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Dermatan 4-O-sulfotransferase1 ablation accelerates peripheral nerve regeneration
Nuray Akyüz1, Sandra Rost, Ali Mehanna
1Center for Molecular Neurobiology Hamburg, University Hospital Hamburg-Eppendorf, Martinistrasse 52, D-20246 Hamburg, Germany.
Experimental Neurology
|January 31, 2013
Summary
Dermatan sulfate (DS) proteoglycans, unlike chondroitin sulfate (CS), were not previously assessed for their role in neural regeneration. Mice lacking a key DS synthesis enzyme showed improved initial nerve repair, suggesting DS may inhibit adult nerve regeneration.
Area of Science:
- Neuroscience
- Biochemistry
- Extracellular Matrix Biology
Background:
- Chondroitin sulfate (CS) and dermatan sulfate (DS) proteoglycans are extracellular matrix components vital for neural development and plasticity.
- CS is known to inhibit neural regeneration, but the role of DS remains uncharacterized.
Purpose of the Study:
- To investigate the specific roles of DS in neural development and regeneration by creating a mouse model lacking a key DS synthesis enzyme.
- To compare the effects of DS deficiency with CS in the context of neural repair.
Main Methods:
- Generated mice deficient in dermatan 4-O-sulfotransferase1 (Chst14), a key enzyme for DS synthesis.
- Assessed developmental phenotypes, in vitro neuronal and Schwann cell behavior, and functional recovery after peripheral nerve injury.
Main Results:
- Chst14 deficiency led to developmental defects but did not affect brain anatomy.
- Neurons and Schwann cells from deficient mice exhibited enhanced process outgrowth and proliferation in vitro.
- Initial nerve regeneration and functional recovery were accelerated in Chst14(-/-) mice, but long-term outcomes were similar to wild-type.
Conclusions:
- Chst14 and its DS products have limited impact on neural development.
- DS may contribute to the inhibitory environment for neural regeneration in the adult mammalian nervous system.
