Regenerating endothelial cells express insulin-like growth factor-I immunoreactivity after arterial injury |
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Authors: | Dr. Hans-Arne Hansson Eva Jennische Anna Skottner |
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Affiliation: | (1) Department of Histology, University of Gothenburg, Gothenburg, Sweden;(2) KabiVitrum AB, Stockholm, Sweden;(3) Department of Histology, University of Göteborg, P.O.B. 33031, S-40033 Göteborg, Sweden |
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Abstract: | Summary In the present study the expression of insulin-like growth factor I (IGF-I; somatomedin C) immunoreactivity was examined in endothelial cells during repair after injury to the intima in the femoral artery of adult rats. Two types of injury were examined: (1) endothelial denudation induced by the use of a catheter, and (2) vessel compression by short-term ligation. In untreated rats, arterial endothelial cells showed no or, only infrequently, low IGF-I immunoreactivity in their cytoplasm. Endothelial cells at the border to the denuded area showed increased IGF-I immunoreactivity one day after injury to the intima of the femoral artery. Thrombocytes and fibrin deposits as well as vital endothelial cells, covered by clots, were immunonegative. The maximal intensity of IGF-I immunoreactivity was reached within 3 days after insult. The IGF-I immunoreactivity in the endothelial cells remained elevated for at least 4 weeks, compared to the controls. Intimai thickenings appeared within a week after injury and many cells in these thickenings showed intense IGF-I immunoreactivity as did the covering endothelial cells. Smooth muscle cells in the media were generally immunonegative during control conditions and after endothelial denudation. Spontaneously hypertensive rats (SHR) showed, similarly to their matched controls (WKY), approximately the same patterns of IGF-I immunoreactivity in their endothelial cells both under normal conditions and after injury. It is concluded that IGF-I is likely to be involved in the repair of the intima in injured arteries. |
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Keywords: | Insulin-like growth factor I Somatomedin C Arterial injury Endothelial regeneration Intimai thickening Macrophages Smooth muscle cells Rat |
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