Cdc42 deletion yielded enamel defects by disrupting mitochondria and producing reactive oxygen species in dental epithelium
作者机构：Hospital of StomatologyGuanghua School of StomatologyGuangdong Provincial Key Laboratory of StomatologySun Yat-sen UniversityGuangzhouGuangdong 510055China Guangdong Provincial Key Laboratory of Oral DiseasesGuangzhouGuangdong 510055China Department of Cariology and EndodontologyPeking University School and Hospital of Stomatology&National Center for Stomatology&National Clinical Research Center for Oral Diseases&National Engineering Research Center of Oral Biomaterials and Digital Medical DevicesBeijing 100081China Department of Oral and Maxillofacial SurgeryUniversity at BuffaloBuffaloNY 14214USA Department of OrthodonticsStomatological HospitalSouthern Medical UniversityGuangzhouGuangdong 510280China
出 版 物：《Genes & Diseases》 (基因与疾病（英文）)
年 卷 期：2024年第11卷第5期
页 面：335-349页
核心收录：
基 金：the National Natural Science Foundation of China(No.81900958,82170987,82073378,81974146,82101053) the Natural Science Foundation of Guangdong Province,China(No.2020A1515-010059,2021A1515012535) Sun Yat-Sen University Clinical Research 5010 Program(No.2023009) Science and Technology Planning Project of Guangzhou,China(No.2023-A04J2148) Open Funding of Guangdong Provincial Key Laboratory of Stomatology(China)(No.KF2021120104)
主 题：Cdc42 Enamel defects Mitochondrial dysfunction Rho GTPase Tooth repair
摘 要：Developmental defects of enamel are common due to genetic and environmental factors before and after ***42,a Rho family small GTPase,regulates prenatal tooth development in ***,its role in postnatal tooth development,especially enamel formation,remains ***,we investigated Cdc42 functions in mouse enamel development and tooth repair after ***42 showed highly dynamic temporospatial patterns in the developing incisors,with robust expression in ameloblast and odontoblast ***,epithelium-specific Cdc42 deletion resulted in enamel defects in *** differentiation was inhibited,and hypomineralization of enamel was observed upon epithelial Cdc42 *** analysis showed that abnormal mitochondrial components,phosphotransferase activity,and ion channel regulator activity occurred in the Cdc42 mutant dental *** oxygen species accumulation was detected in the mutant mice,suggesting that abnormal oxidative stress occurred after Cdc42 ***,Cdc42 mutant mice showed delayed tooth repair and generated less calcified *** dysfunction and abnormal oxygen consumption were evidenced by reduced Apool and Timm8a1 expression,increased Atp5j2 levels,and reactive oxygen species overproduction in the mutant repair ***-specific Cdc42 deletion attenuated ERK1/2 signaling in the labial cervical *** Sox2 expression in the mutant labial cervical loop after clipping might lead to delayed tooth *** findings suggested that mitochondrial dysfunction,up-regulated oxidative stress,and abnormal ion channel activity may be among multiple factors responsible for the observed enamel defects in Cdc42 mutant ***,Cdc42 exerts multidimensional and pivotal roles in enamel development and is particularly required for ameloblast differentiation and enamel matrix formation.
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