{"title":"ELK1-CDKL5-Rac1信号通路调控内皮细胞迁移，促进纳米铌颗粒诱导的血管生成","authors":"Xiao-He Zhou, Min-Hua Mo, Zi-Wei Chen, Wen-Jing Liu, Yan-Li Zhang, Janak L. Pathak, Li-Jing Wang, Chang Liu, Long-Quan Shao, Liang-Jiao Chen","doi":"10.1007/s12598-024-02939-8","DOIUrl":null,"url":null,"abstract":"<div><p>Promotion of angiogenesis is crucial for bone tissue repair, and the poor activity of angiogenic cells and growth factors is the main problem in angiogenesis. New proangiogenic nanomaterials are urgently needed to be a promising strategy for this issue. Nb promotes bone formation and fracture healing, possibly by increasing vascular endothelial growth factor (VEGF) production. Nanoniobium particles (nNb) may promote angiogenesis. However, the effect of nNb on angiogenesis is unclear, limiting its application. This study confirmed that nNb significantly promoted angiogenesis. nNb increased and Ras-related C3 botulinum toxin substrate (Rac) family small guanosine triphosphatase (GTPase) 1 (Rac1) expression, inducing F-actin aggregation at the front edge of cells and the formation of pseudopodia to mediate cell migration, further promoting angiogenesis. We discovered that cyclin-dependent kinase-like 5 (CDKL5) is a new signaling molecule that activates Rac1. V-ets erythroblastosis virus E26 oncogene homolog (ETS) domain-containing protein (ELK1), regulating CDKL5 and Rac1, plays an upstream regulatory role. When ELK1 was inhibited, CDKL5 and Rac1 levels were decreased. ELK1, CDKL5 or Rac1 are effective regulatory targets of angiogenesis. Inhibiting expression of ELK1, CDKL5 or Rac1 decreased angiogenesis. Thus, nNb has good angiogenic effects. The ELK1-CDKL5-Rac1 signaling pathway regulates the migration of endothelial cells to promote angiogenesis. nNb can be used in bone tissue engineering as a new nanomaterial, and it will promote the development of a new strategy for tissue engineering.</p><h3>Graphical abstract</h3>\n<div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":749,"journal":{"name":"Rare Metals","volume":"44 1","pages":"444 - 460"},"PeriodicalIF":9.6000,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"ELK1-CDKL5-Rac1 signaling pathway regulates the migration of endothelial cells to promote angiogenesis induced by nanoniobium particles\",\"authors\":\"Xiao-He Zhou, Min-Hua Mo, Zi-Wei Chen, Wen-Jing Liu, Yan-Li Zhang, Janak L. Pathak, Li-Jing Wang, Chang Liu, Long-Quan Shao, Liang-Jiao Chen\",\"doi\":\"10.1007/s12598-024-02939-8\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Promotion of angiogenesis is crucial for bone tissue repair, and the poor activity of angiogenic cells and growth factors is the main problem in angiogenesis. New proangiogenic nanomaterials are urgently needed to be a promising strategy for this issue. Nb promotes bone formation and fracture healing, possibly by increasing vascular endothelial growth factor (VEGF) production. Nanoniobium particles (nNb) may promote angiogenesis. However, the effect of nNb on angiogenesis is unclear, limiting its application. This study confirmed that nNb significantly promoted angiogenesis. nNb increased and Ras-related C3 botulinum toxin substrate (Rac) family small guanosine triphosphatase (GTPase) 1 (Rac1) expression, inducing F-actin aggregation at the front edge of cells and the formation of pseudopodia to mediate cell migration, further promoting angiogenesis. We discovered that cyclin-dependent kinase-like 5 (CDKL5) is a new signaling molecule that activates Rac1. V-ets erythroblastosis virus E26 oncogene homolog (ETS) domain-containing protein (ELK1), regulating CDKL5 and Rac1, plays an upstream regulatory role. When ELK1 was inhibited, CDKL5 and Rac1 levels were decreased. ELK1, CDKL5 or Rac1 are effective regulatory targets of angiogenesis. Inhibiting expression of ELK1, CDKL5 or Rac1 decreased angiogenesis. Thus, nNb has good angiogenic effects. The ELK1-CDKL5-Rac1 signaling pathway regulates the migration of endothelial cells to promote angiogenesis. nNb can be used in bone tissue engineering as a new nanomaterial, and it will promote the development of a new strategy for tissue engineering.</p><h3>Graphical abstract</h3>\\n<div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>\",\"PeriodicalId\":749,\"journal\":{\"name\":\"Rare Metals\",\"volume\":\"44 1\",\"pages\":\"444 - 460\"},\"PeriodicalIF\":9.6000,\"publicationDate\":\"2024-08-13\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Rare Metals\",\"FirstCategoryId\":\"88\",\"ListUrlMain\":\"https://link.springer.com/article/10.1007/s12598-024-02939-8\",\"RegionNum\":1,\"RegionCategory\":\"材料科学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"MATERIALS SCIENCE, MULTIDISCIPLINARY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Rare Metals","FirstCategoryId":"88","ListUrlMain":"https://link.springer.com/article/10.1007/s12598-024-02939-8","RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"MATERIALS SCIENCE, MULTIDISCIPLINARY","Score":null,"Total":0}
ELK1-CDKL5-Rac1 signaling pathway regulates the migration of endothelial cells to promote angiogenesis induced by nanoniobium particles
Promotion of angiogenesis is crucial for bone tissue repair, and the poor activity of angiogenic cells and growth factors is the main problem in angiogenesis. New proangiogenic nanomaterials are urgently needed to be a promising strategy for this issue. Nb promotes bone formation and fracture healing, possibly by increasing vascular endothelial growth factor (VEGF) production. Nanoniobium particles (nNb) may promote angiogenesis. However, the effect of nNb on angiogenesis is unclear, limiting its application. This study confirmed that nNb significantly promoted angiogenesis. nNb increased and Ras-related C3 botulinum toxin substrate (Rac) family small guanosine triphosphatase (GTPase) 1 (Rac1) expression, inducing F-actin aggregation at the front edge of cells and the formation of pseudopodia to mediate cell migration, further promoting angiogenesis. We discovered that cyclin-dependent kinase-like 5 (CDKL5) is a new signaling molecule that activates Rac1. V-ets erythroblastosis virus E26 oncogene homolog (ETS) domain-containing protein (ELK1), regulating CDKL5 and Rac1, plays an upstream regulatory role. When ELK1 was inhibited, CDKL5 and Rac1 levels were decreased. ELK1, CDKL5 or Rac1 are effective regulatory targets of angiogenesis. Inhibiting expression of ELK1, CDKL5 or Rac1 decreased angiogenesis. Thus, nNb has good angiogenic effects. The ELK1-CDKL5-Rac1 signaling pathway regulates the migration of endothelial cells to promote angiogenesis. nNb can be used in bone tissue engineering as a new nanomaterial, and it will promote the development of a new strategy for tissue engineering.
期刊介绍：
Rare Metals is a monthly peer-reviewed journal published by the Nonferrous Metals Society of China. It serves as a platform for engineers and scientists to communicate and disseminate original research articles in the field of rare metals. The journal focuses on a wide range of topics including metallurgy, processing, and determination of rare metals. Additionally, it showcases the application of rare metals in advanced materials such as superconductors, semiconductors, composites, and ceramics.
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