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TGF-beta1 calcium signaling in osteoblasts
Leon J Nesti1, E J Caterson, Wan-Ju Li
1Department of Orthopaedics and Rehabilitation, Walter Reed Army Medical Center, Washington, DC 20307, USA.
Journal of Cellular Biochemistry
|January 11, 2007
Summary
Transforming growth factor-beta1 (TGF-beta1) rapidly increases intracellular calcium in human osteoblasts, which is essential for enhanced cell adhesion. This calcium signaling pathway is independent of Smad proteins.
Area of Science:
- Cell Biology
- Biochemistry
- Molecular Biology
Background:
- Transforming growth factor-beta1 (TGF-beta1) signaling regulates various cellular processes.
- TGF-beta1 binding to cell surface receptors initiates intracellular signaling cascades.
- Previous studies showed TGF-beta1 enhances human osteoblast (HOB) adhesion.
Purpose of the Study:
- To investigate the role of intracellular calcium ([Ca(2+)](i)) in TGF-beta1-mediated HOB adhesion.
- To determine if TGF-beta1 signaling affects Smad protein phosphorylation in HOBs.
Main Methods:
- Measurement of intracellular calcium concentration ([Ca(2+)](i)) using calcium indicators.
- Treatment of HOBs with TGF-beta1, calcium channel modulators (nifedipine, Bay K 8644), and thapsigargin.
- Assessment of HOB adhesion to tissue culture polystyrene.
- Analysis of Smad protein phosphorylation.
Main Results:
- TGF-beta1 induced a rapid, transient, and oscillatory rise in [Ca(2+)](i) in HOBs.
- This calcium rise was dependent on extracellular calcium and L-type calcium channels.
- TGF-beta1-induced HOB adhesion was inhibited by nifedipine and required the calcium rise.
- Smad protein phosphorylation was not altered by TGF-beta1 treatment.
Conclusions:
- Intracellular calcium signaling is a critical component of TGF-beta1 signal transduction in osteoblasts.
- TGF-beta1 enhances HOB adhesion via a calcium-dependent pathway, distinct from Smad signaling.
- This highlights a novel role for calcium as a second messenger in TGF-beta1 action on osteoblasts.
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