Somatolactin (SL), the latest member of the growth hormone/prolactin family, is a novel pituitary hormone with diverse functions. At present, SL can be identified only in fish but not in tetrapods and its regulation at the pituitary level has not been fully characterized. Using grass carp as a model, we examined the direct effects of pituitary adenylate cyclase-activating polypeptide (PACAP) on SL secretion and synthesis at the pituitary cell level. As a first step, the structural identity of grass carp SL, SLalpha and SLbeta, was established by 5'/3'-rapid amplification of cDNA ends. These two SL isoforms are single-copy genes and are expressed in two separate populations of pituitary cells located in the pars intermedia. In the carp pituitary, PACAP nerve fibers were detected in the nerve tracts of the neurohypophysis and extended into the vicinity of pituitary cells forming the pars intermedia. In primary cultures of grass carp pituitary cells, PACAP was effective in stimulating SL release, cellular SL content, and total SL production. The increase in SL production also occurred with parallel rises in SLalpha and SLbeta mRNA levels. With the use of a combination of molecular and pharmacological approaches, PACAP-induced SL release and SL gene expression were shown to be mediated by pituitary PAC-I receptors. These findings, as a whole, suggest that PACAP may serve as a hypophysiotropic factor in fish stimulating SL secretion and synthesis at the pituitary level. Apparently, PACAP-induced SL production is mediated by upregulation of SLalpha and SLbeta gene expression through activation of PAC-I receptors.
MicroRNA-16 (miR-16) has been demonstrated to regulate proliferation and apoptosis in many types of cancers, but its biological function in bladder cancer remains unknown. Here, we found expression of miR-16 to be downregulated in bladder cancer in comparison with the adjacent normal tissues. Enforced expression of miR-16 was able to inhibit cell proliferation in TCHu-1 cells, in line with results for miR-16 antisense oligonucleotides (antisense miR-16). At the molecular level, our results further revealed that cyclin D1 expression was negatively regulated by miR-16. Therefore, the data reported here demonstrate that miR-16 is an important regulator in bladder cancer, which will contribute to better understanding of important mis-regulated miRNAs.
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