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Silencing of FABP3 leads to apoptosis-induced mitochondrial dysfunction and stimulates Wnt signaling in zebrafish

  • Authors:
    • Yao-Qiu Liu
    • Gui-Xian Song
    • Hai-Lang Liu
    • Xue-Jie Wang
    • Ya-Hui Shen
    • Li-Juan Zhou
    • Jin Jin
    • Ming Liu
    • Chun-Mei Shi
    • Ling-Mei Qian

  • View Affiliations

  • Published online on: July 11, 2013     https://doi.org/10.3892/mmr.2013.1586
  • Pages: 806-812
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Abstract

Fatty acid binding protein 3 (FABP3, also termed heart‑type fatty acid binding protein) is a member of the intracellular lipid‑binding protein family that may be essential in fatty acid transport, cell growth, cellular signaling and gene transcription. Previously, we demonstrated that FABP3 was involved in apoptosis‑associated congenital cardiac malformations; however, its mechanism of regulation remains unclear. Apoptosis has increasingly been considered to be important in cardiac development. In the present study, a zebrafish model was used to investigate the involvement of FABP3‑morpholino (MO)‑induced apoptosis and mitochondrial dysfunction in cardiac development. During the early stages of cardiac development, injection of FABP3‑MO into zebrafish resulted in significant impairment in cardiac development and promoted the rate of apoptosis which was correlated with significant dysfunction of the mitochondria. For example, the ATP content was markedly decreased at 24 and 48 h post‑fertilization (pf), reactive oxygen species production was significantly enhanced at 24 and 48 h pf and the mitochondrial DNA copy number was reduced at 24, 48 and 72 h pf. Additionally, Nkx2.5 expression was upregulated in FABP3-MO zebrafish, and Wnt signaling molecules (Wnt1, Wnt5 and Wnt11) were also highly expressed in FABP3-MO zebrafish at 24, 48 and 72 h pf. In conclusion, the results indicated that FABP3 knockdown exhibited significant toxic effects on cardiac development and mitochondrial function, which may be responsible for the knockdown of FABP3‑induced apoptosis. Apoptosis was one of the mechanisms underlying this effect, and was correlated with the activation of Wnt signaling. These studies identified FABP3 as a candidate gene underlying the etiology of congenital heart defects.
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September 2013
Volume 8 Issue 3

Print ISSN: 1791-2997
Online ISSN:1791-3004

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  • Journal Metrics
  • Impact Factor: 3.4
  • Ranked Medicine Research and Experimental
    (total number of cites)
  • CiteScore: 6.9
  • CiteScore Rank: Q2: #98/328 Biochemistry, Genetics and Molecular Biology
  • Source Normalized Impact per Paper (SNIP): 0.721
  • SCImago Journal Rank (SJR): 0.65
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Spandidos Publications style
Liu Y, Song G, Liu H, Wang X, Shen Y, Zhou L, Jin J, Liu M, Shi C, Qian L, Qian L, et al: Silencing of FABP3 leads to apoptosis-induced mitochondrial dysfunction and stimulates Wnt signaling in zebrafish. Mol Med Rep 8: 806-812, 2013
APA
Liu, Y., Song, G., Liu, H., Wang, X., Shen, Y., Zhou, L. ... Qian, L. (2013). Silencing of FABP3 leads to apoptosis-induced mitochondrial dysfunction and stimulates Wnt signaling in zebrafish. Molecular Medicine Reports, 8, 806-812. https://doi.org/10.3892/mmr.2013.1586
MLA
Liu, Y., Song, G., Liu, H., Wang, X., Shen, Y., Zhou, L., Jin, J., Liu, M., Shi, C., Qian, L."Silencing of FABP3 leads to apoptosis-induced mitochondrial dysfunction and stimulates Wnt signaling in zebrafish". Molecular Medicine Reports 8.3 (2013): 806-812.
Chicago
Liu, Y., Song, G., Liu, H., Wang, X., Shen, Y., Zhou, L., Jin, J., Liu, M., Shi, C., Qian, L."Silencing of FABP3 leads to apoptosis-induced mitochondrial dysfunction and stimulates Wnt signaling in zebrafish". Molecular Medicine Reports 8, no. 3 (2013): 806-812. https://doi.org/10.3892/mmr.2013.1586