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Nitrogen deposition and biodiversity alter plant flowering phenology through abiotic factors and functional traits. However, few studies have considered their combined effects on flowering phenology. A common garden experiment with two nitrogen addition levels (0 and 6 g N m−2 year−1) and five species richness levels (1, 2, 4, 6, and 8) was established. We assessed the effects of nitrogen addition and plant species richness on three flowering phenological events of Medicago sativa L. via changes in functional traits, soil nutrients, and soil moisture and temperature. The first flowering day was delayed, the last flowering day advanced, and the flowering duration shortened after nitrogen addition. Meanwhile, the last flowering day advanced, and flowering duration shortened along plant species richness gradients, with an average of 0.64 and 0.95 days change per plant species increase, respectively. Importantly, it was observed that plant species richness affected flowering phenology mainly through changes in plant nutrient acquisition traits (i.e., leaf nitrogen and carbon/nitrogen ratio). Our findings illustrate the non-negligible effects of intraspecific variation in functional traits on flowering phenology and highlight the importance of including functional traits in phenological models to improve predictions of plant phenology in response to nitrogen deposition and biodiversity loss. [ABSTRACT FROM AUTHOR]

Natural infrastructure is essential in reducing thermal discomfort caused by the urban heat island (UHI) effect. Optimizing and planning green and blue spaces can help establish nature-based urban heat mitigation strategies that benefit sustainable urban development. Most current studies on urban heat mitigation have focused on the single heat reduction effect of green space or blue space, while there has been a lack of research on the combined cooling effects of blue and green spaces. Moreover, existing heat mitigation models and methods cannot directly guide the optimization of blue–green spatial patterns at the urban scale. This has led to an unclear relationship between heat mitigation effects and blue–green spatial patterns. Based on land use data, meteorological data, and biophysical information as inputs, this paper utilized the InVEST urban cooling model (UCM) and scenario analysis method to simulate urban heat mitigation patterns by setting up different blue–green space configuration scenarios. The relative contribution of blue–green space changes to the variation of heat mitigation benefits was quantitatively estimated using the difference comparison method, and the relationship between heat reduction effects and urban blue–green spatial patterns was elucidated using spatial analysis methods. The results show that the InVEST UCM captured some of the variability in the surface thermal response of Wuhan and can be applied to the modeling of urban heat mitigation patterns. Furthermore, they show that consideration of the cooling effect of water evaporation can improve the simulation accuracy to some extent. In Wuhan, there were regional differences in heat mitigation patterns and the heat mitigation effect was significantly higher in the suburbs than in the city. Additionally, urban parks, lakes, and mountains with surface or block distribution had noticeable cooling benefits. Finally, the scenario simulation results demonstrate that green space was more efficient at mitigating heat, while blue space was more critical for the geographical partitioning of the UHI. These findings can provide a reference for the planning and optimal management of urban blue and green spaces, as well as for the design of heat reduction policies. [ABSTRACT FROM AUTHOR]

The Han River Basin is a main agricultural production area and a water source for the middle route of the South-to-North Water Diversion Project in China. Over the past 20 years, human exploitation and ecological construction have disturbed the sustainability of land productivity in the Han River Basin. Theil–Sen trend analysis, Mann–Kendall statistical test, and Hurst index methods were applied to examine spatial–temporal trends and sustainability characteristics of land net primary productivity (NPP) change in the Han River Basin from 2001 to 2019 using MOD17A3 NPP product, natural, and socio-economic data obtained from Google Earth Engine (GEE). The findings demonstrated that the interannual variation of land NPP exhibited a fluctuating upward trend, with a more pronounced growth rate from 2001 to 2010 than from 2011 to 2019. The spatial heterogeneity of land NPP was evident, with high values in the west and low values in the east. Of the basin area, 57.82% presented a significant increase in land NPP, while only 0.96% showed a significant decrease. In the future, land NPP in the Han River Basin will present sustained growth. The results were also compared with Trends.Earth's calculations for the SDG 15.3.1 sub-indicator of land productivity. In addition, the spatial heterogeneity of factors influencing land NPP change was explored using a multiscale geographically weighted regression (MGWR) model. Precipitation and population count were the dominant factors in most regions. Besides, precipitation, population count, and human modification all exhibited inhibitory effects on the increase in land NPP except for elevation. The research can provide a scientific basis for tracking land degradation neutrality (LDN) progress and achieving sustainable socio-ecological development of the Han River Basin. [ABSTRACT FROM AUTHOR]

High-dose dexamethasone (DEX) is used to treat chemotherapy-induced nausea and vomiting or to control immunotherapy-related autoimmune diseases in clinical practice. However, the underlying mechanisms of high-dose DEX in tumor progression remain unaddressed. Therefore, we explored the effects of high-dose DEX on tumor progression and the potential mechanisms of its anti-tumor function using immunohistochemistry, histological examination, real-time quantitative PCR (qPCR), and Western blotting. Tumor volume, blood vessel invasion, and levels of the cell proliferation markers Ki67 and c-Myc and the anti-apoptotic marker Bcl2 decreased in response to high-dose DEX. However, the cell apoptosis marker cleaved caspase 3 increased significantly in mice treated with 50 mg/kg DEX compared with controls. Some genes associated with immune responses were significantly downregulated following treatment with 50 mg/kg DEX e.g., Cxcl9, Cxcl10, Cd3e, Gzmb, Ifng, Foxp3, S100a9, Arg1, and Mrc1. In contrast, the M1-like tumor-associated macrophages (TAMs) activation marker Nos2 was shown to be increased. Moreover, the expression of peroxisome proliferator-activated receptors α and γ (Pparα and Pparg, respectively) was shown to be significantly upregulated in livers or tumors treated with DEX. However, high-dose DEX treatment decreased the expression of glucose and lipid metabolic pathway-related genes such as glycolysis-associated genes (Glut1, Hk2, Pgk1, Idh3a), triglyceride (TG) synthesis genes (Gpam, Agpat2, Dgat1), exogenous free fatty acid (FFA) uptake-related genes (Fabp1, Slc27a4, and CD36), and fatty acid oxidation (FAO) genes (Acadm, Acaa1, Cpt1a, Pnpla2). In addition, increased serum glucose and decreased serum TG and non-esterified fatty acid (NEFA) were observed in DEX treated-xenografted tumor mice. These findings indicate that high-dose DEX-inhibited tumor progression is a complicated process, not only activated by M1-like TAMs, but also decreased by the uptake and consumption of glucose and lipids that block the raw material and energy supply of cancer cells. Activated M1-like TAMs and inefficient glucose and lipid metabolism delayed tumor cell growth and promoted apoptosis. These findings have important implications for the application of DEX combined with drugs that target key metabolism pathways for tumor therapy in clinical practice. [ABSTRACT FROM AUTHOR]

PPP3CB belongs to the phosphoprotein phosphatases (PPPs) group. Although the majority of the PPP family play important roles in the epithelial-to-mesenchymal transition (EMT) of tumor cells, little is known about the function of PPP3CB in the EMT process. Here, we found PPP3CB had high expression in kidney mesenchymal-like cells compared with kidney epithelial-like cells. Knock-down of PPP3CB downregulated epithelial marker E-cadherin and upregulated mesenchymal marker Vimentin, promoting the transition of cell states from epithelial to mesenchymal and reorganizing the actin cytoskeleton which contributed to cell migration. Conversely, overexpression of PPP3CB reversed EMT and inhibited migration of tumor cells. Besides, in vitro and in vivo experiments indicated that the loss of PPP3CB suppressed the tumor growth. However, the deletion of the phosphatase domain of PPP3CB showed no effect on the expression of E-cadherin, migration, and G401 cell proliferation. Together, we demonstrate that PPP3CB inhibits G401 cell migration through regulating EMT and promotes cell proliferation, which are both associated with the phosphatase activity of PPP3CB. [ABSTRACT FROM AUTHOR]

Apobec-1 complementation factor (A1CF) is a member of the heterogeneous nuclear ribonucleoproteins (hnRNP) family, which participates in site-specific posttranscriptional RNA editing of apolipoprotein B (apoB) transcript. The posttranscriptional editing of apoB mRNA by A1CF in the small intestine is required for lipid absorption. Apart from the intestine, A1CF mRNA is also reported to be highly expressed in the kidneys. However, it is remained unknown about the functions of A1CF in the kidneys. The aim of this paper is to explore the potential functions of A1CF in the kidneys. Our results demonstrated that in C57BL/6 mice A1CF was weakly expressed in embryonic kidneys from E15.5dpc while strongly expressed in mature kidneys after birth, and it mainly existed in the tubules of inner cortex. More importantly, we identified A1CF negatively regulated the process of epithelial-mesenchymal transition (EMT) in kidney tubular epithelial cells. Our results found ectopic expression of A1CF up-regulated the epithelial markers E-cadherin, and down-regulated the mesenchymal markers vimentin and α-smooth muscle actin (α-SMA) in NRK52e cells. In addition, knockdown of A1CF enhanced EMT contrary to the overexpression effect. Notably, the two A1CF variants led to the similar trend in the EMT process. Taken together, these data suggest that A1CF may be an antagonistic factor to the EMT process of kidney tubular epithelial cells.

Accumulating evidence demonstrated that miRNAs are highly involved in kidney fibrosis and Epithelial-Eesenchymal Transition (EMT), however, the mechanisms of miRNAs in kidney fibrosis are poorly understood. In this work, we identified that miR542-3p could promote EMT through down-regulating bone morphogenetic protein 7 (BMP7) expression by targeting BMP7 3'UTR. Firstly, real-time PCR results showed that miR542-3p was significantly up-regulated in kidney fibrosis in vitro and in vivo. Moreover, Western blot results demonstrated that miR542-3p may promote EMT in the NRK52e cell line. In addition, we confirmed that BMP7, which played a crucial role in anti-kidney fibrosis and suppressed the progression of EMT, was a target of miR542-3p through Dual-Luciferase reporter assay, as did Western blot analysis. The effects of miR542-3p on regulating EMT could also be suppressed by transiently overexpressing BMP7 in NRK52e cells. Taken together, miR542-3p may be a critical mediator of the induction of EMT via directly targeting BMP7.

MicroRNAs (miRNAs) possess an important regulating effect among numerous renal diseases, while their functions in the process of epithelial-to-mesenchymal transition (EMT) after podocyte injury remain unclear. The purpose of our study is to identify the potential functions of miR-30a in EMT of podocytes and explore the underlying mechanisms of miR-30a in the impaired podocytes. The results revealed that downregulation of miR-30a in podocyte injury animal models and patients, highly induced the mesenchymal markers of EMT including Collagen I, Fibronectin and Snail. Furthermore, overexpression of miR-30a enhances epithelial markers (E-cadherin) but diminished mesenchymal markers (Collagen I, Fibronectin and Snail) in podocytes. In addition, we established miR-30a target NFATc3, an important transcription factor of Non-canonical Wnt signaling pathway. More importantly, our findings demonstrated that the augmentation of miR-30a level in podocytes inhibits the nuclear translocation of NFATc3 to protect cytoskeleton disorder or rearrangement. In summary, we uncovered the protective function of miR30a targeting NFATc3 in the regulation of podocyte injury response to EMT.