Junjun Shu, ShiXin Lin, Yuehua Wu, Jun Zhu, X. Zou, Hong Zhu, Jun Gao
{"title":"ITGB3和PPIF质粒构建对宫内粘连大鼠子代影响的机制及生物信息学分析","authors":"Junjun Shu, ShiXin Lin, Yuehua Wu, Jun Zhu, X. Zou, Hong Zhu, Jun Gao","doi":"10.1166/sam.2023.4500","DOIUrl":null,"url":null,"abstract":"This study aimed to develop an animal model of pathologic regeneration of intrauterine adhesions (IUA) and assess the impact of ITGB3 and PPIF plasmid construction on the offspring of rats with IUA. Thirty female SD rats were divided into an experimental group and a control group. In\n the experimental group, the rats’ left and right endometrium underwent mild and severe mechanical damage using a self-made curette. The control group underwent a sham operation without endometrial injury. At various time points after surgery, uteruses were collected for analysis. Immunohistochemical\n staining was performed to evaluate changes in major histocompatibility complex II molecule (MHC II) and 5-bromodeoxyuridine (BrdU) in endometrial cells. The study observed the inflammatory and hyperplastic changes in endometrial tissue and the repair process in rats with different endometrial\n gland injuries. RNA interference (RNAi) sequences targeting the rat PPIF gene were designed and cloned into a lentivirus vector transfer plasmid, ITGB3. The number of endometrial glands decreased with increased mechanical injury. The PPIF short hairpin RNA (shRNA) fragment was successfully\n cloned into the lentiviral vector. After mild mechanical injury, the endometrial tissue regenerated to a basic repair level, while severe mechanical injury led to incomplete repair and tissue fibrosis, resulting in IUA.","PeriodicalId":21671,"journal":{"name":"Science of Advanced Materials","volume":null,"pages":null},"PeriodicalIF":0.9000,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The Mechanism of ITGB3 and PPIF Plasmid Construction on the Offspring of Rats with Intrauterine Adhesion and Bioinformatics Analysis\",\"authors\":\"Junjun Shu, ShiXin Lin, Yuehua Wu, Jun Zhu, X. Zou, Hong Zhu, Jun Gao\",\"doi\":\"10.1166/sam.2023.4500\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"This study aimed to develop an animal model of pathologic regeneration of intrauterine adhesions (IUA) and assess the impact of ITGB3 and PPIF plasmid construction on the offspring of rats with IUA. Thirty female SD rats were divided into an experimental group and a control group. In\\n the experimental group, the rats’ left and right endometrium underwent mild and severe mechanical damage using a self-made curette. The control group underwent a sham operation without endometrial injury. At various time points after surgery, uteruses were collected for analysis. Immunohistochemical\\n staining was performed to evaluate changes in major histocompatibility complex II molecule (MHC II) and 5-bromodeoxyuridine (BrdU) in endometrial cells. The study observed the inflammatory and hyperplastic changes in endometrial tissue and the repair process in rats with different endometrial\\n gland injuries. RNA interference (RNAi) sequences targeting the rat PPIF gene were designed and cloned into a lentivirus vector transfer plasmid, ITGB3. The number of endometrial glands decreased with increased mechanical injury. The PPIF short hairpin RNA (shRNA) fragment was successfully\\n cloned into the lentiviral vector. After mild mechanical injury, the endometrial tissue regenerated to a basic repair level, while severe mechanical injury led to incomplete repair and tissue fibrosis, resulting in IUA.\",\"PeriodicalId\":21671,\"journal\":{\"name\":\"Science of Advanced Materials\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.9000,\"publicationDate\":\"2023-07-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Science of Advanced Materials\",\"FirstCategoryId\":\"88\",\"ListUrlMain\":\"https://doi.org/10.1166/sam.2023.4500\",\"RegionNum\":4,\"RegionCategory\":\"材料科学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Science of Advanced Materials","FirstCategoryId":"88","ListUrlMain":"https://doi.org/10.1166/sam.2023.4500","RegionNum":4,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
The Mechanism of ITGB3 and PPIF Plasmid Construction on the Offspring of Rats with Intrauterine Adhesion and Bioinformatics Analysis
This study aimed to develop an animal model of pathologic regeneration of intrauterine adhesions (IUA) and assess the impact of ITGB3 and PPIF plasmid construction on the offspring of rats with IUA. Thirty female SD rats were divided into an experimental group and a control group. In
the experimental group, the rats’ left and right endometrium underwent mild and severe mechanical damage using a self-made curette. The control group underwent a sham operation without endometrial injury. At various time points after surgery, uteruses were collected for analysis. Immunohistochemical
staining was performed to evaluate changes in major histocompatibility complex II molecule (MHC II) and 5-bromodeoxyuridine (BrdU) in endometrial cells. The study observed the inflammatory and hyperplastic changes in endometrial tissue and the repair process in rats with different endometrial
gland injuries. RNA interference (RNAi) sequences targeting the rat PPIF gene were designed and cloned into a lentivirus vector transfer plasmid, ITGB3. The number of endometrial glands decreased with increased mechanical injury. The PPIF short hairpin RNA (shRNA) fragment was successfully
cloned into the lentiviral vector. After mild mechanical injury, the endometrial tissue regenerated to a basic repair level, while severe mechanical injury led to incomplete repair and tissue fibrosis, resulting in IUA.