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EGF receptor kinase suppresses ciliogenesis through activation of USP8 deubiquitinase

Chemokines protect vascular smooth muscle cells from cell death induced by cyclic mechanical stretch.

New photic stimulating system with white light-emitting diodes to elicit electroretinograms from zebrafish larvae.

Potential protective function of the sterol regulatory element binding factor 1-fatty acid desaturase 12 axis in early-stage age-related macular degeneration

Activation of Sterol Regulatory Element Binding Factors by Fenofibrate and Gemfibrozil Stimulates Myelination in Zebrafish

tDNA Damage Response Is Involved in the Developmental Toxicity of Mebendazole in Zebrafish Retina


Front Pharmacol. 2016 Mar 14;7:57. doi: 10.3389/fphar.2016.00057. eCollection 2016.
DNA Damage Response Is Involved in the Developmental Toxicity of Mebendazole in Zebrafish Retina.
Sasagawa S, Nishimura Y, Kon T, Yamanaka Y, Murakami S, Ashikawa Y, Yuge M, Okabe S, Kawaguchi K, Kawase R, Tanaka T.

Intestinal helminths cause iron-deficiency anemia in pregnant women, associated with premature delivery, low birth weight, maternal ill health, and maternal death. Although benzimidazole compounds such as mebendazole (MBZ) are highly efficacious against helminths, there are limited data on its use during pregnancy. In this study, we performed in vivo imaging of the retinas of zebrafish larvae exposed to MBZ, and found that exposure to MBZ during 2 and 3 days post-fertilization caused malformation of the retinal layers. To identify the molecular mechanism underlying the developmental toxicity of MBZ, we performed transcriptome analysis of zebrafish eyes. The analysis revealed that the DNA damage response was involved in the developmental toxicity of MBZ. We were also able to demonstrate that inhibition of ATM significantly attenuated the apoptosis induced by MBZ in the zebrafish retina. These results suggest that MBZ causes developmental toxicity in the zebrafish retina at least partly by activating the DNA damage response, including ATM signaling, providing a potential adverse outcome pathway in the developmental toxicity of MBZ in mammals.