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Elevated PTH induces endothelial-to-chondrogenic transition in aortic endothelial cells.

Publication ,  Journal Article
Wu, M; Zhang, J-D; Tang, R-N; Crowley, SD; Liu, H; Lv, L-L; Ma, K-L; Liu, B-C
Published in: Am J Physiol Renal Physiol
March 1, 2017

Previous studies have shown that increased parathyroid hormone (PTH) attributable to secondary hyperparathyroidism in chronic kidney disease accelerates the arteriosclerotic fibrosis and calcification. Although the underlying mechanisms remain largely unknown, endothelial cells (ECs) have recently been demonstrated to participate in calcification in part by providing chondrogenic cells via the endothelial-to-mesenchymal transition (EndMT). Therefore, this study aimed to investigate whether elevated PTH could induce endothelial-to-chondrogenic transition in aortic ECs and to determine the possible underlying signaling pathway. We found that treatment of ECs with PTH significantly upregulated the expression of EndMT-related markers. Accordingly, ECs treated with PTH exhibited chondrogenic potential. In vivo, lineage-tracing model-subjected mice with endothelial-specific green fluorescent protein fluorescence to chronic PTH infusion showed a marked increase in the aortic expression of chondrocyte markers, and confocal microscopy revealed the endothelial origin of cells expressing chondrocyte markers in the aorta after PTH infusion. Furthermore, this in vitro study showed that PTH enhanced the nuclear localization of β-catenin in ECs, whereas β-catenin siRNA or DKK1, an inhibitor of β-catenin nuclear translocation, attenuated the upregulation of EndMT-associated and chondrogenic markers induced by PTH. In summary, our study demonstrated that elevated PTH could induce the transition of ECs to chondrogenic cells via EndMT, possibly mediated by the nuclear translocation of β-catenin.

Duke Scholars

Published In

Am J Physiol Renal Physiol

DOI

EISSN

1522-1466

Publication Date

March 1, 2017

Volume

312

Issue

3

Start / End Page

F436 / F444

Location

United States

Related Subject Headings

  • beta Catenin
  • Urology & Nephrology
  • Transfection
  • Signal Transduction
  • RNA Interference
  • Phenotype
  • Parathyroid Hormone
  • Mice, Transgenic
  • Humans
  • Epithelial-Mesenchymal Transition
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Wu, M., Zhang, J.-D., Tang, R.-N., Crowley, S. D., Liu, H., Lv, L.-L., … Liu, B.-C. (2017). Elevated PTH induces endothelial-to-chondrogenic transition in aortic endothelial cells. Am J Physiol Renal Physiol, 312(3), F436–F444. https://doi.org/10.1152/ajprenal.00210.2016
Wu, Min, Jian-Dong Zhang, Ri-Ning Tang, Steven D. Crowley, Hong Liu, Lin-Li Lv, Kun-Ling Ma, and Bi-Cheng Liu. “Elevated PTH induces endothelial-to-chondrogenic transition in aortic endothelial cells.Am J Physiol Renal Physiol 312, no. 3 (March 1, 2017): F436–44. https://doi.org/10.1152/ajprenal.00210.2016.
Wu M, Zhang J-D, Tang R-N, Crowley SD, Liu H, Lv L-L, et al. Elevated PTH induces endothelial-to-chondrogenic transition in aortic endothelial cells. Am J Physiol Renal Physiol. 2017 Mar 1;312(3):F436–44.
Wu, Min, et al. “Elevated PTH induces endothelial-to-chondrogenic transition in aortic endothelial cells.Am J Physiol Renal Physiol, vol. 312, no. 3, Mar. 2017, pp. F436–44. Pubmed, doi:10.1152/ajprenal.00210.2016.
Wu M, Zhang J-D, Tang R-N, Crowley SD, Liu H, Lv L-L, Ma K-L, Liu B-C. Elevated PTH induces endothelial-to-chondrogenic transition in aortic endothelial cells. Am J Physiol Renal Physiol. 2017 Mar 1;312(3):F436–F444.

Published In

Am J Physiol Renal Physiol

DOI

EISSN

1522-1466

Publication Date

March 1, 2017

Volume

312

Issue

3

Start / End Page

F436 / F444

Location

United States

Related Subject Headings

  • beta Catenin
  • Urology & Nephrology
  • Transfection
  • Signal Transduction
  • RNA Interference
  • Phenotype
  • Parathyroid Hormone
  • Mice, Transgenic
  • Humans
  • Epithelial-Mesenchymal Transition