Soil water content and nitrogen differentially correlate with multidimensional leaf traits of two temperate broadleaf species.

The variation and correlation of leaf economics and vein traits are crucial for predicting plant ecological strategies under different environmental changes. However, correlations between these two suites of traits and abiotic factors such as soil water and nitrogen content remain ambiguous. We measured leaf economics and vein traits as well as soil water and nitrogen content for two different shade-tolerant species (Betula platyphylla and Acer mono) in four mixed broadleaved-Korean pine (Pinus koraiensis) forests along a latitudinal gradient in Northeast China. We found that leaf economics traits and vein traits were decoupled in shade-intolerant species, Betula platphylla, but significantly coupled in a shade-tolerant species, A. mono. We found stronger correlations among leaf traits in the shade tolerant species than in the shade intolerant species. Furthermore, leaf economic traits were positively correlated with the soil water gradient for both species, whereas vein traits were positively correlated with soil water gradient for the shade intolerant species but negatively correlated in the shade tolerant species. Although economic traits were positively correlated with soil nitrogen gradient in shade intolerant species but not correlated in shade tolerant species, vein traits were negatively correlated with soil nitrogen gradient in shade tolerant species but not correlated in shade intolerant species. Our study provides evidence for distinct correlations between leaf economics and vein traits and local abiotic factors of species differing in light demands. We recommend that the ecological significance of shade tolerance be considered for species when evaluating ecosystem functions and predicting plant responses to environmental changes.

Bone morphogenetic protein (BMP) 7 expression is regulated by the E3 ligase UBE4A in diabetic nephropathy.

Mesangial cells played a central role in the pathophysiology of diabetic nephropathy (DN). Our goal was to evaluate the molecular mechanism that regulates loss of BMP7 protein expression in DN. The mRNA and protein levels of BMP7 or UBE4A were detected using qRT-PCR and Western blot respectively. Mass spectrometry and co-immunoprecipitation were used to explore the E3 ligase which regulated BMP7 post-translationally. We initially confirmed that BMP7 protein, but not mRNA, is downregulated when cultured under high glucose mimicking DN conditions, which was rescued by MG-132 treatment. Proteomic analysis of NRK-52E cells ± MG-132 revealed a list of ubiquitin ligases associated with BMP7. Knockdown of the ubiquitin ligase UBE4A stabilized BMP7 expression in NRK-52E cells grown under high glucose conditions. Concurrent overexpression experiments confirmed that UBE4A is the ubiquitin ligase that degrades BMP7. Co-immunoprecipitation analysis confirmed that BMP7 and UBE4A interact. BMP7 expression in DN is regulated by post-translational mechanism.

Proteasome subunit-α type-6 protein is post-transcriptionally repressed by the microRNA-4490 in diabetic nephropathy.

A common complication of both type I and type II diabetes is nephropathy, characterized by accumulation of extracellular matrix in the glomerular mesangium. This indicates a central role of mesangial cells in the pathophysiology of diabetic nephropathy. Using the proteomic approach, it was earlier elucidated in a rat model that the proteasome subunit-α type-6 protein (PSMA6) is suppressed in the renal cortex in nephropathic kidney. However, the underlying mechanism effecting suppression of PSMA6 protein in the renal cortex is not yet known. Twenty diabetic patients were enrolled and the expression level of PSMA6 in them was detected by immunohistochemistry. The protein and mRNA expression levels of PSMA6 in NRK-52E cells under high glucose condition were determined by Western blot and quantitative real-time PCR, respectively. Dual luciferase assay was used to detect the relationship of PSMA6 and miR-4490. Our results show that PSMA6 protein is down-regulated in patients with diabetic nephropathy compared with healthy control. Using the NRK-52E cell line cultured under high glucose condition as an in vitro model of diabetic nephropathy, we show that loss of PSMA6 protein expression occured independent of changes the in PSMA6 mRNA expression. We next elucidate that PSMA6 mRNA is post-transcriptionally regulated by the microRNA (miRNA)-4490, whose expression is inversely correlated to PSMA6 protein expression. Using reporter assays we show that PSMA6 is a direct target of the miR-4490. Exogenous manipulation of miR-4490 levels modulated expression of PSMA6, indicating that miR-4490 can be tested as a biomarker for nephropathy in diabetic patients.