作者: Yupeng Dong , Yoshitaka Kimura , Takuya Ito , Clarissa Velayo , Takafumi Sato
DOI: 10.1016/J.BBRC.2015.10.125
关键词: Internal medicine 、 Fetus 、 Activating transcription factor 2 、 Medicine 、 Immunology 、 Endocrinology 、 Inflammation 、 Vagina 、 Transcriptional regulation 、 Reperfusion injury 、 Tumor necrosis factor alpha 、 Phosphorylation
摘要: During pregnancy, both ischemic reperfusion and bacterial agent LPS are known risk factors for fetal brain damage. However, there is a lack of evidence to explain whether vaginal affects the fetus response reperfusion. Here we reported that was more than 2 folds higher vulnerability hemorrhage when mother mouse treated with LPS. As our previously reported, induces P53-dependent damage based on molecular mechanism: transcriptional pattern changed from HIF-1alpha-dependent immediately. In present work, only precondition, phosphorylation activated factor (ATF) at Thr71 appeared in Moreover, this completely blocked by pre-treatment P53 inhibitor, pifithrin-α. We concluded precondition trigged p53-dependent ATF2 reperfusion, which played an important role increasing fetus.