-100 M) significantly decreased the degree of H2O2-induced apoptosis in a dose dependent manner. The addition of serum (1%) blunted the effects of estrogen on H2O2-induced apoptosis, and TSH totally abrogated the estrogen effect.Physiologic doses of estrogen (10~100 nM) showed no suppressive effects on H2O2-induced apoptosis in FRTL-5 cells. CONCLUSION: A system for evaluating apoptosis in FRTL-5 cells triggered by hydrogen peroxide (H2O2), a highly likely apoptogenic signal in physiologic condition, was set up, and found for the first time that high dose estrogen suppressed the H2O2-induced apoptosis in FRTL-5 cells

The Effect of Ghrelin on Ca2+ Concentration in Thyroid FRTL-5 Cells

Ghrelin is a newly discovered peptide, which is released from the stomach and neurons in the hypothalamic arcuate nucleus (ARC), and potently stimulates growth hormone release and food intake. In the present study, we investigated the effect of ghrelin on [Ca2+]i in thyroid FRTL-5 cells. Ghrelin (5 nM) increased [Ca2+]i and TSH (1 unit/l) had an additive effect on [Ca2+]i when extracellular normal solution was 1.1mM Ca2+ containing Coon's modified Ham's F12 medium. When Ca2+-free medium containing 2 mM EGTA replaced the above normal solution, ghrelin also induced a similar rise in [Ca2+]i. In the middle of [Ca2+]i increment by ghrelin, nifedipine (1 micrometer), nickel (100micrometer) and La3+ (100micrometer) had no effect on [Ca2+]i. After endoplasmic reticulum was depleted by cyclopiazonic acid (CPA; 10micrometer), ghrelin caused no visible change on [Ca2+]i in Ca2+-free/2 mM EGTA solution. These results suggest that ghrelin can increase [Ca2+]i through endoplasmic reticulum in thyroid FRTL-5 cells.

Effects of USF-1, USF-2, PTEN and Thyroid Transcription Factors on the Function and Growth in FRTL-5 Cells / 대한내분비학회지

BACKGROUND: Upstream stimulatory factors (USFs) and PTEN are known to be tumor suppressants. USFs and PAX-8 were reported to be the functional competitors in sodium iodide symporter (NIS) gene expression. We investigated the effects of USF-1, USF-2, PTEN, and thyroid-specific transcription factors (TTF-1, PAX-8) on the function and growth of thyrocytes of FRTL 5 rat thyroid cells. METHODS: Complementary DNAs of the USF-1, USF-2, PTEN, TTF-1 (homeodomain), and PAX-8 were synthesized from RNA extracted from FRTL-5using an RT-PCR kit. Each of them was transiently transfected to the FRTL-5 cells using the lipofectamine after being cloned into the pcDNA3.1 vectors. Stable cell lines, which were transfected by USF-1, PTEN, TTF-1, and PAX-8, were also obtained from the FRTL-5 cells, respectively. Extracellular cAMP concentrations were measured after 24 hours of incubation with varying concentrations of bTSH (0.1~100 mIU/mL). After, [Methyl-3H] thymidine uptake or 5-bromo-2'-deoxyuridine (BrdU) assay was performed. RESULTS: USF-1 and USF-2 significantly increased cAMP levels and decreased thymidine uptake in both transiently and stably transfected cells (p<0.01). PTEN had a tendency to increase both the cAMP levels and BrdU uptake in stable cells, but had a tendency to decrease thymidine uptake in transiently transfected cells. TTF-1 significantly increased the cAMP levels and either thymidine or BrdU uptake in both transiently and stably transfected cells (p<0.05). PAX-8 significantly increased both the cAMP levels and BrdU assay in stable cells, but in transiently transfected cells, it significantly decreased cAMP concentrations (p<0.01). CONCLUSIONS: These results suggested that both the USF-1 and USF-2 play a role in suppressing the growth of thyrocytes but at the same time, they kept the ability to produce cAMP after TSH stimulation. They had opposing effects on TTF-1 and PAX-8 in terms of the proliferation of thyrocytes

Regulatory Mechanism of p66 Shc Expression by TSH in FRTL-5 Cells / 대한내분비학회지

BACKGROUND: Thyroid goiters are very common, however, the mechanism of development is not fully understood. A TSH receptor has been known to activate two different signaling pathways the cAMP/protein kinase A(PKA) and phospholipase C(PLC)/protein kinase C(PKC) systems. However, both systems are limited in the degree to which they explain the discrepancy between a goiter and TSH receptor activation. It has recently been reported that the expression of p66 Shc was increased by TSH stimulation in thyrocytes, suggesting that the p66 Shc molecule may play a critical role in the transition of the TSH-induced growth signals. METHODS AND RESULTS: In this study, we examined the expression of p66 Shc by stimulation of TSH, and the regulatory mechanisms of the TSH-induced expression of the p66 Shc in FRTL-5 cells. In FRTL-5 cells, TSH could increase the expression of the p66 Shc, and the this expression was decreased to basal levels after the removal of TSH. The TSH-induced p66 Shc expression was competitively inhibited by TSH receptor blocking antibodies. The increments of the expression of the p66 Shc protein caused by TSH were both time and concentration dependent, and it was same in the mRNA levels. Cholera toxin increased the expression of the p66 Shc, while pertussis toxin did not. The activators of the cAMP/PKA pathway (8-bromo-cAMP and forskolin) also stimulated the expression of p66 Shc, and the PKA inhibitor H89 decreased the expression, while the inhibition of the PKC pathway by GF109203X, or PMA, affected the expression of p66 Shc very little. CONCLUSION: Our data suggests that p66 Shc may play an important role in regulating the growth of thyrocytes. The TSH receptor - Gs protein - adenylate cyclase - cAMP - PKA pathway mainly mediates the TSH effects on the expression of p66 Shc molecules.

Effect of ceramide on apoptosis and phospholipase D activity in FRTL-5 thyroid cells

Ceramide, a product of sphingomyelin hydrolysis, is now recognized as an intracellular lipid messenger, which mediates the effects of extracellular agents on cellular growth, differentiation and apoptosis. Recently, ceramide has been implicated in the regulation of phospholipase D (PLD). In this study, we examined the effects of ceramide on the activity and mRNA level of PLD during apoptotic process in FRTL-5 thyroid cells. C2-ceramide (N-acetyl sphingosine) induced apoptosis in FRTL-5 thyroid cells. Fluorescent staining showed that ceramide induced the typical features of apoptosis including condensed or fragmented nuclei. DNA fragmentation was also observed by agarose gel electrophoresis. Flow cytometric cell cycle analysis showed more clearly that ceramide induced apoptotic cell death in FRTL-5 thyroid cells. The treatment of FRTL-5 thyroid cells with thyroid-stimulating hormone (TSH) resulted in an increased PLD activity in a dose- and time-dependent manner. However, the TSH-induced increase in PLD activity was down-regulated within 2 h after ceramide treatment. Furthermore, the levels of PLD mRNA were found to be decreased throughout apoptotic process as inferred by reverse transcription-polymerase chain reaction. However, the decreases in PLD mRNA levels were not correlated with those in PLD activities after ceramide treatment. Taken together, these data suggest that ceramide inhibits the PLD activity in an early apoptotic phase and down-regulation of the levels of PLD mRNA may be implicated in apoptotic process in FRTL-5 thyroid cells.

Differential Roles of Transcriptional Coactivators: CBP and CIITA on GAS (Interferon-r Activated Site) - Mediated Transcription in Thyroid Cells / 대한내분비학회지

BACKGROUND: In the previous studies, we identified that the interferon-gamma activated sequence (GAS) in the 5-flanking region of rat ICAM-1 gene is major element for interferon-y-inducible expression of the gene in rat thyroid cells, FRTL-5. We here, investigated the role of transcriptional coactivators, CBP (CREB binding protein) and CIITA (class II transactivator) in the modulation of the activity of GAS which could interacts with signal transducers and activators of transcription-1 and 3 (STAT1 and STAT3). METHODS: The expression of CBP RNA and protein were quantitated in FRTL-5 after stimulation with interferon-y (IFN-gamma), thyroid stimulating hormone (TSH), forskolin and methimazole. Direct association of CBP with STAT were analyzed by irnmunoprecipitation. The transcriptional roles of CBP and CIITA in the regulation of GAS were assessed by the cotransfection with their expression vectors with reporters; 5-deletion constructs of rat ICAM-1 promoter or 8xGAS-luc constructs, into FRTL-5 thyroid cells. RESULTS: The level of CBP RNA and protein were not changed by the treatment with TSH, IFN-y, forskolin and methimazole in FRTL-5, FRT and BRL liver cells. The CBP could be directly associated with STAT1. Furthernmore, the overexpression of CBP significantly increases the both promoter activities; rat ICAM-1 gene promoter which has GAS element and 8xGAS-luc cassette constructs. However the cotransfection of CI1TA decreased the constitutive and CBP-mediated transactivation of rat ICAM-1 promoter and SxGAS-luc cassette constructs. CONCLUSION: We identified that the two transcriptional coactivators; CBP and CIITA has differential roles in the regulation of transcriptional activity of GAS drived promoter. CBP increases the GAS activity through the direct binding with STATl, but CIITA inhibited the CBP-mediated transactivation of GAS activity.

Hormonal regulation of ICAM-1 gene expression in thyroid cells, FRTL-5

Our previous works have shown that human thyroid follicular cells from Graves' disease and FRTL-5 rat thyroid cells express the intercellular adhesion molecule-1 (ICAM-1) molecule and its expression is upregulated by several cytokines, interferon-gamma, tumor necrosis factor-alpha, interleukin-1 beta and interleukin-6. We used FRTL-5 cells which show hormonal dependence of growth and function for the study of hormonal regulation of ICAM-1 gene, We studied ICAM-1 mRNA expression and promoter regulation after cloning of rat ICAM-1 promoter. We found very interesting findings that thyroid stimulating hormone (TSH) and forskolin downregulates steady state MHC class land ICAM-1 mRNA levels in FRTL-5 cells; furthermore, TSH/cAMP inhibit cytokines (interferon-gamma,tumor necrosis factor-alpha)-mediated maximal ICAM-1 mRNA expression, In addition, hydrocortisone and insulin differentially regulate the ICAM-1 mRNA levels; hydrocortisone markedly suppresses the mRNA level but insulin partially recovers hydrocortisone mediated ICAM-1 suppression, The interferon-gamma and tumor necrosis factor-alpha increases full ICAM-1 promoter (pCAM-1822) activity and this cytokine mediated increase of the promoter activity is also inhibited by TSH and forskolin, Thus TSH/cAMP pathways play roles as a antagonistic action for maximal expression of ICAM-1 gene by these cytokines. We propose this TSH action is one of physiologic mechanisms to preserve self tolerance in face of abnormal cytokine challenges in systemic inflammatory condition or acute phase response.

Difference of Thyroid Stimulating Antidody Activities Measured in Chinese Hamster Ovary Cells Stably Transfected with Human TSH Receptor and in FRTL-5 Cells in Graves Disease and Its Clinical Correlations / 대한내분비학회지

Background : Thyroid stimulating antibodies result in the development of hyperthyroidism and goiter in Graves disease. However, thyroid stimulating antibody activities do not correlate with the clinical features in many patients with Graves disease. The purpose of this study is to address this discrepancy between thyroid stimulating antibody activities and clinical features of Graves patients. Methods: We measured thyroid stimulating antibody activities simultaneously using human TSH receptor transfected Chinese hamster(hTSHR-CHO) cells and rat thyroid(FRTL-5) cells in 57 untreated patients with Graves disease, and compared their activities with clinical features including thyroid hormone levels. Results : The detection rate of thyroid stimulating antibody measured by hTSHR-CHO cells was 90% in 57 untreated Graves patients and it was higher than that measured by FRTL-5 cells. Thyroid stimulating antibody activity by hTSHR-CHO cells was significantly correlated with that by FRTL-5 cells(r=0.5, p<0.001), however, 18 of 57(32%) patients showed marked discrepancy of thyroid stimulating antibody activity between in hTSHR-CHO and FRTL-5 systems. Thyroid stimulating antibody activity measured by hTSHR-CHO cells was significantly correlated with serum total T3, free T4 levels, and goiter size but not 99mTc-thyroid uptake. On the other hand, thyroid stimulating antibody activity measured by FRTL-5 cells was significantly correlated with goiter size and 99mTc-thyroid uptake but not thyroid hormone levels. The difference between function and goiter size with respect to thyroid stimulating antibody measurement in two cells system is, nevertheless, particularly evident in the free T4/goiter ratio in patients with high hTSHR-CHO and low FRTL-5 cell assay values. Conclusion: These findings suggest that thyroid stimulating antibodies in Graves disease are heterogeneous population in terms of responses to different origin of cells. Further, thyroid stimulating antibody activities measured by FRTL-5 cells tend to correlate better with goiter size and Tc-thyroid uptake, whereas thyroid stimulating antibody activities measured by hTSH-CHO cells correlate better with thyroid hormone levels.

Assay of Thyrotropin Receptor Antibodies with Recombinant Human Thyrotropin Receptor Expressed on Chinese Hamster Ovary Cells / 대한내분비학회지

Thyroid stimulating antibody which results in the development of hyperthyroidism and goiter in Graves' patients used to be measured by using rat thyroid cells, FRTL-5. However, this assay has disadvantages: decreased sensitivity due to differences in species, and fastidious culture conditions for FRTL-5 cells. Thus, we recently created stably transfected Chinese hamster ovary(CHO) cells containing the human TSH receptor(hTSHR-CHO) and developed optimal conditions for the measurement of thyroid stimulating antibody using hTSHR-CHO cells. In this study, to evaluate the clinical relevance of thyroid stimulating antibody measurement using hTSHR-CHO cells, we measured thyroid stimulating antibody activities of IgGs from Graves' disease and other thyroid disease using hTSHR-CHO cells, and compared to those of thyroid stimulating antibody assays using FRTL-5 cells. 1) The cut off value of positive thyroid stimulating antibody activity measured in hTSHR-CHO cells was 145%(above the mean +2SD) which was lower than 165% in FRTL-5 cells. The intra-assay and inter-assay variances were 3.9% to 9.0% and 12.7% to 1.6%, respectively. 2) Thyroid stimulating antibody activity was detected in 90% of patients with untreated Graves' disease when patients initially presented. Further, in patients seen initially but already under therapy, 75% had positive values if they were hyperthyroid but only 43% had IgGs with activity if they were euthyroid. Patients in clinical remission after therapy showed positive values in 23% of cases. Only 2 of 25 patients with Hashimoto's thyroiditis showed weak thyroid stimulating antibody activity, none of 18 patients with nodular nontoxie goiter, 1 of 15 patients with primary myxedema, and 2 of 33 control patients with no thyroid disease. Thus, the detection frequency and specificity of the assay with hTSHR-CHO cells was excellent for this type bioassay.3) The detection frequency of thyroid stimulating antibody activity by hTSHR-CHO cells assay system(90%) was higher than that by FRTL-5 cells assay system(66%) in untreated Graves' patients. Those two activities were positively correlated with each other(r=0.52, p<0.001). However, some IgGs showed discrepancy of the thyroid stimulating antibody activity measured in hTSHR-CHO cells and in FRTL-5 cells; 56 of 87 patients were positive in both cells system, 8 of 87 were negative in both cells system, 1 of 87 was only positive in FRTL-5 cells and 22 of 87 were only positive in hTSHR-CHO cell system. Thus, 73%(22/30) of IgGs showing negative values of thyroid stimulating antibody activities in FRTL-5 cells were detected its activities in hTSHR-CHO cells system.In summary, thyroid stimulating antibody assay with hTSHR-CHO cells exhibited so excellent sensitivity and specificity that this technique should be used for clinical practice as well as basic research.

Changes of sodium iodide symporter expression in FRTL cells during acute iodine excess / 中华内分泌代谢杂志

FRTL cells were incubated in the culture medium containing 10 -6 -10-3 mol/L KI for 24, 48 and 72 h, and the levels of sodium iodide symporter (NIS) mRNA and protein were measured using RT-PCR and Western blot. The levels of NIS mRNA in FRTL cells incubated with different concentrations of iodide for 24 and 48 h showed no significant difference as compared with the control group, however, NIS protein was reduced gradually in FRTL cells incubated with different concentrations of iodide for 48 and 72 h as compared with that in control group. The higher the iodide concentration, the lower the levels of NIS protein. The results show that acute iodine excess does not affect the expression of NIS mRNA, but down-regulates NIS protein expression. Iodine excess may regulate the expression of NIS through post-transcription.

STUDY OF SERUM TRAb IN AUTOIMMUNE THYROID DISEASE WITH ABC- ELISA / 西安交通大学学报(医学版)

In this paper the investigation of using a new method-ABC-ELISA in assay of Autoimmune Thyroid Disease are presented. The sensitivity of ABC-ELISA is compared with that of standard ELISA; Its reliability is proven by the methods of detecting TSAb with FRTL-5. TRAb is detected by ABC-ELISA in 91% of untreated Graves'. TRAb is detected by Standard ELISA in 70% of untreated Graves'. The results of ABC-ELISA in 26 untreated Graves' are equal to that of the method of detecting TSAb with FRTL-5. Therefore, we consider that ABC-ELISA is a sensitive, reproducible, convenient method applicable to clinical practice.