Heart-targeted overexpression of Nip3a in zebrafish embryos causes abnormal heart development and cardiac dysfunction

Wang, Wen-Der; Huang, Chang‐Jen; Lu, Yu-Fen; Hsin, Jin-Ping; Prabhakar, V; Cheng, Ching Feng; Hwang, Sheng-Ping L.

doi:10.1016/j.bbrc.2006.06.174

Cited by 14 publications

(10 citation statements)

References 42 publications

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“…Recent investigations from another research team coincide well with ours: they transiently expressed a pro-apoptotic protein, Nip3a, by a heart-specific BMP4 promoter in zebrafish embryos, further revealed the absence of a proper atrioventricular boundary and no endocardial cells lining this region. In addition, induced apoptotic myocardium cells were clustered in the presumptive atrioventricular boundary as well as in the adjacent atrium of Nip3a-overexpressing embryo (Wang et al, 2006). In our work, apoptosis in the right auricle adjacent to atrial septum may reflect the status of atrial septum from osASD patients.…”

Section: Discussionmentioning

confidence: 64%

Cardiomyocyte apoptosis in the right auricle of patients with ostium secundum atrial septal defect diseases

et al. 2007

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Section: Discussionmentioning

confidence: 64%

Cardiomyocyte apoptosis in the right auricle of patients with ostium secundum atrial septal defect diseases

et al. 2007

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“…The ECs undergo further remodeling to form the actual valve leaflets at the AV boundary. Many aspects of this process have been observed directly and recently reported ( Bartman et al , 2004 ; Beis et al , 2005 ; Hu et al , 2000 ; Hurlstone et al , 2003 ; Stainier et al , 2002 ; Wang et al , 2006 )…”

mentioning

confidence: 77%

2,3,7,8-Tetrachlorodibenzo-p-dioxin Exposure Prevents Cardiac Valve Formation in Developing Zebrafish

Mehta

Peterson

Heideman

2008

Toxicological Sciences

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Cardiovascular malformations are one of the most common congenital birth defects observed in humans. Defects in cardiac valves disrupt normal blood flow. Zebrafish are an outstanding experimental model for studying the effects that environmental contaminants have on developmental processes. Previous research has shown that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes blood regurgitation in the heart and reduces peripheral blood flow in embryonic zebrafish, suggesting some form of valve failure. To test this we used video microscopy to examine valve function and structure in developing zebrafish exposed to TCDD. TCDD exposure produced blood regurgitation at both the atrioventricular (AV) and bulboventricular (BV) junctions. In marked contrast to control embryos exposed to the vehicle dimethyl sulfoxide, embryos exposed to TCDD failed to form valve leaflets as the heart matured. In addition, whereas TCDD did not block initial formation of the bulbus arteriosus, we found that TCDD exposure prevented the normal growth and development of this portion of the outflow tract. TCDD altered the localization of endothelial cells at the AV and BV junctions and altered the localized expression of mRNAs bmp4 and notch1b normally associated with the nascent valves. Taken together, our results demonstrate that although TCDD does not prevent the initial specification of the presumptive valve locations, TCDD exposure produces severe alterations in valve development, leading to blood regurgitation and failing circulation in the developing zebrafish.

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“…The following in situ probes were used: cas [37], cmlc2 [38], fgfr2 [ 36 ], foxA3 [39], foxj1a [25], lefty1 and spaw (both were provided by Dr. Karuna Sampath, The National University of Singapore), and pitx2c [40]. The DIG-labeled probes were generated by in vitro transcription using a DIG RNA labeling kit (Roche).…”

Section: Methodsmentioning

confidence: 99%

A Variant of Fibroblast Growth Factor Receptor 2 (Fgfr2) Regulates Left-Right Asymmetry in Zebrafish

et al. 2011

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Many organs in vertebrates are left-right asymmetrical located. For example, liver is at the right side and stomach is at the left side in human. Fibroblast growth factor (Fgf) signaling is important for left-right asymmetry. To investigate the roles of Fgfr2 signaling in zebrafish left-right asymmetry, we used splicing blocking morpholinos to specifically block the splicing of fgfr2b and fgfr2c variants, respectively. We found that the relative position of the liver and the pancreas were disrupted in fgfr2c morphants. Furthermore, the left-right asymmetry of the heart became random. Expression pattern of the laterality controlling genes, spaw and pitx2c, also became random in the morphants. Furthermore, lefty1 was not expressed in the posterior notochord, indicating that the molecular midline barrier had been disrupted. It was also not expressed in the brain diencephalon. Kupffer's vesicle (KV) size became smaller in fgfr2c morphants. Furthermore, KV cilia were shorter in fgfr2c morphants. We conclude that the fgfr2c isoform plays an important role in the left-right asymmetry during zebrafish development.

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Heart-targeted overexpression of Nip3a in zebrafish embryos causes abnormal heart development and cardiac dysfunction

Cited by 14 publications

References 42 publications

Cardiomyocyte apoptosis in the right auricle of patients with ostium secundum atrial septal defect diseases

Cardiomyocyte apoptosis in the right auricle of patients with ostium secundum atrial septal defect diseases

2,3,7,8-Tetrachlorodibenzo-p-dioxin Exposure Prevents Cardiac Valve Formation in Developing Zebrafish

A Variant of Fibroblast Growth Factor Receptor 2 (Fgfr2) Regulates Left-Right Asymmetry in Zebrafish

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