Insulin-Like Growth Factor-I (IGF-I)/IGF-I Receptor Axis and Increased Invasion Activity of Fibroblasts in Keloid.

Accession number;00A0416110
Title;Insulin-Like Growth Factor-I (IGF-I)/IGF-I Receptor Axis and Increased Invasion Activity of Fibroblasts in Keloid.
Author; OHTSURU A (Nagasaki Univ. School Of Medicine, Jpn) YOSHIMOTO H (Nagasaki Univ. School Of Medicine, Jpn) ISHIHARA H (Nagasaki Univ. School Of Medicine, Jpn) NAMBA H (Nagasaki Univ. School Of Medicine, Jpn) YAMASHITA S (Nagasaki Univ. School Of Medicine, Jpn)
Journal Title;Endocr J
Journal Code:F0625A
ISSN:0918-8959
VOL.47;NO.Supplement;PAGE.S41-S44(2000)
Figure&Table&Reference;TBL.2, REF.3
Pub. Country;Japan
Language;English
Abstract;Activation of signals for insulin-like growth factor-I receptor (IGF-IR) is thought to be closely linked to abnormal cell proliferation and differentiation in various diseases. The keloid in which fibroblasts invade beyond the margins of the original wound, is a dermal fibroproliferative tissue of unknown etiology. Clinically, keloids are most commonly observed in subjects at ages between 10 and 30 years. Interestingly, plasma levels of growth hormone and IGF-I are also high during the same period, suggesting that IGF-I might be involved in the patho-physiology of keloid fibroblasts. We therefore first examined the expression level of IGF-IR in normal and keloid tissues. Immunohistochemical analysis confirmed increased expression of IGF-IR in keloid fibroblasts, but not in normal fibroblasts. On the other hand, the staining intensity of IGF-IR in the epidermis of normal tissues was almost equal to that in keloids. Next, to study the functional properties of the IGF-I/IGF-IR axis in both normal and keloid fibroblasts, we investigated invasion activities. The invasive activity of IGF-IR overexpressing keloid fibroblasts was greatly increased in the presence of IGF-I, and inhibited by a neutralizing antibody to IGF-I. In contrast, its activity of IGF-IR weak-expressing normal fibroblasts was not changed. Our results indicate the involvement of the activated IGF-I/IGF-IR axis in the pathogenesis of the invasive activity of fibroblasts. (author abst.)
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