Engineered Alignment in Media Equivalents: Magnetic Prealignment and Mandrel Compaction

1998 ◽  
Vol 120 (5) ◽  
pp. 660-666 ◽  
Author(s):  
V. H. Barocas ◽  
T. S. Girton ◽  
R. T. Tranquillo

We predicted and measured the evolution of smooth muscle cell (SMC) orientation in media-equivalents (MEs) for four fabrication conditions (F−, M−, F+, M+) under Free or Mandrel compaction (F/M) with and without magnetic prealignment of the collagen fibrils in the circumferential direction (±). Mandrel compaction refers to SMC-induced compaction of the ME that is constrained by having a nonadhesive mandrel placed in the ME lumen. Predictions were made using our anisotropic biphasic theory (ABT) for tissue-equivalent mechanics. Successful prediction of trends of the SMC orientation data for all four fabrication cases was obtained: maintenance of the initial isotropic state for F−, loss of initial circumferential alignment for F+, development of circumferential alignment for M−, and enhancement of initial circumferential alignment for M+. These results suggest two mechanisms by which the presence of the mandrel leads to much greater mechanical stiffness in the circumferential direction reported for mandrel compacted MEs relative to free compacted MEs: (1) by inducing an increasing circumferential alignment of the SMC and collagen, and (2) by inducing a large stress on the SMC, resulting in secretion and accumulation of stiffening components.

Biomaterials ◽  
2009 ◽  
Vol 30 (29) ◽  
pp. 5486-5496 ◽  
Author(s):  
Tighe A. Spurlin ◽  
Kiran Bhadriraju ◽  
Koo-Hyun Chung ◽  
Alessandro Tona ◽  
Anne L. Plant

2007 ◽  
Vol 92 (5) ◽  
pp. 1759-1769 ◽  
Author(s):  
Dennis P. McDaniel ◽  
Gordon A. Shaw ◽  
John T. Elliott ◽  
Kiran Bhadriraju ◽  
Curt Meuse ◽  
...  

2004 ◽  
Vol 171 (4S) ◽  
pp. 376-377
Author(s):  
Yongmu Zheng ◽  
Shaohua Chang ◽  
Alan J. Wein ◽  
Samuel Chacko ◽  
Michael E. DiSanto

1990 ◽  
Vol 63 (02) ◽  
pp. 291-297 ◽  
Author(s):  
Herm-Jan M Brinkman ◽  
Marijke F van Buul-Worteiboer ◽  
Jan A van Mourik

SummaryWe observed that the growth of human umbilical arterysmooth muscle cells was inhibited by the phospholipase A2 inhibitors p-bromophenacylbromide and mepacrine. Thesefindings suggest that fatty acid metabolism might be integrated in the control mechanism of vascular smooth muscle cell proliferation. To identify eicosanoids possibly involved in this process, we studied both the metabolism of arachidonic acid of these cells in more detail and the effect of certain arachidonic acid metabolites on smooth muscle cells growth. We found no evidence for the conversion of arachidonic acid via the lipoxygenase pathway. In contrast, arachidonic acid was rapidly converted via the cyclooxy-genase pathway. The following metabolites were identified: prostaglandin E2 (PGE2), 6-keto-prostaglandin F1α (6-k-PGF1α), prostaglandin F2α (PGF2α), 12-hydroxyheptadecatrienoic acid (12-HHT) and 11-hydroxyeicosatetetraenoic acid (11-HETE). PGE2 was the major metabolite detected. Arachidonic acid metabolites were only found in the culture medium, not in the cell. After synthesis, 11-HETE was cleared from the culture medium. We have previously reported that PGE2 inhibits the serum-induced [3H]-thymidine incorporation of growth-arrested human umbilical artery smooth muscle cells. Here we show that also 11-HETEexerts this inhibitory property. Thus, our data suggeststhat human umbilical artery smooth muscle cells convert arachidonic acid only via the cyclooxygenase pathway. Certain metabolites produced by this pathway, including PGE2 and 11-HETE, may inhibit vascular smooth muscle cell proliferation.


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