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Please use this identifier to cite or link to this item: http://hdl.handle.net/10271/3144

Title: Decrease in sphingomyelin (d18:1/16:0) in stem villi and phosphatidylcholine (16:0/20:4) in terminal villi of human term placentas with pathohistological maternal malperfusion
Other Titles: 病理組織学的に母体循環不全を示唆する胎盤では、幹絨毛でsphingomyelin (d18:1/16:0) が、終末絨毛でphosphatidylcholine (16:0/20:4) の発現が低下する
Authors: Yamazaki, Kaori
山﨑, 香織
Issue Date: 16-Nov-2015
Publisher: PLOS
Abstract: Placental villi play pivotal roles in feto-maternal transportation and phospholipids constitute a major part of the villous membrane. We have been developing and optimizing an imaging system based on a matrix-assisted laser desorption/ionization (MALDI)-based mass spectrometer, which provides clear two-dimensional molecular distribution patterns using highly sensitive mass spectrometry from mixtures of ions generated on tissue surfaces. We recently applied this technology to normal human uncomplicated term placentas and detected the specific distribution of sphingomyelin (SM) (d18:1/16:0) in stem villi and phosphatidylcholine (PC) (16:0/20:4) in terminal villi. In the present study, we applied this technology to nine placentas with maternal or fetal complications, and determined whether a relationship existed between these specific distribution patterns of phospholipid molecules and the six representative pathological findings of placentas, i.e., villitis of unknown etiology (VUE), thrombus, atherosis, chorioamnionitis (CAM), immature terminal villi, and multiple branched terminal villi. In two placentas with the first and second largest total number of positive pathological findings, i.e., five and three positive findings, the specific distribution of SM (d18:1/16:0) in stem villi and PC (16:0/20:4) in terminal villi disappeared. The common pathological findings in these two placentas were atherosis, immature terminal villi, and multiple branched terminal villi, suggesting the possible involvement of the underperfusion of maternal blood into the intervillous space. On the other hand, the number of pathological findings were two or less in the seven other placentas, in which no specific relationships were observed between the differential expression patterns of these two phospholipids in stem and terminal villi and the pathological findings of the placentas; however, the specific distribution pattern of SM (d18:1/16:0) in stem villi disappeared in four placentas, while that of PC (16:0/20:4) in terminal villi was preserved. These results suggested that the absence of the specific distribution of PC (16:0/20:4) in terminal villi, possibly in combination with the absence of SM (d18:1/16:0) in stem villi, was linked to placental morphological changes in response to maternal underperfusion of the placenta.
Description: 浜松医科大学学位論文 医博第722号(平成28年3月14日)
URI: http://hdl.handle.net/10271/3144
DOI: Info:doi/10.1371/journal.pone.0142609
PubMed ID: info:pmid/26569622
Academic Degrees and number: 13802甲第722号
Degree-granting date: 2016-03-14
Degree name: 博士(医学)
Degree-granting institutions: 浜松医科大学
Appears in Collections:2010 博士(論文)

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