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Extracellular matrix molecules and cell adhesion molecules induce neurites through different mechanisms
1Department of Pharmacology, University of Miami School of Medicine, Florida 33136.
The Journal of Cell Biology
|December 1, 1990
Summary
Protein kinase C is crucial for sustained neurite outgrowth on extracellular matrix (ECM) glycoproteins and cell adhesion molecules (CAMs). However, its role differs in initial growth responses to ECM versus CAM substrates.
Area of Science:
- Neuroscience
- Cell Biology
- Molecular Biology
Background:
- Extracellular matrix (ECM) glycoproteins and cell adhesion molecules (CAMs) promote neurite outgrowth in primary neurons.
- Intracellular signaling mechanisms for these processes are not fully understood.
- Protein kinase C (PKC) has been implicated in neuronal responses to laminin.
Purpose of the Study:
- To investigate whether the neurite outgrowth response to CAMs is dependent on protein kinase C.
- To compare the intracellular mechanisms of neurite outgrowth on ECM versus CAM substrates.
Main Methods:
- Tested the effect of protein kinase C inhibition on neurite outgrowth using various substrates (laminin, fibronectin, collagen, L1, N-cadherin).
- Utilized phorbol esters to modulate protein kinase C activity.
- Examined both initial and later phases of outgrowth.
Main Results:
- Protein kinase C inhibition impaired outgrowth on ECM substrates (fibronectin, collagen) and laminin.
- PKC inhibition potentiated initial outgrowth on L1 and N-cadherin but inhibited later outgrowth.
- Phorbol esters potentiated outgrowth on L1 and N-cadherin, unlike on laminin.
Conclusions:
- Different intracellular mechanisms mediate initial neurite outgrowth on ECM and CAM substrates.
- Protein kinase C is essential for sustained neurite growth on both ECM glycoproteins and CAMs.