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Updated: Dec 30, 2025

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model
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CFTR deletion affects mouse osteoblasts in a gender-specific manner.

Valérie Orlando1, Geneviève Morin1, Alisson Laffont1

  • 1Research Centre, CHU Sainte-Justine, Montreal, Montreal, Quebec, Canada.

Journal of Cellular Physiology
|January 28, 2020
PubMed
Summary

Cystic fibrosis (CF) bone disease shows gender differences. In CFTR-deficient mice, osteoblast dysfunction occurred in females, while males showed more severe bone loss, impacting bone strength similarly in both genders.

Keywords:
CFTRcystic fibrosisdifferentiationgenderosteoblast

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Area of Science:

  • Bone Biology
  • Genetics
  • Cystic Fibrosis Research

Background:

  • Increased life expectancy in cystic fibrosis (CF) patients leads to higher prevalence of CF bone disease.
  • CF bone disease is characterized by low bone mass and impaired quality, with notable gender-based differences in severity.
  • The underlying pathophysiological mechanisms for these gender disparities in CF bone disease remain largely unexplored.

Purpose of the Study:

  • To investigate the gender-specific impact of CF transmembrane conductance regulator (CFTR) deletion on osteoblast and osteoclast cellular differentiation and function.
  • To determine if in vitro findings regarding CFTR deletion effects translate to in vivo observations in a mouse model.

Main Methods:

  • Utilized bone marrow-derived osteoblasts and osteoclasts from Cftr+/+ (wild-type) and Cftr-/- (knockout) mice.
  • Employed in vitro cell culture techniques to assess cellular differentiation and function.
  • Applied in vivo imaging techniques and three-point bending tests to evaluate bone phenotype and strength in knockout mice.

Main Results:

  • In vitro studies showed no osteoclast defect, but impaired osteoblast differentiation and function in Cftr-/- females.
  • Aberrant responses to stimuli were observed in osteoblasts from Cftr-/- females.
  • Cftr-/- mice exhibited a trabecular osteopenic phenotype, more pronounced in males than females.
  • Bone strength was similarly reduced in both male and female Cftr-/- mice compared to controls.

Conclusions:

  • A trabecular bone phenotype exists in Cftr-/- mice, slightly more pronounced in males, mirroring patient observations.
  • Pathophysiological mechanisms driving this bone phenotype differ between genders at the osteoblast level.
  • These gender-specific osteoblast behaviors in the absence of CFTR may explain observed clinical differences in CF bone disease.