|
|
|
|
|
|
|
|
|||||
| Home Help Feedback Subscriptions Archive Search Table of Contents | |||||
Journal of Cell Science, Vol 57, Issue 1 331-350, Copyright © 1982 by Company of Biologists
JOURNAL ARTICLES |
P Thorogood, L Smith, A Nicol, R McGinty and D Garrod
It has been proposed elsewhere that the teratogenic effects of retinoids on craniofacial morphogenesis are caused by a disturbance of the migration of cranial neural crest cells. The effects of 3.5 X 10(-5) M and 3.5 X 10(-6) M-retinol on the migration of avian neural crest cells in vitro have been investigated by monitoring cell morphology, locomotory behaviour, fibronectin distribution and actin-microfilament organization. Retinol retards migration by affecting cell-to-substratum adhesiveness. Cells exposed to medium containing retinol are less adherent to the substratum, and although the cell surface is very mobile, are unable to extend or maintain lamellipodia. As a consequence the cells do not actively translocate. Fibronectin distribution at the cell surface is sparse, possibly as a result of shedding, and actin distribution remains diffuse. At the retinol molarities used all these effects are reversible. Thus cells allowed to recover in normal medium flatten out, display lamellipodia and commence active translocation. Fibronectin becomes organized into a fibrillar array and actin microfilaments become organized into cables. The period needed for this recovery is directly related to the molarity of retinol during the initial exposure; after recovery the retinol-treated cells are virtually indistinguishable from control cells. We propose that in vivo the effects of retinoids might be to impair cell-extracellular matrix interaction, thus impeding a cell's ability to migrate through that matrix. Contrary to previous suggestions, the in vivo effects are probably not in any way 'specific' to neural crest cells but are more accurately considered as 'selective', in that any cell undergoing migration would be similarly affected.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati 
Twitter What's this?
This article has been cited by other articles:
|
|
 |
|
  S. S. Williams, J. P. Mear, H.-C. Liang, S. S. Potter, B. J. Aronow, and M. C. Colbert Large-scale reprogramming of cranial neural crest gene expression by retinoic acid exposure Physiol Genomics, October 4, 2004; 19(2): 184 - 197. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E Gale, V Prince, A Lumsden, J Clarke, N Holder, and M Maden Late effects of retinoic acid on neural crest and aspects of rhombomere Development, January 3, 1996; 122(3): 783 - 793. [Abstract] [PDF]
|
|
|
|
 |
|
 M.C. Johnston and P.T. Bronsky Prenatal Craniofacial Development: New Insights On Normal and Abnormal Mechanisms Critical Reviews in Oral Biology & Medicine, January 1, 1995; 6(1): 25 - 79. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M.C. Johnston and P.T. Bronsky Prenatal Craniofacial Development: New Insights on Normal and Abnormal Mechanisms Critical Reviews in Oral Biology & Medicine, January 1, 1995; 6(4): 368 - 422. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. J. Schuh, B. L. Hall, J. C. Kraft, M. L. Privalsky, and D. Kimelman v-erbA and citral reduce the teratogenic effects of all-trans retinoic acid and retinol, respectively, in Xenopus embryogenesis Development, November 1, 1993; 119(3): 785 - 798. [Abstract] [PDF]
|
|
|
|
|
|
E Ruberte, V Friederich, P Chambon, and G Morriss-Kay Retinoic acid receptors and cellular retinoid binding proteins. III. Their differential transcript distribution during mouse nervous system development Development, January 5, 1993; 118(1): 267 - 282. [Abstract] [PDF]
|
|
|
|
 |
|
 Teratology Society Position Paper: Recommendations for Vitamin A Use During Pregnancy International Journal of Toxicology, July 1, 1987; 6(4): 525 - 533. [PDF]
|
|
