Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2005: ¥1,700,000 (Direct Cost: ¥1,700,000)
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Research Abstract |
In the seawater (SW)-acclimated euryhaline fishes, the ion/water permeability of the gastrointestinal tract is generally greater than that of freshwater (FW)-acclimated fish. The esophageal epithelium of SW fishes is simple columnar in form, whereas that of FW fishes is stratified. We have previously shown that esophageal epithelium of a euryhaline goby and tilapia displays elevated cell proliferation in FW fish, but undergoes apoptosis during SW acclimation (1). In-vivo cortisol treatment of the goby stimulated not only the apoptosis but also cell proliferation in the esophageal epithelium, whereas 11-deoxycorticosterone, the putative teleostean mineralocorticoid (2), did not have any impact on cell proliferation or apoptosis (3). To understand the possible dual mode of action of cortisol on the esophageal cell turnover, we have developed a method of culture tissue explants of the esophagus from euryhaline medaka (Oryzias latipes). Oligonucleotide detection assay and an oxidation-reduction indicator were used as indicators of apoptosis and cell proliferations, respectively. Addition of cortisol (10 nM) to the culture medium for 8 days stimulated apoptosis in the medaka esophagus, as a well-established glucocorticoid function. No effects were seen at higher doses (100 and 1000 nM). On the other hand, addition of cortisol (1000 nM) for 8 days induced the cell proliferation. The response of cell proliferation was dose-dependent within physiological range (10-1000 nM). Thus, it is likely that cortisol induces directly not only apoptosis but also cell proliferation at the esophagus in euryhaline fishes, possibly via glucocorticoid receptor, since glucocorticoid receptor shows lower sensitivity for cortisol than mineralocorticoid receptor (2). References (1) Takahashi et al. (2006). J. Comp. Physiol. B, 176, 463-468. (2) Prunet et al. (2006). Gen. Comp. Endocrinol., 147, 17-23. (3) Takahashi et al. (2006). Life Sci., 79, 1873-1880.
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