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Somatostatin analog Lanreotide inhibits myocyte replication and several growth factors in allograft arteriosclerosis
Author(s) -
Häyry Pekka,
Räisänen Anne,
Ustinov Jarkko,
Mennander Ari,
Paavonen Timo
Publication year - 1993
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.7.11.8370476
Subject(s) - lanreotide , somatostatin , medicine , octreotide , replication (statistics) , myocyte , arteriosclerosis , chemistry , cardiology , endocrinology , growth hormone , acromegaly , hormone , virology
Chronic rejection is the most common reason for late loss of a transplant. The molecular mechanism of chronic rejection is not known and there is no treatment for this disorder. The characteristic histological feature in chronic rejection is increased smooth muscle cell replication in the vascular wall, leading to allograft arteriosclerosis. In this study we demonstrate that nonimmunosuppressed rat aortic allografts undergoing chronic rejection synthesize increased quantitites of several smooth muscle cell growth‐promoting substances in the vascular wall including interleukin‐1, eicosanoids, and several peptide growth factors. Administration of a stable somatostatin analog lanreotide, BIM 23014, strongly inhibits myocyte proliferation in the allograft in vivo. It has no inhibitory effect on the proliferation of smooth muscle cells in vitro. Concomitantly, the locally produced peptide growth factors, i.e., epidermal growth factor, insulin‐like growth factor 1, and BB‐isomer of platelet‐derived growth factor, but not other mediators of inflammation, are significantly reduced. The results suggest that growth factors are the main effector molecules leading to myocyte proliferation in allograft arteriosclerosis and that allograft arteriosclerosis (chronic rejection) may be specifically inhibited by lanreotide administration.—Häyry, P., Räisänen, A., Ustinov, J., Mennander, A., Paavonen, T. Somatostatin analog lanreotide inhibits myocyte replication and several growth factors in allograft arteriosclerosis. FASEB J. 7: 1055‐1060; 1993.