Effect of decidualization on the expression of bax and bcl-2 in the rat uterine endometrium

During early pregnancy, the uterine endometrium responds to an implanting blastocyst with the extensive growth and differentiation of decidualization. This transformation of endometrial stromal cells begins in the antimesometrial side of the uterus to form a primary decidual zone, expands to form a...

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Veröffentlicht in:Endocrinology (Philadelphia) 1996-07, Vol.137 (7), p.3123-3130
Hauptverfasser: Akcali, K C, Khan, S A, Moulton, B C
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Moulton, B C
description During early pregnancy, the uterine endometrium responds to an implanting blastocyst with the extensive growth and differentiation of decidualization. This transformation of endometrial stromal cells begins in the antimesometrial side of the uterus to form a primary decidual zone, expands to form a secondary zone in the antimesometrium, and eventually transforms stromal cells in the mesometrial region. During pregnancy, both decidual zones regress by apoptosis, leaving decidual cells in the mesometrial region to form decidua basalis and the mature placenta. Molecular mechanisms controlling cell death during blastocyst implantation and decidualization are unknown. We examined the hypothesis that progesterone and estrogen control of endometrial differentiation and eventual apoptosis involves control of bcl-2 gene family expression. Ovariectomized rats were primed with estradiol and treated with progestin (medroxyprogesterone acetate, 3.5 mg) and estradiol (200 ng) before an intrauterine stimulus to initiate decidualization. Expression of the two bax messenger RNA transcripts, 1.0 and 1.5 kilobases, was examined by Northern blot analysis after hormone treatment and decidualization, and only the 1.0-kilobase transcript was induced. After the same treatments, the expression of bcl-2, a suppressor of apoptosis, decreased. In situ analysis revealed a cell type-specific increase in bax expression after the hormonal treatment and decidualization. This increase was first seen in luminal and glandular epithelial cells and then in the periluminal stroma 24 h after intrauterine stimulation, with eventual progressive expression throughout the stroma. Expression of bcl-2 decreased after hormone treatment and decidualization. Immunohistochemical studies of Bax showed that expression of Bax protein accompanied decidualization of the stroma. Bcl-2 protein was only seen in the luminal and glandular epithelia, and its level decreased as decidualization progressed. These data indicate that the balance between bax and bcl-2 expression is altered during stromal cell differentiation. Increased expression of bax precedes nucleosomal DNA fragmentation and eventual apoptosis, which plays a significant role in placental development.
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This transformation of endometrial stromal cells begins in the antimesometrial side of the uterus to form a primary decidual zone, expands to form a secondary zone in the antimesometrium, and eventually transforms stromal cells in the mesometrial region. During pregnancy, both decidual zones regress by apoptosis, leaving decidual cells in the mesometrial region to form decidua basalis and the mature placenta. Molecular mechanisms controlling cell death during blastocyst implantation and decidualization are unknown. We examined the hypothesis that progesterone and estrogen control of endometrial differentiation and eventual apoptosis involves control of bcl-2 gene family expression. Ovariectomized rats were primed with estradiol and treated with progestin (medroxyprogesterone acetate, 3.5 mg) and estradiol (200 ng) before an intrauterine stimulus to initiate decidualization. Expression of the two bax messenger RNA transcripts, 1.0 and 1.5 kilobases, was examined by Northern blot analysis after hormone treatment and decidualization, and only the 1.0-kilobase transcript was induced. After the same treatments, the expression of bcl-2, a suppressor of apoptosis, decreased. In situ analysis revealed a cell type-specific increase in bax expression after the hormonal treatment and decidualization. This increase was first seen in luminal and glandular epithelial cells and then in the periluminal stroma 24 h after intrauterine stimulation, with eventual progressive expression throughout the stroma. Expression of bcl-2 decreased after hormone treatment and decidualization. Immunohistochemical studies of Bax showed that expression of Bax protein accompanied decidualization of the stroma. Bcl-2 protein was only seen in the luminal and glandular epithelia, and its level decreased as decidualization progressed. These data indicate that the balance between bax and bcl-2 expression is altered during stromal cell differentiation. 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This transformation of endometrial stromal cells begins in the antimesometrial side of the uterus to form a primary decidual zone, expands to form a secondary zone in the antimesometrium, and eventually transforms stromal cells in the mesometrial region. During pregnancy, both decidual zones regress by apoptosis, leaving decidual cells in the mesometrial region to form decidua basalis and the mature placenta. Molecular mechanisms controlling cell death during blastocyst implantation and decidualization are unknown. We examined the hypothesis that progesterone and estrogen control of endometrial differentiation and eventual apoptosis involves control of bcl-2 gene family expression. Ovariectomized rats were primed with estradiol and treated with progestin (medroxyprogesterone acetate, 3.5 mg) and estradiol (200 ng) before an intrauterine stimulus to initiate decidualization. Expression of the two bax messenger RNA transcripts, 1.0 and 1.5 kilobases, was examined by Northern blot analysis after hormone treatment and decidualization, and only the 1.0-kilobase transcript was induced. After the same treatments, the expression of bcl-2, a suppressor of apoptosis, decreased. In situ analysis revealed a cell type-specific increase in bax expression after the hormonal treatment and decidualization. This increase was first seen in luminal and glandular epithelial cells and then in the periluminal stroma 24 h after intrauterine stimulation, with eventual progressive expression throughout the stroma. Expression of bcl-2 decreased after hormone treatment and decidualization. Immunohistochemical studies of Bax showed that expression of Bax protein accompanied decidualization of the stroma. Bcl-2 protein was only seen in the luminal and glandular epithelia, and its level decreased as decidualization progressed. These data indicate that the balance between bax and bcl-2 expression is altered during stromal cell differentiation. Increased expression of bax precedes nucleosomal DNA fragmentation and eventual apoptosis, which plays a significant role in placental development.</description><subject>17β-Estradiol</subject><subject>Acetic acid</subject><subject>Apoptosis</subject><subject>BAX protein</subject><subject>Bcl-2 protein</subject><subject>Cell death</subject><subject>Cell differentiation</subject><subject>Decidua</subject><subject>Differentiation (biology)</subject><subject>DNA fragmentation</subject><subject>Endocrine therapy</subject><subject>Endometrium</subject><subject>Epithelial cells</subject><subject>Epithelium</subject><subject>Estrogens</subject><subject>Gene expression</subject><subject>Implantation</subject><subject>Medroxyprogesterone acetate</subject><subject>Molecular modelling</subject><subject>Ovariectomy</subject><subject>Placenta</subject><subject>Pregnancy</subject><subject>Progesterone</subject><subject>Progestin</subject><subject>Proteins</subject><subject>Sex hormones</subject><subject>Stromal cells</subject><subject>Uterus</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><recordid>eNqNkN1KxDAQhYMouK6-gFcBr1vz2ySXsqw_sOCNXnkR0mSKXXbbmrSw-vRm7T6AMDDM8J2Zw0HolpKSMkruoQt9SbkqVamVIobrM7SgRshCUUXO0YIQygvFmLpEVylt8yiE4Av0sW4a8CPuGxzAt2Fyu_bHjW3f4VzjJ2A4DBFS-ts0uHYH7LqAa78rGG5nJLoRTyPEtst4drKHMbbT_hpdNG6X4ObUl-j9cf22ei42r08vq4dN4RkTpmBKKOqN9DKAEbRylfSm0toQojmQQGWodZAaTCBGas8rMDVI6YkyDITjS3Q33x1i_zVBGu22n2KXX1pOORHGSGoyxWbKxz6lCI0dYrt38dtSYo8h2qN1m0O0yp5CzKJiFvXT8B_-F-x3cwE</recordid><startdate>19960701</startdate><enddate>19960701</enddate><creator>Akcali, K C</creator><creator>Khan, S A</creator><creator>Moulton, B C</creator><general>Oxford University Press</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope></search><sort><creationdate>19960701</creationdate><title>Effect of decidualization on the expression of bax and bcl-2 in the rat uterine endometrium</title><author>Akcali, K C ; 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This transformation of endometrial stromal cells begins in the antimesometrial side of the uterus to form a primary decidual zone, expands to form a secondary zone in the antimesometrium, and eventually transforms stromal cells in the mesometrial region. During pregnancy, both decidual zones regress by apoptosis, leaving decidual cells in the mesometrial region to form decidua basalis and the mature placenta. Molecular mechanisms controlling cell death during blastocyst implantation and decidualization are unknown. We examined the hypothesis that progesterone and estrogen control of endometrial differentiation and eventual apoptosis involves control of bcl-2 gene family expression. Ovariectomized rats were primed with estradiol and treated with progestin (medroxyprogesterone acetate, 3.5 mg) and estradiol (200 ng) before an intrauterine stimulus to initiate decidualization. Expression of the two bax messenger RNA transcripts, 1.0 and 1.5 kilobases, was examined by Northern blot analysis after hormone treatment and decidualization, and only the 1.0-kilobase transcript was induced. After the same treatments, the expression of bcl-2, a suppressor of apoptosis, decreased. In situ analysis revealed a cell type-specific increase in bax expression after the hormonal treatment and decidualization. This increase was first seen in luminal and glandular epithelial cells and then in the periluminal stroma 24 h after intrauterine stimulation, with eventual progressive expression throughout the stroma. Expression of bcl-2 decreased after hormone treatment and decidualization. Immunohistochemical studies of Bax showed that expression of Bax protein accompanied decidualization of the stroma. Bcl-2 protein was only seen in the luminal and glandular epithelia, and its level decreased as decidualization progressed. These data indicate that the balance between bax and bcl-2 expression is altered during stromal cell differentiation. Increased expression of bax precedes nucleosomal DNA fragmentation and eventual apoptosis, which plays a significant role in placental development.</abstract><cop>Washington</cop><pub>Oxford University Press</pub><doi>10.1210/endo.137.7.8770938</doi><tpages>8</tpages></addata></record>
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source Oxford University Press Journals All Titles (1996-Current); Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
subjects 17β-Estradiol
Acetic acid
Apoptosis
BAX protein
Bcl-2 protein
Cell death
Cell differentiation
Decidua
Differentiation (biology)
DNA fragmentation
Endocrine therapy
Endometrium
Epithelial cells
Epithelium
Estrogens
Gene expression
Implantation
Medroxyprogesterone acetate
Molecular modelling
Ovariectomy
Placenta
Pregnancy
Progesterone
Progestin
Proteins
Sex hormones
Stromal cells
Uterus
title Effect of decidualization on the expression of bax and bcl-2 in the rat uterine endometrium
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