Developmental changes in extracellular matrix messenger RNAs in the mouse placenta during the second half of pregnancy: Possible factors involved in the regulation of placental extracellular matrix expression
Developmental changes in extracellular matrix messenger RNAs in the mouse placenta during the second half of pregnancy: Possible factors involved in the regulation of placental extracellular matrix expression
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DOI：
10.1095/biolreprod.107.061382
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发表时间：
2007-12-01
影响因子：
3.6
通讯作者：
Nishiyama, Toshio
中科院分区：
文献类型：
--
作者：
Arai, Koji Y.;Nishiyama, Toshio
在妊娠后半期小鼠胎胎盘组织中检测前胶原（Col1a1/2、Col3a1、Col4a1/2、Col5a1/2）和纤维连接蛋白1 （Fn1）的表达。核糖核酸酶保护试验（RPAs）显示，这些mrna的水平在怀孕第10天至第14天显著增加，此后它们保持相对稳定的水平。原位杂交表明，Col1a1和Col4a1主要定位于迷路，而Fn1主要表达于海绵滋养细胞。由于转化生长因子- β (TGFB)超家族成员参与各种组织中细胞外基质（ECM）表达的调控，TGFB家族成员及其结合蛋白的mRNA水平也通过RPAs进行了检测。胎盘中表达转化生长因子- β -3 （Tgfb1-3）、激活素亚基（Inhba、lnhbb）、卵泡抑素（Fst）和卵泡抑素样3 (Fstl3)，而未检测到肌生长抑制素（Mstn）的显著表达。虽然Tgfbl-3和Inhba在胎盘中的表达模式提示TGFBs和激活素A可能参与了胎盘ECM表达的调节，但TGFBs和激活素A在体外均未影响ECM mRNA水平。另一方面，缺氧显著降低培养的胎盘细胞Col1a1/2和Col4a1/2 mrna，高糖状态显著增加Col1a1和Col3a1 mrna。高糖条件下Fn1表达增加，缺氧也使Fn1表达增加，但程度较轻。这些数据表明，胎盘中氧张力和营养供应的增加，而不是TGFB家族成员，可能是导致胎盘ECM mRNA表达增加的原因。
Expression of procollagens (Col1a1/2, Col3a1, Col4a1/2, Col5a1/2) and fibronectin 1 (Fn1) in the mouse fetal placental tissue was examined during the second half of pregnancy. Ribonuclease protection assays (RPAs) revealed that levels of these mRNAs noticeably increased between Days 10 and 14 of pregnancy, and they remained at relatively constant levels thereafter. In situ hyridization showed that Col1a1 and Col4a1 mainly localized in the labyrinth, whereas Fn1 was expressed mainly in the spongiotrophoblast. Since members of the transforming growth factor-beta (TGFB) superfamily are involved in the regulation of extracellular matrix (ECM) expression in various tissues, mRNA levels of TGFB family members and their binding proteins were also examined by RPAs. Transforming growth factor-betal-3 (Tgfb1-3), activin subunits (Inhba, lnhbb), follistatin (Fst), and follistatin-like 3 (Fstl3) were expressed in the placenta, whereas significant expression of myostatin (Mstn) was not detected. Although the expression patterns of Tgfbl-3 and Inhba in the placenta suggest possible involvement of TGFBs and activin A in the regulation of placental ECM expression, neither TGFBs nor activin A affected ECM mRNA levels in vitro. On the other hand, hypoxia significantly decreased Col1a1/2 and Col4a1/2 mRNAs in cultured placental cells, and a high-glucose condition significantly increased Col1a1 and Col3a1 mRNAs. Fn1 expression was increased under the high-glucose condition, although hypoxia also increased Fn1 expression to a lesser degree. These data suggest that an increase in oxygen tension and nutrient supply during placentation rather than TGFB family members may be responsible for the increase in the placental ECM mRNA expression.