Response of photosynthetic nitrogen use efficiency in Betula utilis to altitudinal variation along Balang Mountain, Sichuan, China.

To better understand the response and adaptation of plants to altitudinal changes, four sites at the altitude of 2200 m, 2500 m, 3100 m and 3400 m on Balang Mountain were selected to test and calculate the eco-physiological parameters in leaves of Betula utilis, including photosynthetic nitrogen use efficiency (PNUE), CO2 diffusion conductance (stomatal conductance gs and mesophyll conductance gm) and nitrogen allocation in each component (fractions of leaf nitrogen allocated to Rubisco PR, to bioenergetics PB, to light-harvesting components PL, and to cell wall PCW). Their changes with altitudinal variations and the relationships between leaf PNUE and the other parameters were analyzed. The results showed that PNUE, PR, and PB of the leaves were relatively higher at 2500 m and 3100 m. With the increases of altitude, gs and gm increased and PL decreased. The correlations between PR, PB and PNUE were significant, indicating that PR and PB were the main factors driving the changes in leaf PNUE in response to altitudinal variations. Besides, the fraction of leaf nitrogen allocated to photosynthetic apparatus (PP) was relatively higher at 2500 m and 3100 m. With increasing altitude, PCW decreased and the fraction of leaf nitrogen allocated to the other components (Pother) increased, which suggested that B. utilis leaves tended to allocate more nitrogen to the other components instead of the photosynthetic apparatus and cell wall with the increasing altitude to well adapt environmental changes.

p38 MAPK is Crucial for Wnt1- and LiCl-Induced Epithelial Mesenchymal Transition.

Idiopathic pulmonary fibrosis (IPF) is characterized by myofibroblast foci in lung parenchyma. Myofibroblasts are thought to originate from epithelial-to-mesenchymal transition (EMT). Wnt1 and lithium chloride (LiCl) induce EMT in alveolar epithelial cells (AECs), but the mechanisms are unclear. AECs were treated with Wnt1 and LiCl, respectively; morphological change and molecular changes of EMT, including E-cadherin, fibronectin, and vimentin, were observed. SB203580 was administrated to test the role of p38 МАРК signaling in EMT. Then AECs were treated with siRNAs targeting p38 МАРК to further test the effects of p38 МАРК, and the role was further confirmed by re-expression of p38 МАРК. At last P-catenin siRNA was used to test the role of ß-catenin in the EMT process and relationship of ß-catenin and p38 МАРК was concluded. Exposure of AECs to Wnt1 and LiCl resulted in upregulation of vimentin and fibronectin with subsequent downregulation of E-cadherin. Wnt1 and LiCl stimulated the p38 МАРК signaling pathways. Perturbing the p38 МАРК pathway either by SB203580 or through p38 МАРК siRNA blocked EMT and inhibited fibronetin synthesis, which were reversed by transfection of p38 МАРК expression plasmid. ß-catenin siRNA attenuated the EMT process and decreased p38 МАРК phosphorylation, indicating that ß-catenin is involved in the EMTrelated changes through regulation of p38 МАРК phosphorylation. These findings suggest that p38 МАРК participates in the pathogenesis of EMT through Wnt pathway and that p38 МАРК may be a novel target for IPF therapy.