Activin-A up-regulates type I activin receptor mRNA levels in human immortalized extravillous trophoblast cells.
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Activin-A up-regulates type I activin receptor mRNA levels in human immortalized extravillous trophoblast cells. Victor TS Chen1, Chun Peng2 and Peter CK Leung*1 Address: 1Department of Obstetrics and Gynecology, University of British Columbia, Vancouver, BC, Canada and 2Department of Biology, York University, Toronto, Ontario, Canada Email: Victor TS Chen - [email protected]; Chun Peng - [email protected]; Peter CK Leung* - [email protected] * Corresponding author
Published: 24 March 2003 Reproductive Biology and Endocrinology 2003, 1:29
Received: 7 March 2003 Accepted: 24 March 2003
This article is available from: http://www.RBEj.com/content/1/1/29 © 2003 Chen et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.
ActivinFollistatinActivin ReceptorImmortalized Extravillous Trophoblast CellsCompetitive PCR
Abstract Activin is known to play an important regulatory role in reproduction, including pregnancy. To further examine the role and signaling mechanism of activin in regulating placental function, the steady-state level of activin type I receptor (ActRI) mRNA in immortalized extravillous trophoblasts (IEVT) cells was measured using competitive PCR (cPCR). An internal standard of ActRI cDNA for cPCR was constructed for the quantification of ActRI mRNA levels in IEVT cells. ActRI mRNA levels were increased in a dose-dependent manner by activin-A with the maximal effect observed at the dose of 10 ng/ml. Time course studies revealed that activin-A had maximal effects on ActRI mRNA levels at 6 hours after treatment. The effects of activin-A on ActRI mRNA levels was blocked by follistatin, an activin binding protein, in a dose-dependent manner. In addition, inhibin-A inhibited basal, as well as activin-A-induced ActRI mRNA levels. These findings provide evidence, for the first time, that activin-A modulates ActRI mRNA levels in human trophoblast cells.
Introduction Although activins and inhibins were originally isolated from follicular fluids and identified as stimulators and inhibitors, respectively, of pituitary follicle-stimulating hormone (FSH), the identification of inhibins and activins in a wide variety of tissues suggest that these factors play much greater roles than the control of FSH secretion [1– 5]. Also, it has become evident that these factors exert their effects mostly in autocrine/paracrine manners. Similar to other members of the transforming growth factor-β (TGF-β) family, activins exert their actions by interacting with both type I and type II membrane serine/ threonine kinase receptors [6,7]. Two type I (ActRI and ActRIB) and two type II (ActRII and ActRIIB) receptors have
been shown to interact with activins [5] and their mRNAs have been detected in human placental trophoblast cells [8–10], as well as in choriocarcinoma cells [11]. Activins, particularly activin-A,
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