Molecular networks regulating cell division during Arabidopsis leaf growth

Leaves are the primary organs for photosynthesis, and as such have a pivotal role for plant growth and development. Leaf development is a multifactorial and dynamic process involving many genes that regulate size, shape, and differentiation. The processes that mainly drive leaf development are cell proliferation and cell expansion, and numerous genes have been identified that, when ectopically expressed or down-regulated, increase cell number and/or cell size during leaf growth. Many of the genes regulating cell proliferation are functionally interconnected and can be grouped into regulatory modules. Here, we review our current understanding of six important gene regulatory modules affecting cell proliferation during Arabidopsis leaf growth: ubiquitin receptor DA1–ENHANCER OF DA1 (EOD1), GROWTH REGULATING FACTOR (GRF)–GRF-INTERACTING FACTOR (GIF), SWITCH/SUCROSE NON-FERMENTING (SWI/SNF), gibberellin (GA)–DELLA, KLU, and PEAPOD (PPD). Furthermore, we discuss how post-mitotic cell expansion and these six modules regulating cell proliferation make up the final leaf size.

Endocrine and other physiologic modulators of perinatal cardiomyocyte endowment

Immature contractile cardiomyocytes proliferate to rapidly increase cell number, establishing cardiomyocyte endowment in the perinatal period. Developmental changes in cellular maturation, size and attrition further contribute to cardiac anatomy. These physiological processes occur concomitant with a changing hormonal environment as the fetus prepares itself for the transition to extrauterine life. There are complex interactions between endocrine, hemodynamic and nutritional regulators of cardiac development. Birth has been long assumed to be the trigger for major differences between the fetal and postnatal cardiomyocyte growth patterns, but investigations in normally growing sheep and rodents suggest this may not be entirely true; in sheep, these differences are initiated before birth, while in rodents they occur after birth. The aim of this review is to draw together our understanding of the temporal regulation of these signals and cardiomyocyte responses relative to birth. Further, we consider how these dynamics are altered in stressed and suboptimal intrauterine environments.

Inhibition of Peroxisome Proliferator-Activated Receptor Gamma Prevents the Melanogenesis in Murine B16/F10 Melanoma Cells

The purpose of this study was to investigate if PPARγplays a role in the melanogenesis. B16/F10 cells were divided into five groups: control, melanin stimulating hormone (α-MSH),α-MSH+retinol,α-MSH+GW9662 (PPARγantagonist), and GW9662. Cells in the control group were cultured in the Dulbecco’s modified Eagle’s medium (DMEM) for 48 hrs. To initiate the melanogenesis, cells in allα-MSH groups were cultured in medium containingα-MSH (10 nM) for 48 hrs. Cells were treated simultaneously with retinol (5 μM) in theα-MSH+retinol group. Instead of retinol, GW9662 (10 μM) was cocultured in theα-MSH+GW9662 group. Cells in the final group were cultured in the DMEM with GW9662. All the analyses were carried out 48 hours after treatments. Theα-MSH was able to increase cell number, melanin production, and the activity of tyrosinase, the limiting enzyme in melanogenesis. Theseα-MSH-induced changes were prevented either by retinol or by GW9662. Further analyses of the activities of antioxidant enzymes including glutathione, catalase, and the superoxide dismutase (SOD) showed thatα-MSH treatment raised the activity of SOD which was dependent on PPARγlevel. According to our results, theα-MSH-induced melanogenesis was PPARγdependent, which also modulated the expression of SOD.

Acute stressor exposure both suppresses acquired immunity and potentiates innate immunity

Acute stressor exposure alters immune function. Rats exposed to inescapable tail shock stress (IS) generate less antibody to a benign, antigenic protein, keyhole limpet hemocyanin (KLH). The following studies examined the effect of IS on peritoneal cavity, spleen, and mesenteric lymph node cell number, interferon-γ (IFN-γ) production, and nitrite production. Rats were injected intraperitoneally with KLH (200 μg) or saline immediately before IS exposure and killed 0, 48, and 96 h after IS termination. KLH immunization resulted in elevated cell numbers and IFN-γ levels 2–4 days later in nonstressed control rats. In contrast, rats exposed to IS failed to increase cell number and IFN-γ levels in response to KLH. The T cell subpopulations affected were CD4 T cells, specifically the Th1-like subset. In addition, in rats exposed to IS + KLH, nitrite production was potentiated 2–4 days after stressor termination. IS had little effect on these measures in saline-injected rats. These data support the conclusion that exposure to IS suppresses the expansion of anti-KLH lymphocytes, possibly anti-KLH Th1 cells. In addition, stressor exposure potentiates the production of nitrite. Importantly, this potentiated response occurred only in KLH-immunized animals, suggesting that macrophages may be primed by stressor exposure and thus respond more vigorously to antigen. The potential links between these changes are discussed.