|
|
![]() |
|
|||
| Home Help Feedback Subscriptions Archive Search Table of Contents | |||||
Journal of Cell Science, Vol 107, Issue 4 1007-1018, Copyright © 1994 by Company of Biologists
JOURNAL ARTICLES |
RI Clyman, J Tannenbaum, YQ Chen, D Cooper, PD Yurchenco, RH Kramer and NS Waleh
Cardiovascular Research Institute, Department of Pediatrics, San Francisco, CA 94143-0544.
During permanent closure of the ductus arteriosus, smooth muscle cells migrate through the extracellular matrix (ECM) to form intimal mounds that occlude the vessel's lumen. Smooth muscle cells (SMC) migrate over surfaces coated with collagen in vitro. During the migration SMC also synthesize fibronectin (FN) and laminin (LN). Antibodies against FN and LN inhibit migration on collagen by 30% and 67%, respectively. Because of the apparent importance of LN in migration, we examined how SMC interact with LN and LN fragments (P1, E8, P1', E1', E3, E4, and G). Ductus SMC adhere to high concentrations of LN and two fragments of the molecule: P1 and E8. They use a unique set of integrin receptors to bind to LN (alpha 1 beta 1, alpha 6 beta 1 and alpha v beta 3), to P1 (alpha 1 beta 1, alpha v beta 3), and to E8 (alpha 6 beta 1, alpha v beta 3). The alpha v beta 3 integrin binds to the P1 fragment of LN in an RGD peptide-dependent manner, and to the E8 fragment in an RGD-independent manner; the RGD site on the P1 fragment probably is not available to the cell in intact LN. Antibodies against beta 1 integrins completely inhibit SMC adhesion to LN; antibodies against the alpha v beta 3 integrin do not block SMC adhesion to LN, but do prevent cell spreading. LN is also capable of interfering with SMC adhesion to other ECM components. The antiadhesive effect of LN is located in the E1' domain. Both exogenous and endogenous LN increase SMC motility on collagen I. The locomotion-promoting activity of LN resides in the E1' antiadhesive domain, and not in its adhesive (P1, E8) domains. LN causes a decrease in the number of focal contacts on collagen I. This might enable SMC to alter their mobility as they move through the extracellular matrix to occlude the ductus arteriosus lumen.
This article has been cited by other articles:
![]() |
K.-J. Lee, A. Hinek, R. R. Chaturvedi, C. L. Almeida, O. Honjo, G. Koren, and L. N. Benson Rapamycin-Eluting Stents in the Arterial Duct: Experimental Observations in the Pig Model Circulation, April 21, 2009; 119(15): 2078 - 2085. [Abstract] [Full Text] [PDF] |
||||
![]() |
U. Yokoyama, Y. Sato, T. Akaike, S. Ishida, J. Sawada, T. Nagao, H. Quan, M. Jin, M. Iwamoto, S. Yokota, et al. Maternal vitamin A alters gene profiles and structural maturation of the rat ductus arteriosus Physiol Genomics, September 11, 2007; 31(1): 139 - 157. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Costa, S. Barogi, N. D. Socci, D. Angeloni, M. Maffei, B. Baragatti, C. Chiellini, E. Grasso, and F. Coceani Gene expression in ductus arteriosus and aorta: comparison of birth and oxygen effects Physiol Genomics, April 13, 2006; 25(2): 250 - 262. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. P. Moiseeva Adhesion receptors of vascular smooth muscle cells and their functions Cardiovasc Res, December 1, 2001; 52(3): 372 - 386. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Seki, N. Koyama, N. L. Kovach, T. Yednock, A. W. Clowes, and J. M. Harlan Regulation of ß1-Integrin Function in Cultured Human Vascular Smooth Muscle Cells Circ. Res., April 1, 1996; 78(4): 596 - 605. [Abstract] [Full Text] |
||||
![]() |
H. Colognato-Pyke, J. J. O'Rear, Y. Yamada, S. Carbonetto, Y.-S. Cheng, and P. D. Yurchenco Mapping of Network-forming, Heparin-binding, and [IMAGE]1[IMAGE]1 Integrin-recognition Sites within the [IMAGE]-Chain Short Arm of Laminin-1 J. Biol. Chem., April 21, 1995; 270(16): 9398 - 9406. [Abstract] [Full Text] [PDF] |
||||