Anti-apoptotic effects of IGF-I on mortality and dysmorphogenesis in <Emphasis Type="Italic">tbx5</Emphasis>-deficient zebrafish embryos |
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Authors: | Tzu-Chun Tsai Chun-Che Shih Hsin-Ping Chien An-Hang Yang Jenn-Kan Lu Jen-Her Lu |
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Institution: | 1.Institutes of Clinical Medicine, School of Medicine,National Yang-Ming University,Taipei,Taiwan, Republic of China;2.Departments of Surgery, Pediatrics and Pathology, Veterans General Hospital-Taipei,Taipei,Taiwan, Republic of China;3.Laboratory of Molecular Biology, Institute of Aquaculture,National Taiwan Ocean University,Keelung,Taiwan, Republic of China;4.Department of Pediatrics, Veterans General Hospital-Taipei,Taipei,Taiwan, Republic of China |
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Abstract: | BackgroundTbx5 deficiency in zebrafish causes several abnormal phenotypes of the heart and pectoral fins. It has been reported that exogenous human growth hormone can enhance expression of downstream mediators in the growth hormone and insulin-like growth factor I (IGF-I) pathway and partially restore dysmorphogenesis in tbx5 morphants. This study aimed to further evaluate the effects of IGF-I on cell apoptosis and dysmorphogenesis in zebrafish embryos deficient for tbx5.ResultsAmong the five studied groups of zebrafish embryos (wild-type embryos WT], tbx5 morphants MO], mismatched tbx5 morpholino-treated wild-type embryos MIS], IGF-I-treated wild-type embryos WTIGF1], and IGF-I-treated tbx5 morphants MOIGF1]), the expression levels of the ifg1, igf1-ra, ifg-rb, erk1, and akt2 genes as well as the ERK and AKT proteins were significantly reduced in the MO group, but were partially restored in the MOIGF1 group. These expression levels remained normal in the WT, MIS, and WTIGF1 groups. Exogenous human IGF-I also reduced the incidence of phenotypic anomalies, decreased the expression levels of apoptotic genes and proteins, suppressed cell apoptosis, and improved survival of the MOIGF1 group.ConclusionsThese results suggest that IGF-I has an anti-apoptotic protective effect in zebrafish embryos with tbx5 deficiency. |
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