Abstract

BackgroudWidespread endothelial injury contributes to the occurrence of preeclampsia. Maspin, first identified as a tumor suppressor, plays a critical role in cell invasion and angiogenesis. Our previous studies found that the expression of maspin was increased in preeclampsic placenta. In this research, we studied the function of human umbilical vein endothelial cells (HUVECs) to explore the role and possible mechanism of maspin gene in the pathogenesis of preeclampsia.MethodsHUVECs were treated with different concentration of recombinant human maspin protein (r-maspin) during normoxia and hypoxia, we detected the proliferation, apoptosis, migration and tube formation of HUVECs. We also assessed nitride oxide (NO) synthesis and the expression of matrix metalloproteinase 2 (MMP2) to further explore the underlying molecular mechanism.ResultsThere was only slight maspin expression at mRNA level in HUVECs. Treated HUVECs with r-maspin, the proliferation of HUVECs was significantly promoted both under normoxia and hypoxia. The tubes formed by HUVECs were significantly inhibited and NO synthesis was significantly reduced by r-maspin. Meantime, r-maspin also inhibited MMP2 expression and activity in HUVECs. However, there was no significant change in the migration and apoptosis of HUVECs.ConclusionsMaspin may be an important participant for mediating endothelial function and ultimately leads to the occurence of preeclamsia.

Highlights

  • Preeclampsia (PE) is a pregnancy disorder that is characterized by the onset of hypertension and proteinuria in previously normotensive women after the twentieth week of gestation [1]

  • The tubes formed by human umbilical vein endothelial cells (HUVECs) were significantly inhibited and nitride oxide (NO) synthesis was significantly reduced by r-maspin

  • There was no significant change in the migration and apoptosis of HUVECs

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Summary

Introduction

Preeclampsia (PE) is a pregnancy disorder that is characterized by the onset of hypertension and proteinuria in previously normotensive women after the twentieth week of gestation [1]. It is generally considered that widespread endothelial injuries contribute to the occurrence of preeclampsia [3]. Mammary serine protease inhibitor (maspin) is an epithelial-specific Class II tumor suppressor gene and belongs to the serine protease inhibitor (serpin) superfamily [4]. Maspin has inhibitory effect on the invasion, motility, and metastasis of tumor cells [5,6,7]. Maspin is an important inhibitor of angiogenesis. Zhang et al [8] have first demonstrated that maspin can effectively block neovascularization by the rat cornea pocket model in vivo and inhibit the migration of endothelial cells in vitro. Cher et al [9] have shown that the vasculature density is reduced by maspin in a prostate xenograft model

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