Reh, University of Washington, United States of America The data show, for the first time, that JNK is activated in mitotic progenitor cells of developing retinal tissue, suggesting a new role of JNK in the control of progenitor cell proliferation in the retina.Ĭitation: Ribas VT, Gonçalves BS, Linden R, Chiarini LB (2012) Activation of c-Jun N-Terminal Kinase (JNK) during Mitosis in Retinal Progenitor Cells. Moreover, cells with aberrant chromatin morphology were found after treatment with the JNK inhibitor. Treatment with the JNK inhibitor decreased the number of cells in anaphase, but did not alter the number of cells in either prophase/prometaphase or metaphase. Inhibition of JNK induced cell cycle arrest, specifically in mitosis. JNK1 and/or JNK2 were preferentially phosphorylated in mitotic cells. The results showed that in the retina of newborn rats (P1), JNK is phosphorylated during mitosis of progenitor cells, mainly during the early stages of mitosis. Phosphorylation of JNK was also examined by western blot. The subcellular localization of proteins was analyzed by double staining with both a DNA marker and an antibody to each protein. Mitotic cells were identified by chromatin morphology, histone-H3 phosphorylation, and location in the retinal tissue. Sections of retinal explants or freshly fixed retinal tissue were used to detect JNK phosphorylation by immunohistochemistry, and were examined through both fluorescence and confocal microscopy. Retinal explants from newborn rats were kept in vitro for 3 hours and under distinct treatments. In this study, we investigated the behavior of JNK during mitosis of progenitor cells in the retina of newborn rats. Most studies of c-Jun N-terminal Kinase (JNK) activation in retinal tissue were done in the context of neurodegeneration.

Jnk1 regulate jun protein turnover