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Lead induces chondrogenesis and alters transforming growth factor-beta and bone morphogenetic protein signaling in

Michael J Zuscik1, Lin Ma, Taylor Buckley

  • 1Center for Musculoskeletal Research, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA.

Environmental Health Perspectives
|September 7, 2007
PubMed

Insights

Lead exposure enhances chondrogenesis, the process of bone formation, in mesenchymal stem cells (MSCs). This occurs through complex interactions with multiple signaling pathways, impacting skeletal development.

Area of Science:

  • Toxicology
  • Skeletal Biology
  • Cell Signaling

Background:

  • Lead (Pb) exposure is known to stunt skeletal growth in children.
  • Chondrogenesis is a critical process in skeletal development.
  • Understanding Pb's impact on chondrogenesis is key to understanding its skeletal toxicity.

Purpose of the Study:

  • To investigate if lead (Pb) alters the chondrogenic commitment of mesenchymal cells.
  • To assess the effects of Pb on key cellular signaling pathways involved in chondrogenesis.

Main Methods:

  • Murine limb bud mesenchymal stem cells (MSCs) were used for in vitro nodule formation assays and gene analysis.
  • TGF-beta and BMP signaling pathways were studied using reporter assays and Western analysis.
  • In vivo effects were assessed via ectopic bone formation assays in Pb-exposed mice.

Main Results:

  • Pb exposure enhanced chondrogenesis in MSCs, indicated by increased nodule formation and expression of chondrogenic markers (Sox-9, collagen type 2, aggrecan).
  • Pb exposure led to enhanced chondrogenesis in vivo during ectopic bone formation.
  • Pb modulated specific signaling pathways: enhancing TGF-beta, inhibiting BMP-2, inducing NF-kappaB, and inhibiting AP-1 signaling.

Conclusions:

  • Lead (Pb) exposure induces chondrogenesis both in vitro and in vivo.
  • Pb's effect on chondrogenesis involves the modulation and integration of multiple signaling pathways, including TGF-beta, BMP, AP-1, and NF-kappaB.
Abstract

Keywords:
BMP signalingTGF-β signalingchondrogenesisleadmesenchymal stem cells

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