Ciba Foundation Symposium 189 - Cell Adhesion and Human

Specialists of their respective fields current papers all for the variety of human ailments as a result of faulty or irregular functioning of mobile adhesion molecules. Discusses new healing techniques to those maladies.


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Alternatively, VCAM-1 may be important for the growth of the ventricular myocardium. In this regard, it should be noted that although VCAM- 1 is expressed throughout the myocardium, the highest levels were observed specifically in the ventricular septum and in the compact zone of the myocardium (data not shown). A third explanation is that the lack of an epicardium results in the more subtle changes occurring in the ventricle. This seems most likely for several reasons. 5d - / - embryos examined, and although the ventricular myocardium and septum were reduced in size, they were not absent and the 26 Kwee et al extent of this size reduction was variable.

The targeting vector introduced two mutations in the VCAM-1 gene. First the neor gene was inserted within the exon encoding domain I, resulting in a large insertion/frameshift mutation. Second, a deletion was introduced spanning sequences from exons encoding domain I to domain IV. Chimeric animals were produced with two ES cell clones containing the targeted mutation and were bred to see if the VCAM-I-deficient animals were viable. As shown in Table 1, after extensive breeding only one live animal homozygous for the VCAM-I mutation was detected after screening of more than 700 offspring from inter-crosses between heterozygous animals.

The regulation of these processes depends on changes in the affinity of von Willebrand factor for GPIb, since soluble von Willebrand factor does not bind to the receptor unless an appropriate ‘modulator’ of the interaction is present. Two non-physiological modulators such as this have been used extensively-the antibiotic ristocetin (Howard & Firkin 1971, Scott et a1 1991) and the snake protein botrocetin (Read et a1 1978, Sugimoto et a1 1991). At present there is no evidence that the mechanisms through which ristocetin and botrocetin induce binding of von Willebrand factor to GPIb are related to the pathophysiological regulation of this event in vivo; however, it is generally postulated that the two modulators, particularly botrocetin, may induce a conformational change in von Willebrand factor leading to the exposure of a n otherwise hidden GPIb binding site.

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