Biology and applications of Clonostachys rosea.

Clonostachys rosea is a promising saprophytic filamentous fungus that belongs to phylum Ascomycota. Clonostachys rosea is widespread around the world and exists in many kinds of habitats, with the highest frequency in soil. As an excellent mycoparasite, C. rosea exhibits strong biological control ability against numerous fungal plant pathogens, nematodes and insects. These behaviours are based on the activation of multiple mechanisms such as secreted cell-wall-degrading enzymes, production of antifungal secondary metabolites and induction of plant defence systems. Besides having significant biocontrol activity, C. rosea also functions in the biodegradation of plastic waste, biotransformation of bioactive compounds, as a bioenergy sources and in fermentation. This mini review summarizes information about the biology and various applications of C. rosea and expands on its possible uses.

Icariin may benefit the mesenchymal stem cells of patients with steroid-associated osteonecrosis by ABCB1-promoter demethylation: a preliminary study.

UNLABELLED: In this study, we found out a previously undefined function of icariin which restored the dynamic balance between osteogenic and adipogenic differentiation of mesenchymal stem cells (MSCs) in patients with osteonecrosis of femoral head (ONFH) via ABCB1-promoter demethylation. These findings provided important information regarding potential implication of icariin targeting epigenetic changes for the treatment of steroid -associated ONFH. INTRODUCTION: Here, we investigated whether icariin can also exert a beneficial role in the reactivation of MSCs in the patients with steroid-associated ONFH via ABCB1-promoter demethylation. METHODS: Bone marrow was collected from the proximal femur in patients with steroid-associated ONFH (n = 20) and patients with new femoral neck fractures (n = 22), and then MSCs were isolated. We investigated cell viability, intracellular reactive oxygen species (ROS) level, mitochondrial membrane potential (MMP), P-glycoprotein (P-gp) activity, the transcript levels of ABCB1 and oxidative stress-related genes, methylation extent at CpG islands of ABCB1 promoter, and osteogenic and adipogenic differentiation ability of MSCs from the femoral neck fractures group and from the steroid-associated ONFH group treated with or without icariin. RESULTS: We observed that MSCs from the steroid-associated ONFH group showed reduced proliferation ability, elevated ROS level, depressed MMP, weakened osteogenesis, and enhanced adipogenesis while low P-gp activity, transcription level of ABCB1, and oxidative stress-related genes as well as aberrant CpG islands hypermethylation of ABCB1 were also noted in steroid-associated ONFH group. Treatment with icariin obviously induced de novo P-gp expression, decreased oxidative stress, and promoted osteogenesis. CONCLUSION: Icariin may be a potential drug targeting epigenetic changes for the treatment of steroid-associated ONFH.

SCIRR39 promotes neurite extension via RhoA in NGF-induced PC12 cells.

SCIRR39 is an identified upregulated gene in rat primary neuron injury and/or regeneration process with roles largely unexplored. Using real-time quantitative PCR, Western blotting and immunofluorescence, SCIRR39 expression was detected in normal PC12 cells and upregulated in differentiated cells. The results of cell proliferation by Cell Counting Kit and cell cycle by flow cytometry indicated that SCIRR39 inhibited cell proliferation and induced the decrease in S phase. Importantly, immunofluorescent and RhoA pull-down assays showed that SCIRR39 strongly affected the neurite extension of NGF-treated PC12 cells through a RhoA-dependent mechanism, but the truncated mutants of SCIRR39 containing a truncation from 141AA to 211AA or from 397AA to 424AA failed to mock the SCIRR39 effect on neurite extension. Moreover, change of SCIRR39 expression in NGF-treated PC12 cells regulated the expression and phosphorylation of Fyn, a regulator of RhoA activity, but not the expression of ROCK II protein. Finally, immunofluorescence and RhoA pull-down assays revealed that obvious inhibition of neurite extension by SCIRR39 shRNA was reversed by RhoA inhibitor C3-transferase. Our results indicated that SCIRR39 increased the neurite extension in NGF-treated PC12 cells via RhoA, suggesting that SCIRR39 contributes to the regeneration of neuron injury by specifically altering the differentiation program.