Transcriptomic responses of marine medaka’s ovary to hypoxia

•Hypoxia deregulates 287 genes in ovary of medaka.•Hypoxia impairs fish ovarian follicle development and steroid metabolic process.•Hypoxia causes activations of FSH and IGF1R, and inhibition of LIF. Hypoxia, an endocrine disruptor, is pressing global problem affecting marine organisms in over 400 “...

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Veröffentlicht in:Aquatic toxicology 2016-08, Vol.177, p.476-483
Hauptverfasser: Lai, Keng Po, Li, Jing Woei, Tse, Anna Chung Kwan, Cheung, Angela, Wang, Simon, Chan, Ting Fung, Kong, Richard Yuen Chong, Wu, Rudolf Shiu Sun
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Sprache:eng
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Zusammenfassung:•Hypoxia deregulates 287 genes in ovary of medaka.•Hypoxia impairs fish ovarian follicle development and steroid metabolic process.•Hypoxia causes activations of FSH and IGF1R, and inhibition of LIF. Hypoxia, an endocrine disruptor, is pressing global problem affecting marine organisms in over 400 “Dead Zones” worldwide. There is growing evident demonstrated the disruptive effect of hypoxia on reproductive systems of marine fish through the impairments of steroidogenic gene expression, leading to the alteration of sex hormone production in gonads. But the detailed molecular mechanism underlying the responses of female reproductive systems to hypoxic stress remains largely unknown. In the present report, we used marine medaka Oryzias melastigma as a model, together with high-throughput transcriptome sequencing and bioinformatics analysis, aiming to determine the changes in transcriptional signature in the ovary of marine fish under hypoxic stress. Our result discovered over two hundred differential expressed genes in ovary in response to hypoxia. The bioinformatics analysis together with quantitative RT-PCR validation on the deregulated genes highlighted the dysregulations of a number of female reproductive functions including interruptions of ovarian follicle development, gonad development and steroid metabolic process. Additionally, we revealed that these deregulations are through the modulation of leukemia inhibitory factor (LIF), insulin-like growth factor 1 receptor (IGF1R) and follicle stimulating hormone (FSH). The result of this work complements previous studies and provides additional insights into the underlying molecular mechanism of hypoxia-induced impairment of female reproductive system.
ISSN:0166-445X
1879-1514
DOI:10.1016/j.aquatox.2016.06.023