Catsper1 promoter is bidirectional and regulates the expression of a novel lncRNA.

The Catsper1 gene, whose expression is restricted to male germ cells, has great importance in reproductive biology because of its function in sperm motility and fertilization. We previously reported that the promoter of this gene has transcriptional activity in either direction in a heterologous system. In the present study, we found that the Catsper1 promoter has in vitro transcriptional activity in either orientation in GC-1 spg mouse spermatogonial cells. The results also showed that this promoter regulates the expression of a new divergent Catsper1 gene named Catsper1au (Catsper1 antisense upstream transcript). Catsper1au is expressed in adult male mouse testis and liver tissues but not in female mouse liver or ovary tissues. In the testis, Catsper1au is expressed in embryos at 11.5 days post-coitum and from newborns to adults. This gene is also expressed in 1- to 3-week postnatal hearts and in 1-week to adult stage livers. The analysis of the 1402 bp whole genome sequence revealed that Catsper1au is an intronless and polyadenylated lncRNA, located in the nuclei of Sertoli and spermatogenic cells from adult testis. These data indicate that Catsper1au is divergently expressed from the Catsper1 promoter and could regulate gene expression during spermatogenesis.

Effects of 45-nm silver nanoparticles on coronary endothelial cells and isolated rat aortic rings.

This study was undertaken to determine whether silver nanoparticles (Ag-45 nm NPs) induce selective and specific biological effects, such as induction of proliferation and nitric oxide (NO) production, and cytotoxicity in coronary endothelial cells (CECs), and regulation of vascular tone in isolated rat aortic rings. Physical characterization of Ag-45 nm NPs by transmission electron microscopy (TEM) demonstrated that nanoparticles ranging in size from 10 to 90 nm had biological effects on CECs. Increasing concentrations of Ag-45 nm NPs exerted a dual effect on cell proliferation whereby proliferation was inhibited at low concentrations of NPs and stimulated at high concentrations. The effects of high, but not low, concentrations of Ag-45 nm NPs were dependent on NO because the effects were partially blocked by N(G)-nitro-L-arginine methyl ester (L-NAME). We have also shown that high, but not low, concentrations of Ag-45 nm NPs induce NO-dependent proliferation through activation of endothelial nitric oxide synthase (eNOS) by phosphorylation of Serine 1177. Moreover, the antiproliferative and proliferative effects of Ag-45 nm NPs were concentration-dependent and inversely correlated with cellular toxicity. In isolated rat aortic rings, a low concentration of NPs induced vasoconstriction and a high concentration stimulated vasodilation. The physiologic effects induced by a low concentration of Ag-45 nm NPs inhibited acetylcholine- (ACh-) induced NO-mediated relaxation. Vasodilation induced by a high concentration of NPs was partially abolished by L-NAME pretreatment. When the endothelium was removed from the rings, all physiologic responses were blocked. These results clearly demonstrate that the NPs have selective and specific effects on the vascular endothelium in a concentration-dependent manner and suggest that opposite effects could be associated with NPs of different sizes.