PMID- 19508743
OWN - NLM
STAT- MEDLINE
DCOM- 20100329
LR  - 20141120
IS  - 1741-0533 (Electronic)
IS  - 1740-925X (Linking)
VI  - 4
IP  - 4
DP  - 2008 Nov
TI  - The glia-derived extracellular matrix glycoprotein tenascin-C promotes embryonic 
      and postnatal retina axon outgrowth via the alternatively spliced fibronectin 
      type III domain TNfnD.
PG  - 271-83
LID - 10.1017/S1740925X09990020 [doi]
AB  - Tenascin-C (Tnc) is an astrocytic multifunctional extracellular matrix (ECM) 
      glycoprotein that potentially promotes or inhibits neurite outgrowth. To 
      investigate its possible functions for retinal development, explants from 
      embryonic day 18 (E18) rat retinas were cultivated on culture substrates composed 
      of poly-d-lysine (PDL), or PDL additionally coated with Tnc or laminin (LN)-1, 
      which significantly increased fiber length. When combined with LN, Tnc induced 
      axon fasciculation that reduced the apparent number of outgrowing fibers. In 
      order to circumscribe the stimulatory region, Tnc-derived fibronectin type III 
      (TNfn) domains fused to the human Ig-Fc-fragment TNfnD6-Fc, TNfnBD-Fc, 
      TNFnA1A2-Fc and TNfnA1D-Fc were studied. The fusion proteins TNfnBD-Fc and to a 
      lesser degree TNfnA1D-Fc were stimulatory when compared with the Ig-Fc-fragment 
      protein without insert. In contrast, the combination TNfnA1A2-Fc reduced fiber 
      outgrowth beneath the values obtained for the Ig-Fc domain, indicating potential 
      inhibitory properties. The monoclonal J1/tn2 antibody (clone 578) that is 
      specific for domain TNfnD blocked the stimulatory properties of the TNfn-Fc 
      fusions. When postnatal day 7 retinal ganglion cells were used rather that 
      explants, Tnc and Tnc-derived proteins proved permissive for neurite outgrowth. 
      The present study highlights a strong retinal axon growth-promoting activity of 
      the Tnc domain TNfnD, which is modulated by neighboring domains.
FAU - Siddiqui, Sonia
AU  - Siddiqui S
AD  - Department of Cell Morphology and Molecular Neurobiology, Ruhr-University, 
      Bochum, Germany.
FAU - Horvat-Brocker, Andrea
AU  - Horvat-Brocker A
FAU - Faissner, Andreas
AU  - Faissner A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090610
PL  - England
TA  - Neuron Glia Biol
JT  - Neuron glia biology
JID - 101217278
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Fibronectins)
RN  - 0 (Immunoglobulin Fc Fragments)
RN  - 0 (Laminin)
RN  - 0 (Recombinant Fusion Proteins)
RN  - 0 (Tenascin)
RN  - 0 (laminin 1)
SB  - IM
MH  - Age Factors
MH  - Alternative Splicing/*physiology
MH  - Animals
MH  - Animals, Newborn
MH  - Antibodies, Monoclonal/pharmacology
MH  - Axons/*drug effects
MH  - Cells, Cultured
MH  - Dose-Response Relationship, Drug
MH  - Embryo, Mammalian
MH  - Female
MH  - Fibronectins/*genetics/immunology/metabolism
MH  - Gene Expression Regulation, Developmental/drug effects/genetics
MH  - Humans
MH  - Immunoglobulin Fc Fragments/genetics/metabolism
MH  - In Vitro Techniques
MH  - Laminin/metabolism
MH  - Neural Inhibition/drug effects/genetics
MH  - Pregnancy
MH  - Protein Structure, Tertiary/physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Recombinant Fusion Proteins/genetics/metabolism
MH  - *Retina/cytology/embryology/growth & development
MH  - Retinal Ganglion Cells/*cytology
MH  - Tenascin/chemistry/genetics/*pharmacology
EDAT- 2009/06/11 09:00
MHDA- 2010/03/30 06:00
CRDT- 2009/06/11 09:00
PHST- 2009/06/11 09:00 [entrez]
PHST- 2009/06/11 09:00 [pubmed]
PHST- 2010/03/30 06:00 [medline]
AID - S1740925X09990020 [pii]
AID - 10.1017/S1740925X09990020 [doi]
PST - ppublish
SO  - Neuron Glia Biol. 2008 Nov;4(4):271-83. doi: 10.1017/S1740925X09990020. Epub 2009 
      Jun 10.