Effects of mutual intercropping on cadmium accumulation by the accumulator plants Conyza canadensis,Cardamine hirsuta,and Cerastium glomeratum

In this study, three cadmium (Cd) accumulator species (Conyza canadensis, Cardamine hirsuta, and Cerastium glomeratum) were co-cultured in Cd-contaminated soil in pots to study the effects of intercropping on co-remediation. Only C. canadensis intercropped with C. glomeratum, C. hirsuta intercropped with C. glomeratum, and three-species intercropping increased plant biomass compared with their respective monocultures. The treatments of C. canadensis intercropped with C. glomeratum and three-species intercropping increased the Cd contents in roots and shoots of C. canadensis, whereas the other intercropping treatments decreased or had no significant impact on Cd contents. As for Cd accumulation, the treatments of C. canadensis intercropped with C. glomeratum, C. hirsuta intercropped with C. glomeratum, and three-species intercropping increased Cd accumulation in a single plant compared with that of their respective monocultures, whereas other intercropping treatments decreased Cd accumulation in individual plants. Only the treatments of C. canadensis intercropped with C. glomeratum and C. hirsuta intercropped with C. glomeratum increased Cd accumulation in shoots of a single pot compared with that of their respective monocultures. Therefore, C. canadensis intercropped with C. glomeratum and C. hirsuta intercropped with C. glomeratum may improve the phytoremediation efficiency for Cd-contaminated soil.     

UCH-L1 Inhibition Suppresses tau Aggresome Formation during Proteasomal Impairment

In conditions of proteasomal impairment, the damaged or misfolded proteins, collectively known as aggresome, can accumulate in the perinuclear space and be subsequently eliminated by autophagy. Abnormal aggregation of microtubule-associated protein tau in the cytoplasm is a common neuropathological feature of tauopathies. The deficiency in ubiquitin carboxy-terminal hydrolase L1 (UCH-L1), a proteasomal deubiquitinating enzyme, is closely related to tau aggregation; however, the associated mechanisms remain unclear. Here, we showed that UCH-L1 inhibition interrupts proteasomal impairment-induced tau aggresome formation. By reducing the production of lysine (K63)-linked ubiquitin chains, UCH-L1 inhibition decreases HDAC6 deacetylase activity and attenuates the interaction of HDAC6 and tau protein, finally leading to tau aggresome formation impairment. All these results indicated that UCH-L1 plays a key role in the process of tau aggresome formation by regulating HDAC6 deacetylase activity and implied that UCH-L1 may act as a signaling molecule to coordinate the effects of the ubiquitin-proteasome system and the autophagy-lysosome pathway, which mediate protein aggregates degradation in the cytoplasm.     

Extraction and identification of the chyme proteins in the digestive tract of growing pigs

This study aimed to explore the rule of degradation of dietary proteins by identifying chyme proteins in different segments of the digestive tract of growing pigs, using proteomics techniques. Six growing pigs were fed a corn-soybean meal-based diet for 7 days. The feedstuff and chyme proteins were separately extracted and separated with SDS-PAGE. 2D LCMS/MS combined with protein database searching identified 1,513 proteins in different segments of the gastrointestinal tract, the number of identified exogenous proteins gradually decline from the stomach to colon, with large amounts in the duodenum to the large intestine. More corn proteins than soybean proteins were identified both in the feedstuff and chyme, and these were significantly decreased after digestion in the stomach. More membrane proteins than non-membrane proteins were identified in whole digestive tract. These results regarding the profiles of chyme proteins in different segments of the gastrointestinal tract would provide useful information for optimizing feed formula in pigs.     

RNAi targeting STMN alleviates the resistance to taxol and collectively contributes to down regulate the malignancy of NSCLC cells in vitro and in vivo

Stathmin (STMN) plays a vital role in maintaining the malignant behavior of cancer through directly regulating microtubule dynamics equilibrium. Taxol, an effective chemotherapeutics mainly acting to promote microtubule polymerization, has been commercially applied in treating solid tumors, which results in serious drug resistance. Our study demonstrated that STMN RNA interference (RNAi) enlarged taxol-induced inhibitions in cellular proliferation, colony formation, and multidimensional spaces of cell immigration and decreased half maximal inhibitory concentration (IC₅₀) of taxol in nonsmall cell lung cancer (NSCLC) NCI-H1299 cells; STMN RNAi and taxol jointly attenuated the expressions of extracellular regulated kinase (ERK), nuclear factor kappa B (NF-κB) and B cell lymphoma-2 (Bcl-2), but up regulated Bax expression and initiated intrinsic cell death pathway by activating caspase-3 and caspase-9, while inhibited interleukin 10 (IL-10) autocrine from cell culture supernatant and xenografted mouse serum, as well as intracellular expressions of IL-10 protein and mRNA in vitro; additionally, neutralizing IL-10 alone would incur cell apoptosis to some degree; the further study confirmed that RNAi targeting STMN promoted the sensitivity of taxol in different NSCLC cells. In vivo animal experiments proved that STMN RNAi and taxol cooperatively inhibited the tumorigenicity of NCI-H1299 cells and histological atypia and Ki-67 proliferative index of xenografted tumors and promoted cell differentiation to a higher grade with well-differentiated indicators of glandular lumen-like structure and proliferative fibroblasts. These findings suggest that silencing STMN alleviates the resistance to taxol and collectively contributes to induce the dysfunction of multiple signals and down regulate the malignancy of tumors; thus, STMN is a promising target in treating refractory tumors.     

CD10+GPR77+ Cancer-Associated Fibroblasts Promote Cancer Formation and Chemoresistance by Sustaining Cancer Stemness

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Activation of valvular interstitial cells is mediated by transforming growth factor-beta1 interactions with matrix molecules.

Strategies for the tissue-engineering of living cardiac valve replacements are limited by a lack of appropriate scaffold materials that both permit cell viability and actively contribute to the growth of functional tissues. Components of the extracellular matrix can localize and modify growth factor signals, and by doing so impart instructional stimuli for direction of cell phenotype. Fibronectin, collagen I, and heparin were explored as affinity matrices for sequestering and presenting soluble signaling molecules to control differentiation of valvular interstitial cells (VICs) to myofibroblasts. VIC differentiation is commonly characterized by expression of stress fibers containing alpha smooth muscle actin (alpha-SMA), and transforming growth factor-beta1 (TGF-beta1) is a central mediator of this transition. Both fibronectin and heparin, which are known to possess TGF-beta1 binding interactions, were found to increase VIC alpha-SMA expression (120% and 258% of expression in controls), while VICs cultured on collagen I-modified substrates had diminished alpha-SMA expression (66% of control). Heparin treatment significantly stimulated VIC production of TGF-beta1 at all concentrations tested (50 to 400 mug/ml). Heparin-modified substrates were found to alter cell morphology through increased adsorption of serum proteins, specifically TGF-beta1. In sum, heparin produced alpha-SMA-positive myofibroblasts through both the de novo production of TGF-beta1, and its localization in the pericellular environment. The addition of heparin to fibronectin-modified substrates led to a synergistic increase in VIC alpha-SMA expression, produced by the reciprocal binding of fibronectin, heparin, cell-produced TGF-beta1. The characterization of molecules, both soluble and insoluble, that control VIC activation will be important for the development of tailored 3D culture environments for tissue-engineering applications.