Differential data on the responsiveness of multiple cell types to cell death induced by non-thermal atmospheric pressure plasma-activated solutions.

A discovery that cells die of a novel and distinctive process, along with some characteristic events, such as cellular shrinkage and Programmed cell death 4 disappearance, has been done by using non-thermal atmospheric pressure plasma-activated solutions [1]. Data on the responsiveness of multiple cell types to the induction of cellular shrinkage and cell death and the loss of Programmed cell death 4 by exposure to the non-thermal atmospheric pressure plasma-activated solutions were collected. Human neuroblastoma SH-SY5Y cells, murine myoblast C2C12 cells, and murine embryonic fibroblasts were cultured for various periods in each of the non-thermal atmospheric pressure plasma-activated solutions and then examined by light field microscopic observation for their effects on cell morphology, by Trypan blue dye exclusion assay for those on cell death, and by Western blotting for those on Programmed cell death 4 disappearance. The data clarified some differences in the responsiveness to the induction of cellular shrinkage, cell death, and Pdcd4 disappearance by all the non-thermal atmospheric pressure plasma-activated solutions among the cells.

A novel and distinctive mode of cell death revealed by using non-thermal atmospheric pressure plasma: The involvements of reactive oxygen species and the translation inhibitor Pdcd4.

Cells death is indispensable for embryonic development, tissue homeostasis, and the elimination of cancer, virally infected, or degenerated cells in multicellular organisms. It occurs not only via existing modes but also via unidentified modes, whose elucidation requires. Exposure to non-thermal atmospheric pressure plasma (NTAPP) has been demonstrated to induce cell death, probably because of its ability to generate reactive oxygen species (ROS). However, the mode of this cell death and its underlying mechanism remained elusive. Here we show cell death occurring in a novel and distinctive mode different from apoptosis and necrosis/necroptosis through a mechanism that ROS mediate the loss of the translation inhibitor Programmed cell death 4 (Pdcd4) when cells are cultured in solutions activated by NTAPP irradiation. Thus, our study performed with NTAPP-activated solutions may provide insight into the existence of the atypical cell death in cells and some features of its distinguishing mode and underlying mechanism.

Asymmetrical allocation of JAK1 mRNA during spermatogonial stem cell division in Xenopus laevis.

During Xenopus spermatogenesis, each primary spermatogonium (PG), the largest single cell in the testis, undergoes mitotic divisions with a concomitant decrease in size to produce smaller differentiating spermatogonia. The spermatogonial stem cells (SSCs) occur in this PG population. Taking advantage of identifiable and isolatable properties of Xenopus SSCs, we examined JAK1 gene expression during the spermatogenesis because there have been reports on the important role of JAK/STAT pathway in regulating the status of SSCs in Drosophila and mouse. Surprisingly, in situ hybridization revealed the presence of JAK1 mRNA in the differentiating spermatogonia and primary spermatocytes as well as some PGs. Inhibition of JAK1 activity in the testis caused a decrease in percentage of BrdU-incorporating spermatogonia, suggesting that JAK1 was at least involved in regulation of spermatogonial proliferation. Interestingly, single cell reverse transcription-polymerase chain reaction (RT-PCR) clearly showed two different types of SSCs: SSCs with JAK1 mRNA (JAK1+ ) or without JAK1 mRNA (JAK1- ). Since JAK1- SSC level was increased by induction of testis regeneration, self-renewing SSCs were thought to be JAK1- . In addition, we found barrel-shaped PGs, in which JAK1 mRNA was localized asymmetrically to one half of the cell. The stainability with propidium iodide and morphology of two nuclei in the barrel-shaped PG were similar to those of PG nucleus. Based on the above observations, we propose the hypothesis that JAK1+ SSC is preparing for production of PGs destined to differentiate (destined PGs) and the accumulated JAK1 mRNA in the SSC is distributed exclusively into the destined PGs through mitotic division.