Author's information: Ri-Ning Tang as co-first author.
Nuclear Translocation of β-Catenin Mediates the Parathyroid Hormone-Induced Endothelial-to-Mesenchymal Transition in Human Renal Glomerular Endothelial Cells
Article first published online: 13 AUG 2014
© 2014 Wiley Periodicals, Inc.
Journal of Cellular Biochemistry
Volume 115, Issue 10, pages 1692–1701, October 2014
How to Cite
Wu, M., Tang, R.-N., Liu, H., Ma, K.-L., Lv, L.-L. and Liu, B.-C. (2014), Nuclear Translocation of β-Catenin Mediates the Parathyroid Hormone-Induced Endothelial-to-Mesenchymal Transition in Human Renal Glomerular Endothelial Cells. J. Cell. Biochem., 115: 1692–1701. doi: 10.1002/jcb.24832
No conflicts of interest, financial or otherwise, are declared by the authors.
- Issue published online: 13 AUG 2014
- Article first published online: 13 AUG 2014
- Accepted manuscript online: 12 MAY 2014 06:41AM EST
- Manuscript Accepted: 8 MAY 2014
- Manuscript Received: 18 OCT 2013
- National Natural Science Foundation of China (Key Program). Grant Numbers: 81130010, 81370919
- Natural Science Foundation of Jiangsu Province. Grant Numbers: BK 2011603, BK 2012751
- PARATHYROID HORMONE;
- GLOMERULAR ENDOTHELIAL CELL;
- ENDOTHELIAL-TO-MESENCHYMAL TRANSITION;
Emerging evidence shows that increased parathyroid hormone (PTH) accelerates endothelial injury and subsequent organ fibrosis. Although the underlying mechanisms remain largely unknown, the endothelial-to-mesenchymal transition (EndMT) has recently been demonstrated to be a crucial event during fibrotic disorders. Therefore, the present study aimed to investigate whether elevated PTH could induce EndMT in primary human renal glomerular endothelial cells (GECs) and to determine the possible underlying signaling pathway. The expression of EndMT-related markers was determined by real-time PCR, Western blotting, and confocal microscopy. The results showed that PTH receptor (PTHR) was expressed in GECs and its expression was decreased by increasing concentration of PTH. Moreover, PTH significantly inhibited the expression of endothelial marker CD31 and increased the expression of mesenchymal markers FSP1 and α-SMA in concentration- and time-dependent manners. Confocal microscopy revealed an increasing overlap of CD31 with FSP1 in some GECs after PTH treatment. The expression of type I collagen was upregulated by PTH. Furthermore, PTH enhanced the nuclear β-catenin protein levels, and decreased cytoplasmic β-catenin expression in GECs was observed. In contrast, DKK1, an inhibitor of β-catenin nuclear translocation, attenuated such changes in EndMT-related markers induced by PTH. In summary, these data demonstrated that elevated PTH-induced EndMT in human GECs might be partially mediated by the nuclear translocation of β-catenin. J. Cell. Biochem. 115: 1692–1701, 2014. © 2014 Wiley Periodicals, Inc.