PMID- 9651203
OWN - NLM
STAT- MEDLINE
DCOM- 19980727
LR  - 20220309
IS  - 0270-6474 (Print)
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Linking)
VI  - 18
IP  - 14
DP  - 1998 Jul 15
TI  - Neuronal matrix metalloproteinase-2 degrades and inactivates a neurite-inhibiting 
      chondroitin sulfate proteoglycan.
PG  - 5203-11
AB  - Chondroitin sulfate proteoglycans (CSPGs) are implicated in the regulation of 
      axonal growth. We previously reported that the neurite-promoting activity of 
      laminin is inhibited by association with a Schwann cell-derived CSPG and that 
      endoneurial laminin may be inhibited by this CSPG as well [Zuo J, Hernandez YJ, 
      Muir D (1998) Chondroitin sulfate proteoglycan with neurite-inhibiting activity 
      is upregulated after peripheral nerve injury. J Neurobiol 34:41-54]. Mechanisms 
      regulating axonal growth were studied by using an in vitro bioassay in which 
      regenerating embryonic dorsal root ganglionic neurons (DRGn) were grown on 
      sections of normal adult nerve. DRGn achieved slow neuritic growth on sections of 
      normal nerve, which was reduced significantly by treatment with metalloproteinase 
      inhibitors. Similar results were obtained on a synthetic substratum composed of 
      laminin and inhibitory CSPG. DRGn expressed the matrix metalloproteinase, MMP-2, 
      which was transported to the growth cone. Recombinant MMP-2 inactivated the 
      neurite-inhibiting CSPG without hindering the neurite-promoting potential of 
      laminin. Similarly, neuritic growth by DRGn cultured on normal nerve sections was 
      increased markedly by first treating the nerve sections with MMP-2. The 
      proteolytic deinhibition by MMP-2 was equivalent to and nonadditive with that 
      achieved by chondroitinase, suggesting that both enzymes inactivated inhibitory 
      CSPG. Additionally, the increases in neuritic growth resulting from treating 
      nerve sections with MMP-2 or chondroitinase were blocked by anti-laminin 
      antibodies. From these results we conclude that MMP-2 provides a mechanism for 
      the deinhibition of laminin in the endoneurial basal lamina and may play an 
      important role in the regeneration of peripheral nerve.
FAU - Zuo, J
AU  - Zuo J
AD  - Departments of Pediatrics (Neurology Division) and Neuroscience, University of 
      Florida Brain Institute and College of Medicine, Gainesville, Florida 32610-0296, 
      USA.
FAU - Ferguson, T A
AU  - Ferguson TA
FAU - Hernandez, Y J
AU  - Hernandez YJ
FAU - Stetler-Stevenson, W G
AU  - Stetler-Stevenson WG
FAU - Muir, D
AU  - Muir D
LA  - eng
GR  - NS31255/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Chondroitin Sulfate Proteoglycans)
RN  - 0 (Laminin)
RN  - 0 (Recombinant Proteins)
RN  - EC 3.4.24.- (Gelatinases)
RN  - EC 3.4.24.- (Metalloendopeptidases)
RN  - EC 3.4.24.24 (Matrix Metalloproteinase 2)
RN  - EC 4.2.2.- (Chondroitinases and Chondroitin Lyases)
SB  - IM
MH  - Animals
MH  - Biological Transport/drug effects
MH  - Cells, Cultured
MH  - Chick Embryo
MH  - Chondroitin Sulfate Proteoglycans/*physiology
MH  - Chondroitinases and Chondroitin Lyases/pharmacology
MH  - Cryopreservation
MH  - Ganglia, Spinal/cytology/*drug effects
MH  - Gelatinases/*pharmacology
MH  - Laminin/physiology
MH  - Matrix Metalloproteinase 2
MH  - Metalloendopeptidases/*pharmacology
MH  - Nerve Regeneration/*physiology
MH  - Neurites/*drug effects
MH  - Neurons/*drug effects/enzymology
MH  - Recombinant Proteins/pharmacology
PMC - PMC6793496
EDAT- 1998/07/03 00:00
MHDA- 1998/07/03 00:01
PMCR- 1999/01/15
CRDT- 1998/07/03 00:00
PHST- 1998/07/03 00:00 [pubmed]
PHST- 1998/07/03 00:01 [medline]
PHST- 1998/07/03 00:00 [entrez]
PHST- 1999/01/15 00:00 [pmc-release]
AID - 2149 [pii]
AID - 10.1523/JNEUROSCI.18-14-05203.1998 [doi]
PST - ppublish
SO  - J Neurosci. 1998 Jul 15;18(14):5203-11. doi: 10.1523/JNEUROSCI.18-14-05203.1998.