ALTERATIONS OF HUMAN PLACENTAL EPIDERMAL GROWTH-FACTOR RECEPTOR IN INTRAUTERINE GROWTH-RETARDATION
ALTERATIONS OF HUMAN PLACENTAL EPIDERMAL GROWTH-FACTOR RECEPTOR IN INTRAUTERINE GROWTH-RETARDATION
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DOI：
10.1172/jci117067
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发表时间：
1994-03-01
影响因子：
15.9
通讯作者：
EVAINBRION, D
中科院分区：
文献类型：
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作者：
FONDACCI, C;ALSAT, E;EVAINBRION, D
我们研究了14例宫内发育迟缓患者的胎盘微绒毛EGF受体（EGFR）及其与母体和胎盘特征的关系。SDS-PAGE、放射自显像和扫描分析显示，12例小于胎龄的新生儿胎盘EGFR磷酸化明显降低或缺失。特异性[I-125]EGF结合和结合数据的Scatchard图显示，12例中有6例EGFR数量减少，高亲和位点的平均最大结合能力为1.09 +/- 0.32 pmol/mg（平均控制值为2.30 +/- 0.23 pmol/mg）。大多数高血压女性和吸烟者属于这一亚群。其余6例低EGFR磷酸化的小胎龄胎盘中，有3例未见母体病理或明显的胎盘实质病变。通过[I-125]EGF交联和两种多克隆抗EGFR抗体RK2和C-Term的Western blotting检测，其中5种显示出175-kD的EGFR物种，表明EGF诱导的信号转导异常。第六个胎盘产生一个145-kD的单一EGFR带，与EGFR结构异常一致；Western blot分析未见免疫反应条带。综上所述，宫内生长迟缓的母体和胎盘病理与胎盘EGFR的各种改变有关，指出EGFR配体在胎盘和胎儿生长调节通路中的重要性。
We studied human placental microvillous EGF receptor (EGFR) and its relationship with maternal and placental features in 14 cases of intrauterine growth retardation.Placental EGFR phosphorylation was significantly decreased or absent in 12 cases of small for gestational age neonates, as shown by SDS-PAGE, autoradiography, and scanning analysis. Specific [I-125]EGF binding and Scatchard plots of the binding data showed a decreased number of EGFR in 6 of the 12 cases, with a mean maximal binding capacity of 1.09 +/- 0.32 pmol/mg for high affinity sites (mean control value = 2.30 +/- 0.23 pmol/mg). Most of the hypertensive women and smokers belonged to this subgroup. In three of the remaining six cases of small gestational age placentas with low EGFR phosphorylation, there was no maternal pathology or significant parenchymatous placental lesions. Five showed a 175-kD EGFR species when probed by [I-125]EGF cross-linking and Western blotting with RK2 and C-Term, two polyclonal anti-EGFR antibodies, suggesting abnormal transduction of the EGF-induced signal. The sixth placenta yielded a single 145-kD EGFR band consistent with an abnormal EGFR structure; Western blot analysis showed no immunoreactive band.In conclusion, maternal and placental pathologies in intrauterine growth retardation are associated with various alterations of placental EGFR, pointing out the importance of EGFR ligands in the regulatory pathway of placental anf fetal growth.