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Non-Canonical Wnt Signaling Pathways01:41

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Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
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Isolation of Mouse Interstitial Valve Cells to Study the Calcification of the Aortic Valve In Vitro
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Non-Canonical TERT Activity Initiates Osteogenesis in Calcific Aortic Valve Disease.

Rolando A Cuevas1, Luis Hortells2, Claire C Chu1

  • 1Division of Cardiology, Department of Medicine, Pittsburgh Heart, Lung, Blood and Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, PA (R.A.C., C.C.C., R.W., A.C., C.K.B., C.R., W.J.M., M.J. Bashline, A.P., A.M.P., P.B., M.J.B., C.S.H.).

Circulation Research
|January 21, 2025
PubMed
Summary

Telomere-associated enzyme telomerase reverse transcriptase (TERT) drives calcific aortic valve disease by initiating osteogenic reprogramming through non-canonical activity. Inhibiting TERT and its partner STAT5 offers a potential therapeutic strategy for vascular calcification.

Keywords:
aortic valveinflammationosteogenesisvascular calcification

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Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • Cellular Reprogramming

Background:

  • Calcific aortic valve disease involves pathological remodeling of heart valve leaflets.
  • The early stages of valve leaflet osteogenic reprogramming are not fully understood.
  • Telomerase reverse transcriptase (TERT) overexpression primes stem cells for osteogenic differentiation.

Purpose of the Study:

  • Investigate the role of TERT in the osteogenic reprogramming of valve interstitial cells.
  • Determine if TERT contributes to calcific aortic valve disease pathogenesis.
  • Identify novel therapeutic targets for vascular calcification.

Main Methods:

  • Utilized human aortic valve leaflets and patient-derived interstitial cells for in vitro and in vivo calcification assays.
  • Performed loss-of-function studies using TERT knockdown and genetic deletion in mice.
  • Employed in silico modeling, co-immunoprecipitation, and ChIP-seq to identify TERT interactions and DNA binding.

Main Results:

  • TERT protein was highly expressed in calcified valves, independent of telomere length or senescence.
  • TERT expression increased with osteogenic/inflammatory stimuli; TERT inhibition prevented calcification.
  • TERT initiated osteogenic reprogramming via non-canonical activity, interacting with STAT5 to bind the RUNX2 promoter.

Conclusions:

  • TERT's non-canonical activity is crucial for initiating calcific aortic valve disease.
  • TERT, upregulated by inflammation, partners with STAT5 to regulate RUNX2, a key gene in osteogenic reprogramming.
  • Targeting the TERT-STAT5-RUNX2 pathway presents a novel therapeutic strategy for vascular calcification.