Endocrinology and Metabolism

Original Articles

Identification and Validation of the Relationship of the Anabolic Effect of Parathyroid Hormone with the Wnt/beta-catenin Canonical Pathway.: Se Hwa Kim, Juan Ji An, Yumie Rhee, Sung Kil Lim; J Korean Endocr Soc. 2007;22(6):411-418. Published online December 1, 2007; DOI: https://doi.org/10.3803/jkes.2007.22.6.411

3,072 View
21 Download
2 Crossref

BACKGROUND
It has been well established that daily injections of low dose parathyroid hormone (PTH) increase bone mass in animals and humans. However, the precise mechanisms by which PTH exerts its anabolic action on bone are incompletely understood. The canonical Wnt-b-catenin signaling pathway has recently been demonstrated to have an important role in bone cell function. In the present study, we have examined the interaction between the PTH and Wnt signaling pathways in mouse osteoblastic MC3T3-E1 cells. METHODS & RESULTS: MC3T3-E1 cells were treated with 0.01-0.84 micrometer recombinant PTH. beta-catenin expression was significantly increased after 30 minutes of exposure to PTH and reached a maximum 2.7 fold increase at 1 hr and expression then faded at 6 hrs. In addition, treatment with PTH increased nuclear accumulation of activated beta-catenin; the ratio between the nuclear to cytoplasmic protein was more than three fold at 30 minutes and beyond. Moreover, PTH stimulated T-cell factor/lymphoid enhancer factor (TCF/LEF) reporter gene activity in MC3T3-E1 cells. Confocal microscopy revealed nuclear translocation of beta-catenin by PTH as compared with a glycogen synthase kinase-3beta (GSK-3beta) inhibitor. CONCLUSION: These results suggest that the anabolic mechanism of PTH might be partially associated with the Wnt-canonical pathway. The appropriate target of another anabolic agent should be determined through further studies of this pathway.

Citations

Citations to this article as recorded by

Effects of N-acetyl-l-cysteine on fish hepatoma cells treated with mercury chloride and ionizing radiation
Jin Kyu Kim, Min Han, Mohammad Nili
Chemosphere.2011; 85(10): 1635. CrossRef
Bone Forming Effect of PTH through Wnt/β-catenin Signaling System
Dong Jin Chung, Min Young Chung
Journal of Korean Endocrine Society.2007; 22(6): 407. CrossRef

Effects of Wnt-1 on the Growth and Apoptosis of FRTL-5 Cells.: Jung Min Kim, Tae Yong Kim, Young Kee Shong, Yoon Soo Rhee, Eun Jung Park, Hyun Chung Choi, Won Bae Kim; J Korean Endocr Soc. 2007;22(1):35-44. Published online February 1, 2007; DOI: https://doi.org/10.3803/jkes.2007.22.1.35

2,740 View
18 Download

Abstract PDF: BACKGROUND
Wnt proteins are major signaling molecules involved in embryonic induction, generation of cell polarity and the cell fate decision. A central player in the Wnt signaling pathways is beta-catenin. Several studies have suggested that the Wnt/beta-catenin signaling pathway may be involved in the physiologic/pathologic control of thyroid cell growth and function. METHODS: We investigated the effect of thyroid-stimulating hormone (TSH) on the expression of Wnt proteins in FRTL-5 cells. To evaluate the effect of Wnt-1 on FRTL-5 cells growth, we isolated a stable cell line that overexpressed Wnt-1 (W1), and a vector-transfected cell clone (V3) was used as a control. We investigated the differences in the cellular growth rate, the cell cycle and cell apoptosis in the W1 and V3 cell lines. RESULTS: TSH caused a significant increase in the Wnt-1 level and a pronounced decrease in both the active and total beta-catenin levels in the FRTL-5 cells. The growth rate, the percentage of cells in the S/G2/M phase and the c-myc level were significantly higher in the W1 cells compared with the V3 cells. There was no change in the beta-catenin level and the cyclin D1 level in the W1 cells compared with the V3 cells. The cellular apoptosis induced by actinomycin-D seemed to be significantly decreased because the level of bcl-2 was increased in the W1 cells compared with the V3 cells. CONCLUSION: The FRTL-5 cells expressed Wnt-1 protein, and TSH increased the Wnt-1 expression, and it paradoxically decreased beta-catenin in the FRTL-5 cells. Overexpression of Wnt-1 in the FRTL-5 cells increased cell growth and it decreased apoptosis. Growth stimulation by Wnt-1 overexpression was not mediated by beta-catenin (the canonical Wnt pathway), but seemed to be mediated by activation of the Wnt/Ca2+ pathway, which involves an increased c-myc level. Suppression of apoptosis with Wnt-1 overexpression was due to the increased bcl-2 level.

Expression of E-cadherin and a-catenin in Thyroid Carcinomas.: Sang Jin Kim, Min Chul Lee; J Korean Endocr Soc. 1997;12(4):533-540. Published online January 1, 2001

1,631 View
19 Download

Abstract PDF: BACKGROUND
Cell-cell adhesion in tissue is mainly regulated by hornotypic interaction of cadherin molecules, which are anchored to the cytoskeleton via cytoplasmic proteins, including a-and / 3-catenin. Loss of E-cadherin and catenin have been attributed a pathogenetic role in tumor invasion. METHODS: We examined the expression of E-cadherin and a-catenin in human thyroid carcinoma by immunohistochemistry. RESULTS: Normal tissue strongly expressed E-cadherin and a-catenin. However, E-cadherin and a-catenin expression were frequently reduced in thyroid carcinoma (E-cadherin: 62.5%, a-catenin: 81.3%). But the expression of E-cadherin and a-catenin in tumors with metastatic spreading were not different with tumors without metastasis. CONCLUSION: These results suggest that reduced E-eadherin and a-catenin expression may be a sensitive marker for disturbance in the adhesive function of the junctional complex, but further evaluation with more cases is needed for confirmation of the result of the same degree of expression in tumors with metastasis.

First
Prev
Page of 1
Next
Last

Search