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The Mitochondrial Thioredoxin is Required for Liver Development in Zebrafish
Zhang, J.1,2; Cui, X.2; Wang, L.1; Liu, F.1; Jiang, T.1; Li, C.1; Li, D.1; Huang, M.1; Liao, S.1; Wang, J.1; Chen, J.1; Jia, H.1; He, J.3; Tang, Z.1; Yin, Z.3; Liu, M.1
2014
Source PublicationCURRENT MOLECULAR MEDICINE
ISSN1566-5240
Volume14Issue:6Pages:772-782
AbstractThioredoxins (Trxs) are a class of small molecular redox proteins that play an important role in scavenging abnormally accumulated reactive oxygen species (ROS). Thioredoxin 2 (Trx2) is one member of this family located in mitochondria. Trx2 protects cells from increased oxidative stress and has anti-apoptosis function. Knockout of Trx2 in mice led to early embryonic lethality. However, the essential role of Trx2 during embryogenesis remains unclear. To further investigate the role of Trx2 during embryonic development, we performed Trx2 knockdown in zebrafish and investigated the regulation role of Trx2 during embryonic development. Our results indicate that Trx2 had a high expression in early zebrafish embryos and its knockdown in zebrafish led to defective liver development mainly due to increased hepatic cell death. The increased ROS and the imbalance of members of the Bcl-2 family were involved in cell death induced by Trx2 suppression in zebrafish. The dysregulation of Bax, puma and Bcl-xl promoted the reduction of mitochondrial trans-membrane potential and the mitochondria membrane permeabilization (MMP), which initiated the mitochondrial apoptosis pathway. Additionally, we found that the increase of relocated GAPDH in mitochondria may be another factor responsible for the mitochondrial catastrophe.
SubtypeArticle
KeywordApoptosis Bcl-2 Family Liver Morphogenesis Mpp Trx2 Zebrafish
WOS HeadingsScience & Technology ; Life Sciences & Biomedicine
Indexed BySCI
Language英语
WOS Research AreaResearch & Experimental Medicine
WOS SubjectMedicine, Research & Experimental
WOS IDWOS:000341015600007
WOS KeywordOUTER-MEMBRANE PERMEABILIZATION ; CELL-DEATH ; GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE ; OXIDATIVE STRESS ; APOPTOSIS ; BAX ; NUCLEAR ; PUMA ; EXPRESSION ; REDUCTASE
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Cited Times:5[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Identifierhttp://ir.ihb.ac.cn/handle/342005/20390
Collection水生生物分子与细胞生物学研究中心_期刊论文
Affiliation1.Huazhong Univ Sci & Technol, Coll Life Sci & Technol, Ctr Human Genome Res, Key Lab Mol Biophys,Minist Educ, Wuhan 430074, Hubei, Peoples R China
2.Henan Univ, Coll Med, Inst Immunol, Key Lab Cellular & Mol Immunol, Kaifeng, Henan, Peoples R China
3.Chinese Acad Sci, Inst Hydrobiol, Wuhan 430072, Hubei, Peoples R China
Recommended Citation
GB/T 7714
Zhang, J.,Cui, X.,Wang, L.,et al. The Mitochondrial Thioredoxin is Required for Liver Development in Zebrafish[J]. CURRENT MOLECULAR MEDICINE,2014,14(6):772-782.
APA Zhang, J..,Cui, X..,Wang, L..,Liu, F..,Jiang, T..,...&Liu, M..(2014).The Mitochondrial Thioredoxin is Required for Liver Development in Zebrafish.CURRENT MOLECULAR MEDICINE,14(6),772-782.
MLA Zhang, J.,et al."The Mitochondrial Thioredoxin is Required for Liver Development in Zebrafish".CURRENT MOLECULAR MEDICINE 14.6(2014):772-782.
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