ASSA14-03-19 The change of cellular repressor of E1A-stimulated genes during vascular remodelling in a mouse model of arterial injury

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Abstract

Background

Cellular repressor of E1A-stimulated genes (CREG) has been shown to be ubiquitously expressed in human and mouse tissues. However, its physiological functions and possible involvement in pathological processes remain unknown.

Method

To explore pathophysiology pathogenesis of vascular remodelling and possible role of CREG, we established an injury model of the mouse carotid artery in the present study. High-resolution small-animal ultrasound, Masson staining, immunohistochemistry, RT-PCR and western-blot were used to detect the intima-media thickness, collagen content, the change of collagen type I and CREG expression of arterial wall at different time after aterial injury.

Results

CREG was expressed in normal arteries. The expression of CREG mRNA and protein of the arterial wall was marked down-regulated after injury of mouse carotid artery, and reached its lowest value on 3rd day after arterial injury, with close correlation to the process of vascular remodelling (increase in mRNA level of collagen type I). CREG expression gradually restored on the 7th day, and almost returned to normal levels on 14th day and 28th day after arterial injury. In contrast, injured arteries developed marked vascular remodelling after 7 days as manifested by increase in intima-media thickness, narrowing of the vascular lumen, collagen content as well as mRNA and protein level of collagen type I. There were negative relationships between CREG expression and vascular remodelling at the early time of artery injuries. The expression of CREG was decreased at beginning and then increased, but the degree of vascular remodelling was continued to exacerbate.

Conclusion

These data strongly suggest that CREG is involved in the development of vascular remodelling after arterial injury, and that injury-induced CREG down-regulation may contribute to the progression of vascular remodelling.

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