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Pin1 regulates parathyroid hormone mRNA stability.

Rajiv Kumar1

  • 1Division of Nephrology and Hypertension, Department of Medicine, Mayo Clinic and Foundation, 200 First Street SW, Rochester, MN 55905, USA. rkumar@mayo.edu

The Journal of Clinical Investigation
|September 23, 2009
PubMed
Summary

Reduced Pin1 activity in chronic kidney disease (CKD) increases parathyroid hormone (PTH) synthesis by degrading KSRP and stabilizing PTH mRNA. This finding offers new therapeutic targets for treating secondary hyperparathyroidism.

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Nephrology

Background:

  • Secondary hyperparathyroidism is common in chronic kidney disease (CKD) and vitamin D deficiency, leading to fractures and mortality.
  • Parathyroid hormone (PTH) synthesis is regulated by proteins binding to AU-rich elements (AREs) in the 3' UTR of Pth mRNA, affecting mRNA stability.
  • Understanding these regulatory mechanisms is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role of Pin1, a peptidyl-prolyl isomerase, in regulating PTH synthesis in murine models of secondary hyperparathyroidism.
  • To elucidate the molecular mechanisms by which Pin1 activity influences Pth mRNA stability and PTH production in the context of CKD or calcium deficiency.

Main Methods:

  • Assessed Pin1 activity in murine models of secondary hyperparathyroidism (CKD or Ca deficiency).
  • Examined the impact of reduced Pin1 activity on the phosphorylation and degradation of the ARE-binding protein KSRP.
  • Evaluated the effect of altered KSRP and AUF1 levels on Pth mRNA stability and PTH synthesis.

Main Results:

  • Pin1 activity was reduced in murine secondary hyperparathyroidism associated with CKD or Ca deficiency.
  • Reduced Pin1 activity led to KSRP phosphorylation and degradation, diminishing its role in enhancing Pth mRNA degradation.
  • This resulted in increased stability of Pth mRNA and elevated PTH synthesis, partly due to increased activity of AUF1.

Conclusions:

  • Reduced Pin1 activity is a key factor in the molecular pathogenesis of secondary hyperparathyroidism in CKD.
  • The Pin1-KSRP-AUF1 pathway represents a novel regulatory mechanism for PTH synthesis.
  • Targeting Pin1 activity may offer new therapeutic strategies for managing secondary hyperparathyroidism.