Sexual size dimorphism has been observed in European eel and

Sexual size dimorphism has been observed in European eel and half-smooth tongue sole (Cynoglossus semilaevis), as females have a faster growth rate than males, (Degani, G., et al., 2003, Ma, Q., et al., 2012). Ma et al. 2011 reported that the mRNA level of GH was higher in the pituitary gland of both female European eels and half-smooth tongue sole compared to adult males. In addition, the expressions of GH, IGF-1 and IGF-2 in females were significantly higher than males in the post-larval and juvenile stages. Moreover, the concentration of serum IGF-I in mature females was also significantly higher than that of males in half-smooth tongue sole. In our studies, we observed that all the expressions of GH, IGF-1, IGF-2, ghrelin and GHSR in male larval fish were higher than female (Fig. 5) (Ma et al. 2015). Similarly, the expressions of ghrelin and GHSR in hypothalamus and gut of male yellow catfish were higher than female (Fig. 4a and b). Moreover, the expressions of ghrelin and GHSR were observably increased in short and long-term fasting groups compared to their control (Figs. 7 and 8). These results suggested that Ghrelin may act as an orexigenic hormone, like in goldfish (Unniappan, S., et al., 2002, Matsuda, K., et al., 2006, Miura, T., et al., 2009), sea bass (Terova et al. 2008) and zebrafish (Amole and Unniappan 2009). Interestingly, we have found significantly higher Galanthamine level of ghrelin and GHSR in male fish of fasting group than female, during both short and long-term experiments (Fig. 8). Our data indicated that male fish may have better appetite than female in fasting stage, indicating that ghrelin and its receptor GHSR may be induced in response to fasting and may increase food intake and body weight in yellow catfish. Along with appetite stimulation, ghrelin also regulates pituitary GH secretion, GH-releasing hormone and somatostatin (Tschop et al. 2000). Some studies reported that ghrelin specifically stimulates pituitary GH secretion in mammals, though the effect is different in fishes. In tilapia, treatment with ghrelin-C10 significantly increased body weight but couldn't stimulate GH or IGF-I release (Riley et al. 2005). The similar expression patterns between ghrelin/GHSR and GH/IGF axis genes reveals that ghrelin and its receptor GHSR may be involved in the sex biased expression of GH/IGF signaling regulated by sex hormone. Accordingly, we observed that both ghrelin and GHSR expressions were induced after MT treatment. However, long-term MT treatment inhibited ghrelin expression in male fish (Fig. 6c). Similar to the expression of GH, IGF-1 and IGF-2 in male larval fish (Ma et al. 2015), overdose of androgens reduced expression level of genes related to body growth and food intake. In conclusion, our results suggest that MT exerted androgenic effect to promote ghrelin and GHSR expression. Sex difference in growth performance between males and females is probably caused by the expression difference of ghrelin and its receptor GHSR, by regulating feeding and GH/IGF signaling in yellow catfish. The following are the supplementary data related to this article.
Competing interests
Acknowledgments This work was supported by the Fundamental Research Funds for the Central Universities (2662015PY101, 2662015PY072, 2013PY068) and the National Natural Science Foundation of China (31301931). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Introduction Percutaneous coronary intervention (PCI) has been a widely used treatment for ischemic heart disease due to atherosclerosis. However, renarrowing of the treated arteries, known as restenosis still remains a great challenge in a long-term. The pathogeneses of restenosis following mechanical injury of endothelium involve a cascade of processes including platelet aggregation, inflammatory cell infiltration, and the release of growth factors and chemokiens, leading to the phenotypic changes, migration and proliferation of smooth muscle cells, and the synthesis and deposition of proteoglycan, and other extracellular matrix components, leading to neointimal hyperplasia, and vessel remodeling [1], [2].