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When MT1-MMP meets ADAMs.

Hoi Leong Xavier Wong¹, Renhai Cao, Guoxiang Jin

¹Shenzhen Institute of Research and Innovation, The University of Hong Kong, Shenzhen, China.

Cell Cycle (Georgetown, Tex.)

|July 18, 2012

Summary

Matrix metalloproteinase-14 (MT1-MMP) regulates FGF signaling by cleaving ADAM9, crucial for bone development. This interaction is tissue-specific, impacting craniofacial bone formation and offering therapeutic insights.

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Area of Science:

Biochemistry
Developmental Biology
Molecular Biology

Background:

Matrix metalloproteinase-14 (MT1-MMP) is essential for extracellular matrix remodeling and development.
MT1-MMP deficiency causes craniofacial developmental defects, including impaired calvarial bone formation.
Fibroblast Growth Factor (FGF) signaling is critical for various developmental processes.

Purpose of the Study:

To elucidate the role of MT1-MMP in modulating FGF signaling during intramembranous ossification.
To investigate the interaction between MT1-MMP, ADAM9, and FGF receptor 2 (FGFR2) in bone development.
To explore the tissue-specific functions of this regulatory mechanism.

Main Methods:

Analysis of MT1-MMP-deficient mouse models.
Genetic manipulation to deplete ADAM9 in MT1-MMP deficient mice.
Assessment of FGF signaling pathway activation and FGFR2 stability.
Evaluation of calvarial bone formation and corneal angiogenesis.

Main Results:

MT1-MMP protects FGFR2 from ectodomain shedding by cleaving ADAM9, thereby positively modulating FGF signaling.
Depletion of ADAM9 rescued calvarial defects in MT1-MMP-deficient mice by restoring FGF signaling.
The MT1-MMP-ADAM9-FGFR2 regulatory axis is tissue-specific, as demonstrated by the lack of rescue in corneal angiogenesis models.
MT1-MMP also cleaves ADAM15, suggesting broader crosstalk within the ADAM family.

Conclusions:

A novel mechanism for FGF signaling regulation involving MT1-MMP-mediated cleavage of ADAM9 has been identified.
This interplay is crucial for craniofacial development and intramembranous ossification.
Understanding the functional crosstalk between MT1-MMP and ADAM proteases offers potential therapeutic strategies for developmental disorders and diseases like cancer.