PMID- 19394429
OWN - NLM
STAT- MEDLINE
DCOM- 20090907
LR  - 20131121
IS  - 1095-9327 (Electronic)
IS  - 1044-7431 (Linking)
VI  - 41
IP  - 4
DP  - 2009 Aug
TI  - Tenascin-C stimulates contactin-dependent neurite outgrowth via activation of 
      phospholipase C.
PG  - 397-408
LID - 10.1016/j.mcn.2009.04.004 [doi]
AB  - Tenascin-C (Tnc) is transiently expressed during neural development. Within its 
      alternatively spliced fibronectin type III (TNfn) -motifs the TNfnD domain is 
      crucial for a neurite outgrowth-promoting region that is recognized by the 
      GPI-linked adhesion molecule of the Ig-superfamily contactin. In order to 
      understand the downstream signaling mechanisms, embryonic day E18 rat hippocampal 
      neurons were cultivated on TNfnBD-containing and control substrates in the 
      presence of various inhibitors. As predicted, axon outgrowth promotion could be 
      suppressed by antibodies to the TNfnD domain, to contactin, or to the 
      beta1-integrin subunit. The chelators BAPTA/AM or EGTA as well as blockade of 
      membrane-based calcium channels or of the release of calcium from intracellular 
      stores reduced axon growth to control levels. The inhibition of phospholipase C 
      and its downstream targets protein kinase C or calmodulin kinase likewise blocked 
      outgrowth promotion. We propose that TNfnBD stimulates the outgrowth of 
      hippocampal neurons by activating calcium- and phospholipase C-depending 
      pathways. Digital video microscopy studies revealed that increase of fiber length 
      was caused by an augmentation of growth cone velocity.
FAU - Michele, Melanie
AU  - Michele M
AD  - Department of Cell Morphology and Molecular Neurobiology, Ruhr-University Bochum, 
      Building ND 05/593, Universitatsstrabetae 150, D-44801 Bochum, Germany.
FAU - Faissner, Andreas
AU  - Faissner A
LA  - eng
PT  - Journal Article
DEP - 20090424
PL  - United States
TA  - Mol Cell Neurosci
JT  - Molecular and cellular neurosciences
JID - 9100095
RN  - 0 (Antibodies)
RN  - 0 (Antigens, CD19)
RN  - 0 (Calmodulin)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Receptors, Antigen)
RN  - 0 (Tenascin)
RN  - 0 (Tn receptor)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - EC 3.1.4.- (Type C Phospholipases)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Antibodies/pharmacology
MH  - Antigens, CD19/metabolism
MH  - Calcium/metabolism
MH  - Calmodulin/metabolism
MH  - Cells, Cultured
MH  - Dose-Response Relationship, Drug
MH  - Embryo, Mammalian
MH  - Endoplasmic Reticulum/drug effects/metabolism
MH  - Enzyme Activation/drug effects
MH  - Enzyme Inhibitors/pharmacology
MH  - Female
MH  - Hippocampus/cytology
MH  - Mice
MH  - Neural Inhibition/drug effects
MH  - Neurites/*drug effects/enzymology/*physiology/ultrastructure
MH  - Neurons/*cytology
MH  - Pregnancy
MH  - Protein Kinase C/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Antigen/immunology
MH  - Tenascin/metabolism/*pharmacology
MH  - Time Factors
MH  - Type C Phospholipases/*metabolism
EDAT- 2009/04/28 09:00
MHDA- 2009/09/08 06:00
CRDT- 2009/04/28 09:00
PHST- 2009/02/05 00:00 [received]
PHST- 2009/04/03 00:00 [revised]
PHST- 2009/04/17 00:00 [accepted]
PHST- 2009/04/28 09:00 [entrez]
PHST- 2009/04/28 09:00 [pubmed]
PHST- 2009/09/08 06:00 [medline]
AID - S1044-7431(09)00082-7 [pii]
AID - 10.1016/j.mcn.2009.04.004 [doi]
PST - ppublish
SO  - Mol Cell Neurosci. 2009 Aug;41(4):397-408. doi: 10.1016/j.mcn.2009.04.004. Epub 
      2009 Apr 24.