Comparing the expression patterns of placental magnesium/phosphorus‐transporting channels between healthy and preeclamptic pregnancies
Identifieur interne : 001394 ( Istex/Corpus ); précédent : 001393; suivant : 001395Comparing the expression patterns of placental magnesium/phosphorus‐transporting channels between healthy and preeclamptic pregnancies
Auteurs : Hyun Yang ; Tae-Hee Kim ; Geun-Shik Lee ; Eui-Ju Hong ; Eui-Bae JeungSource :
- Molecular Reproduction and Development [ 1040-452X ] ; 2014-09.
Abstract
Preeclampsia is a pregnancy‐specific disorder characterized by de novo development of concurrent hypertension, proteinuria, and placental oxidative stress. During the last trimester of gestation, maternal‐to‐fetal transport of minerals is dramatically increased and becomes tightly mediated by ion channels that are highly permeable to various divalent cations, such as Ca2+, Mg2+, and Zn2+. The regulation of magnesium/inorganic phosphorus ion‐channel transport in the placenta, however, is not incompletely understood. In the present study, we examined the regulation of magnesium/inorganic phosphorus channels (MPCs) in the placenta of pregnant women suffering from preeclampsia as well as in primary human placental cells subjected to oxidative stress. The expression of MPC genes (TRPM6, TRPM7, PiT‐1, and PiT‐2) was down‐regulated in preeclamptic placenta tissues during preterm labor, and generally remained lower at term labor—although TRPM7 expression in the central placenta or PiT‐2 expression in whole placenta was unchanged or up‐regulated. Consistent with this association, expression of MPC genes in the primary placental cells was reduced under hypoxic conditions. TRPM6, TRPM7, and PiT‐1 channels were predominantly detected in the syncytiotrophoblast layers of the placenta. In contrast, PiT‐2 was abundant in the placental intravillous connective tissues. Taken together, our findings indicated that placental MPC expression is down‐regulated in cases of preeclampsia and under hypoxia. This relationship may contribute to a better understanding of the interrelationship between magnesium/inorganic phosphorus imbalances and preeclampsia development during preterm or term labor. Mol. Reprod. Dev. 81: 851–860, 2014. © 2014 Wiley Periodicals, Inc.
Url:
DOI: 10.1002/mrd.22353
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<front><div type="abstract" xml:lang="en">Preeclampsia is a pregnancy‐specific disorder characterized by de novo development of concurrent hypertension, proteinuria, and placental oxidative stress. During the last trimester of gestation, maternal‐to‐fetal transport of minerals is dramatically increased and becomes tightly mediated by ion channels that are highly permeable to various divalent cations, such as Ca2+, Mg2+, and Zn2+. The regulation of magnesium/inorganic phosphorus ion‐channel transport in the placenta, however, is not incompletely understood. In the present study, we examined the regulation of magnesium/inorganic phosphorus channels (MPCs) in the placenta of pregnant women suffering from preeclampsia as well as in primary human placental cells subjected to oxidative stress. The expression of MPC genes (TRPM6, TRPM7, PiT‐1, and PiT‐2) was down‐regulated in preeclamptic placenta tissues during preterm labor, and generally remained lower at term labor—although TRPM7 expression in the central placenta or PiT‐2 expression in whole placenta was unchanged or up‐regulated. Consistent with this association, expression of MPC genes in the primary placental cells was reduced under hypoxic conditions. TRPM6, TRPM7, and PiT‐1 channels were predominantly detected in the syncytiotrophoblast layers of the placenta. In contrast, PiT‐2 was abundant in the placental intravillous connective tissues. Taken together, our findings indicated that placental MPC expression is down‐regulated in cases of preeclampsia and under hypoxia. This relationship may contribute to a better understanding of the interrelationship between magnesium/inorganic phosphorus imbalances and preeclampsia development during preterm or term labor. Mol. Reprod. Dev. 81: 851–860, 2014. © 2014 Wiley Periodicals, Inc.</div>
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<abstract>Preeclampsia is a pregnancy‐specific disorder characterized by de novo development of concurrent hypertension, proteinuria, and placental oxidative stress. During the last trimester of gestation, maternal‐to‐fetal transport of minerals is dramatically increased and becomes tightly mediated by ion channels that are highly permeable to various divalent cations, such as Ca2+, Mg2+, and Zn2+. The regulation of magnesium/inorganic phosphorus ion‐channel transport in the placenta, however, is not incompletely understood. In the present study, we examined the regulation of magnesium/inorganic phosphorus channels (MPCs) in the placenta of pregnant women suffering from preeclampsia as well as in primary human placental cells subjected to oxidative stress. The expression of MPC genes (TRPM6, TRPM7, PiT‐1, and PiT‐2) was down‐regulated in preeclamptic placenta tissues during preterm labor, and generally remained lower at term labor—although TRPM7 expression in the central placenta or PiT‐2 expression in whole placenta was unchanged or up‐regulated. Consistent with this association, expression of MPC genes in the primary placental cells was reduced under hypoxic conditions. TRPM6, TRPM7, and PiT‐1 channels were predominantly detected in the syncytiotrophoblast layers of the placenta. In contrast, PiT‐2 was abundant in the placental intravillous connective tissues. Taken together, our findings indicated that placental MPC expression is down‐regulated in cases of preeclampsia and under hypoxia. This relationship may contribute to a better understanding of the interrelationship between magnesium/inorganic phosphorus imbalances and preeclampsia development during preterm or term labor. Mol. Reprod. Dev. 81: 851–860, 2014. © 2014 Wiley Periodicals, Inc.</abstract>
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<profileDesc><abstract xml:lang="en" style="main"><head>SUMMARY</head>
<p>Preeclampsia is a pregnancy‐specific disorder characterized by de novo development of concurrent hypertension, proteinuria, and placental oxidative stress. During the last trimester of gestation, maternal‐to‐fetal transport of minerals is dramatically increased and becomes tightly mediated by ion channels that are highly permeable to various divalent cations, such as Ca<hi rend="superscript">2+</hi>
, Mg<hi rend="superscript">2+</hi>
, and Zn<hi rend="superscript">2+</hi>
. The regulation of magnesium/inorganic phosphorus ion‐channel transport in the placenta, however, is not incompletely understood. In the present study, we examined the regulation of magnesium/inorganic phosphorus channels (MPCs) in the placenta of pregnant women suffering from preeclampsia as well as in primary human placental cells subjected to oxidative stress. The expression of MPC genes (<hi rend="italic">TRPM6</hi>
, <hi rend="italic">TRPM7</hi>
, <hi rend="italic">PiT‐1</hi>
, and <hi rend="italic">PiT‐2</hi>
) was down‐regulated in preeclamptic placenta tissues during preterm labor, and generally remained lower at term labor—although <hi rend="italic">TRPM7</hi>
expression in the central placenta or <hi rend="italic">PiT‐2</hi>
expression in whole placenta was unchanged or up‐regulated. Consistent with this association, expression of MPC genes in the primary placental cells was reduced under hypoxic conditions. TRPM6, TRPM7, and PiT‐1 channels were predominantly detected in the syncytiotrophoblast layers of the placenta. In contrast, PiT‐2 was abundant in the placental intravillous connective tissues. Taken together, our findings indicated that placental MPC expression is down‐regulated in cases of preeclampsia and under hypoxia. This relationship may contribute to a better understanding of the interrelationship between magnesium/inorganic phosphorus imbalances and preeclampsia development during preterm or term labor. <hi rend="italic">Mol. Reprod. Dev. 81: 851–860, 2014. © 2014 Wiley Periodicals, Inc</hi>
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<correspondenceTo><lineatedText><line>Corresponding author:</line>
<line>Laboratory of Veterinary Biochemistry and Molecular Biology, College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk 361‐763, Republic of Korea. E‐mail: <email>ebjeung@chungbuk.ac.kr</email>
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<contentMeta><titleGroup><title type="main">Comparing the expression patterns of placental magnesium/phosphorus‐transporting channels between healthy and preeclamptic pregnancies</title>
<title type="short">M<sc>AGNESIUM</sc>
/P<sc>HOSPHORUS</sc>
T<sc>RANSPORT</sc>
G<sc>ENES</sc>
A<sc>RE</sc>
R<sc>EGULATED BY</sc>
H<sc>YPOXIC</sc>
S<sc>TRESS</sc>
</title>
<title type="shortAuthors">Y<sc>ANG ET AL</sc>
</title>
</titleGroup>
<creators><creator xml:id="mrd22353-cr-0001" creatorRole="author" affiliationRef="#mrd22353-aff-0001"><personName><givenNames>Hyun</givenNames>
<familyName>Yang</familyName>
</personName>
</creator>
<creator xml:id="mrd22353-cr-0002" creatorRole="author" affiliationRef="#mrd22353-aff-0002"><personName><givenNames>Tae‐Hee</givenNames>
<familyName>Kim</familyName>
</personName>
</creator>
<creator xml:id="mrd22353-cr-0003" creatorRole="author" affiliationRef="#mrd22353-aff-0003"><personName><givenNames>Geun‐Shik</givenNames>
<familyName>Lee</familyName>
</personName>
</creator>
<creator xml:id="mrd22353-cr-0004" creatorRole="author" affiliationRef="#mrd22353-aff-0001"><personName><givenNames>Eui‐Ju</givenNames>
<familyName>Hong</familyName>
</personName>
</creator>
<creator xml:id="mrd22353-cr-0005" creatorRole="author" affiliationRef="#mrd22353-aff-0001" corresponding="yes"><personName><givenNames>Eui‐Bae</givenNames>
<familyName>Jeung</familyName>
</personName>
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<affiliationGroup><affiliation xml:id="mrd22353-aff-0001" countryCode="KR"><orgDiv>Laboratory of Veterinary Biochemistry and Molecular Biology</orgDiv>
<orgDiv>College of Veterinary Medicine</orgDiv>
<orgName>Chungbuk National University</orgName>
<address><city>Cheongju</city>
<countryPart>Chungbuk</countryPart>
<country>Republic of Korea</country>
</address>
</affiliation>
<affiliation xml:id="mrd22353-aff-0002" countryCode="KR"><orgDiv>Department of Obstetrics and Gynecology</orgDiv>
<orgDiv>College of Medicine</orgDiv>
<orgName>Soonchunhyang University</orgName>
<address><city>Bucheon</city>
<country>Republic of Korea</country>
</address>
</affiliation>
<affiliation xml:id="mrd22353-aff-0003" countryCode="KR"><orgDiv>College of Veterinary Medicine</orgDiv>
<orgName>Kangwon National University</orgName>
<address><city>Chuncheon</city>
<countryPart>Gangwon</countryPart>
<country>Republic of Korea</country>
</address>
</affiliation>
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<fundingInfo><fundingAgency>National Research Foundation of Korea</fundingAgency>
<fundingNumber>NRF‐2013R1A2A2A05004582</fundingNumber>
</fundingInfo>
<supportingInformation><p>Additional supporting information may be found in the online version of this article.</p>
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<abstractGroup><abstract type="main" xml:lang="en"><title type="main">SUMMARY</title>
<section xml:id="mrd22353-sec-0001"><p>Preeclampsia is a pregnancy‐specific disorder characterized by de novo development of concurrent hypertension, proteinuria, and placental oxidative stress. During the last trimester of gestation, maternal‐to‐fetal transport of minerals is dramatically increased and becomes tightly mediated by ion channels that are highly permeable to various divalent cations, such as Ca<sup>2+</sup>
, Mg<sup>2+</sup>
, and Zn<sup>2+</sup>
. The regulation of magnesium/inorganic phosphorus ion‐channel transport in the placenta, however, is not incompletely understood. In the present study, we examined the regulation of magnesium/inorganic phosphorus channels (MPCs) in the placenta of pregnant women suffering from preeclampsia as well as in primary human placental cells subjected to oxidative stress. The expression of MPC genes (<i>TRPM6</i>
, <i>TRPM7</i>
, <i>PiT‐1</i>
, and <i>PiT‐2</i>
) was down‐regulated in preeclamptic placenta tissues during preterm labor, and generally remained lower at term labor—although <i>TRPM7</i>
expression in the central placenta or <i>PiT‐2</i>
expression in whole placenta was unchanged or up‐regulated. Consistent with this association, expression of MPC genes in the primary placental cells was reduced under hypoxic conditions. TRPM6, TRPM7, and PiT‐1 channels were predominantly detected in the syncytiotrophoblast layers of the placenta. In contrast, PiT‐2 was abundant in the placental intravillous connective tissues. Taken together, our findings indicated that placental MPC expression is down‐regulated in cases of preeclampsia and under hypoxia. This relationship may contribute to a better understanding of the interrelationship between magnesium/inorganic phosphorus imbalances and preeclampsia development during preterm or term labor. <i>Mol. Reprod. Dev. 81: 851–860, 2014. © 2014 Wiley Periodicals, Inc</i>
.</p>
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<mods version="3.6"><titleInfo lang="en"><title>Comparing the expression patterns of placental magnesium/phosphorus‐transporting channels between healthy and preeclamptic pregnancies</title>
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<titleInfo type="abbreviated" lang="en"><title>MAGNESIUM/PHOSPHORUS TRANSPORT GENES ARE REGULATED BY HYPOXIC STRESS</title>
</titleInfo>
<titleInfo type="alternative" contentType="CDATA" lang="en"><title>Comparing the expression patterns of placental magnesium/phosphorus‐transporting channels between healthy and preeclamptic pregnancies</title>
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<name type="personal"><namePart type="given">Hyun</namePart>
<namePart type="family">Yang</namePart>
<affiliation>Laboratory of Veterinary Biochemistry and Molecular Biology, College of Veterinary Medicine, Chungbuk National University, Chungbuk, Cheongju, Republic of Korea</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
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<name type="personal"><namePart type="given">Tae‐Hee</namePart>
<namePart type="family">Kim</namePart>
<affiliation>Department of Obstetrics and Gynecology, College of Medicine, Soonchunhyang University, Bucheon, Republic of Korea</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
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<name type="personal"><namePart type="given">Geun‐Shik</namePart>
<namePart type="family">Lee</namePart>
<affiliation>College of Veterinary Medicine, Kangwon National University, Gangwon, Chuncheon, Republic of Korea</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Eui‐Ju</namePart>
<namePart type="family">Hong</namePart>
<affiliation>Laboratory of Veterinary Biochemistry and Molecular Biology, College of Veterinary Medicine, Chungbuk National University, Chungbuk, Cheongju, Republic of Korea</affiliation>
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<name type="personal"><namePart type="given">Eui‐Bae</namePart>
<namePart type="family">Jeung</namePart>
<affiliation>Laboratory of Veterinary Biochemistry and Molecular Biology, College of Veterinary Medicine, Chungbuk National University, Chungbuk, Cheongju, Republic of Korea</affiliation>
<affiliation>Corresponding author:Laboratory of Veterinary Biochemistry and Molecular Biology, College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk 361‐763, Republic of Korea. E‐mail:</affiliation>
<affiliation>E-mail: ebjeung@chungbuk.ac.kr</affiliation>
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<abstract lang="en">Preeclampsia is a pregnancy‐specific disorder characterized by de novo development of concurrent hypertension, proteinuria, and placental oxidative stress. During the last trimester of gestation, maternal‐to‐fetal transport of minerals is dramatically increased and becomes tightly mediated by ion channels that are highly permeable to various divalent cations, such as Ca2+, Mg2+, and Zn2+. The regulation of magnesium/inorganic phosphorus ion‐channel transport in the placenta, however, is not incompletely understood. In the present study, we examined the regulation of magnesium/inorganic phosphorus channels (MPCs) in the placenta of pregnant women suffering from preeclampsia as well as in primary human placental cells subjected to oxidative stress. The expression of MPC genes (TRPM6, TRPM7, PiT‐1, and PiT‐2) was down‐regulated in preeclamptic placenta tissues during preterm labor, and generally remained lower at term labor—although TRPM7 expression in the central placenta or PiT‐2 expression in whole placenta was unchanged or up‐regulated. Consistent with this association, expression of MPC genes in the primary placental cells was reduced under hypoxic conditions. TRPM6, TRPM7, and PiT‐1 channels were predominantly detected in the syncytiotrophoblast layers of the placenta. In contrast, PiT‐2 was abundant in the placental intravillous connective tissues. Taken together, our findings indicated that placental MPC expression is down‐regulated in cases of preeclampsia and under hypoxia. This relationship may contribute to a better understanding of the interrelationship between magnesium/inorganic phosphorus imbalances and preeclampsia development during preterm or term labor. Mol. Reprod. Dev. 81: 851–860, 2014. © 2014 Wiley Periodicals, Inc.</abstract>
<note type="funding">National Research Foundation of Korea - No. NRF‐2013R1A2A2A05004582; </note>
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<note type="content"> Additional supporting information may be found in the online version of this article.Supporting Info Item: Supporting Information. - </note>
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<identifier type="ISSN">1040-452X</identifier>
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