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Related Experiment Video

Updated: Jun 12, 2026

Long-term Silencing of Intersectin-1s in Mouse Lungs by Repeated Delivery of a Specific siRNA via Cationic Liposomes. Evaluation of Knockdown Effects by Electron Microscopy
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Published on: June 21, 2013

It's a knockout: CCN3 suppresses neointimal thickening.

Andrew Leask1

  • 1CIHR Group in Skeletal Development and Remodeling, Division of Oral Biology, Department of Dentistry, Schulich School of Medicine and Dentistry, Dental Sciences Building, University of Western Ontario, London, ON Canada N6A 5C1.

Journal of Cell Communication and Signaling
|June 10, 2010
PubMed
Summary

CCN3 protein normally suppresses cell growth. Mice lacking CCN3 showed excessive cell growth after vascular injury, suggesting CCN3 as a potential therapy for hyperproliferative diseases.

Keywords:
CCN3HyperplasiaInjuryNovVasculature

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Last Updated: Jun 12, 2026

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Area of Science:

  • Cellular and Molecular Biology
  • Vascular Biology
  • Protein Function

Background:

  • The CCN protein family plays diverse roles in cellular processes.
  • CCN3, a key member, is known to inhibit cell proliferation.
  • Understanding CCN protein functions in vivo is an emerging area of research.

Purpose of the Study:

  • To investigate the in vivo role of CCN3 in regulating cell proliferation.
  • To examine the effect of CCN3 deficiency on vascular injury response.
  • To explore CCN3 as a potential therapeutic target for hyperproliferative conditions.

Main Methods:

  • Utilizing a mouse model lacking the CCN3 gene.
  • Inducing vascular injury to assess proliferative responses.
  • Analyzing cellular proliferation in response to injury in CCN3-deficient and wild-type mice.

Main Results:

  • Mice deficient in CCN3 exhibited a hyperproliferative response to vascular injury.
  • Absence of CCN3 led to uncontrolled cell growth in the vasculature.
  • These findings highlight CCN3's critical role in preventing excessive cell division.

Conclusions:

  • CCN3 acts as a crucial suppressor of proliferation in vivo.
  • Loss of CCN3 function results in pathological hyperproliferation, particularly after vascular injury.
  • CCN3 represents a promising novel therapeutic candidate for treating hyperproliferative diseases.