Increased endoplasmic reticulum stress in decidual tissue from pregnancies complicated by fetal growth restriction with and without pre-eclampsia.
Increased endoplasmic reticulum stress in decidual tissue from pregnancies complicated by fetal growth restriction with and without pre-eclampsia.
复制标题
妊娠的骨骼组织中内质网应激的增加，由于胎儿生长限制而有和没有子痫前期的胎儿生长限制。
DOI：
10.1016/j.placenta.2011.08.005
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发表时间：
2011-11
期刊：
影响因子：
3.8
通讯作者：
Austgulen, R.
中科院分区：
文献类型：
--
作者：
Lian, I. A.;Loset, M.;Mundal, S. B.;Fenstad, M. H.;Johnson, M. P.;Eide, I. P.;Bjorge, L.;Freed, K. A.;Moses, E. K.;Austgulen, R.
关键词：
Endoplasmic reticulum (ER) stress has been implicated in both pre-eclampsia (PE) and fetal growth restriction (FGR), and is characterised by activation of three signalling branches: 1) PERK-pEIF2α, 2) ATF6 and 3) splicing of XBP1(U) into XBP1(S). To evaluate the contribution of ER stress in the pathogenesis of PE relative to FGR, we compared levels of ER stress markers in decidual tissue from pregnancies complicated by PE and/or FGR. Whole-genome transcriptional profiling was performed on decidual tissue from women with PE (n = 13), FGR (n = 9), PE+FGR (n = 24) and controls (n = 58), and used for pathway- and targeted transcriptional analyses of ER stress markers. The expression and cellular localisation of ER stress markers was assesses by Western blot and immunofluorescence analyses. Increased ER stress was observed in FGR and PE+FGR, including both the PERK-pEIF2α and ATF6 signalling branches, whereas ER stress was less evident in isolated PE. However, these cases demonstrated elevated levels of XBP1(U) protein. ATF6 and XBP1 immunoreactivity was detected in most (> 80%) extravillous trophoblasts, decidual cells and macrophages. No difference in the proportion of immunopositive cells or staining pattern was observed between study groups. Increased PERK-pEIF2α and ATF6 signalling have been associated with decreased cellular proliferation and may contribute to the impaired placental growth characterising pregnancies with FGR and PE+FGR. XBP1(U) has been proposed as a negative regulator of ER stress, and increased levels in PE may reflect a protective mechanism against the detrimental effects of ER stress.
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DOI：
10.1046/j.1525-1373.1999.d01-139.x
发表时间：
1999-12-01
影响因子：
--
作者：
Hubel, CA
通讯作者：
Hubel, CA
影响因子：
30.8
作者：
Goering, Harald H. H.;Curran, Joanne E.;Blangero, John
通讯作者：
Blangero, John
影响因子：
9.8
作者：
Crispi, Fatima;Dominguez, Carmen;Gratacos, Eduard
通讯作者：
Gratacos, Eduard
DOI：
10.1111/j.0001-6349.2004.00395.x
发表时间：
2004-08-01
影响因子：
4.3
作者：
Harsem, NK;Staff, AC;Roald, B
通讯作者：
Roald, B
影响因子：
6.5
作者：
Jakobsen CH;Størvold GL;Bremseth H;Follestad T;Sand K;Mack M;Olsen KS;Lundemo AG;Iversen JG;Krokan HE;Schønberg SA
通讯作者：
Schønberg SA