Increase in collagen turnover but not in collagen fiber content is associated with flow-induced arterial remodeling.
BACKGROUND
Degradation and synthesis of collagen are common features in arterial geometrical remodeling. Previous studies described an association between arterial remodeling and an increase in collagen fiber content after balloon injury. However, this does not exclude that the association between collagen content and remodeling depends on arterial injury since the association of collagen fiber content and arterial remodeling, without arterial injury, has not been investigated. The aim of the present study was to study the relation between flow-induced arterial geometrical remodeling, without arterial injury, and collagen synthesis and degradation, collagen fiber content and cell-migration-associated moesin levels.


RESULTS
In 23 New Zealand White rabbits an arteriovenous shunt (AV shunt) was created in the carotid and femoral artery to induce a structural diameter increase or a partial ligation (n = 27 rabbits) to induce a diameter decrease. In both models, arterial remodeling was accompanied by increased procollagen synthesis, reflected by increased procollagen mRNA or Hsp47 protein levels. In both models, however, no changes were detected in collagen fiber content. Active MMP-2 and moesin levels were increased after AV shunting.


CONCLUSIONS
Collagen synthesis and MMP-2 activation were associated with arterial remodeling. However, a change in collagen fiber content was not observed. These results suggest that, during flow-induced geometrical arterial remodeling, increases in collagen synthesis are used for matrix collagen turnover and cell migration but not to augment collagen fiber content.
Sluijter
Joost P G
JP
University Medical Center, Experimental Cardiology Laboratory, Department of Cardiology, NL-3584 CX Utrecht, The Netherlands.
Smeets
Mirjam B
MB
Velema
Evelyn
E
Pasterkamp
Gerard
G
de Kleijn
Dominique P V
DP
D000818:Animals; D001166:Arteriovenous Shunt, Surgical; D001391:Azo Compounds; D002339:Carotid Arteries / Q000502:physiology* / Q000601:surgery; D002465:Cell Movement / Q000502:physiology; D024042:Collagen Type I / Q000235:genetics* / Q000378:metabolism*; D004396:Coloring Agents; D005263:Femoral Artery / Q000502:physiology* / Q000601:surgery; D015870:Gene Expression; D006360:Heat-Shock Proteins / Q000378:metabolism; D008026:Ligation; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism; D008840:Microfilament Proteins / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis; D011817:Rabbits; D012039:Regional Blood Flow / Q000502:physiology*
D001391:Azo Compounds; D024042:Collagen Type I; D004396:Coloring Agents; D006360:Heat-Shock Proteins; D008840:Microfilament Proteins; D012333:RNA, Messenger; C009798:C.I. direct red 80; C071058:moesin; D020778:Matrix Metalloproteinase 2