The functions of the FoxO family proteins, in particular their transcriptional activities, are modulated by post-translational modifications (PTMs), including phosphorylation, acetylation, ubiquitination, methylation and glycosylation. These PTMs occur in response to different cellular stresses, which in turn regulate the subcellular localization of FoxO family proteins, as well as their half-life, DNA binding, transcriptional activity and ability to interact with other cellular proteins. In this review, we summarize the role of PTMs of FoxO family proteins in linking their biological and functional relevance with various diseases.

Abbreviations: ATG, autophagy related; FOXO1, forkhead box O1; FOXO3, forkhead box O3; GFP, green fluorescent protein; MAP1LC3, microtubule-associated protein 1 light chain 3; PIK3CA, class I PI3K catalytic subunit the BECN1-PtdIns3K complex to promote autophagosome formation. 16,17 Recent evidence has revealed that the FOXO protein family members FOXO1 and FOXO3 promote autophagy. [18][19][20][21][22][23] In skeletal muscle cells, FOXO3 directly upregulates autophagy-related genes, such as microtubule-associated protein 1 light chain 3 (MAP1LC3) and BCL2/adenovirus E1B 19-kDa interacting protein 3 (BNIP3).19 FOXO1 has both transcription-dependent and transcription-independent roles in autophagy. In mouse cardiomyocytes, FOXO1 is deacetylated by the NAD-dependent deacetylase sirtuin-1 (SIRT1) that, in turn, induces the expression of the RAS-related GTP-binding protein RAB7A, which mediates the fusion of mature autophagic vesicles with lysosomes. 21 In addition, FOXO1 mediates starvation-induced autophagy through a transcription-independent mechanism in human cancer cells. We have previously observed that cytoplasmic FOXO1 is required for serum starvation-or H 2 O 2 -induced autophagy in cancer cells. Under these conditions, FOXO1 became acetylated and dissociated from SIRT2 in the cytoplasm, and the acetylated FOXO1, in turn, binds to ATG7 to promote autophagy. 23 Therefore, it is ©2012 Landes Bioscience. Do not distribute.www.landesbioscience.com Autophagy

Microfluidics is characterized by laminar flow at micro-scale dimension, high surface to volume ratio, and markedly improved heat/mass transfer. In addition, together with advantages of large-scale integration and flexible manipulation, microfluidic technology has been rapidly developed as one of the most important platforms in the field of functional biomaterial synthesis. Compared to biomaterials assisted by conventional strategies, functional biomaterials synthesized by microfluidics are with superior properties and performances, due to their controllable morphology and composition, which have shown great advantages and potential in the field of biomedicine, biosensing, and tissue engineering. Take the significance of microfluidic engineered biomaterials into consideration; this review highlights the microfluidic synthesis technologies and biomedical applications of materials. We divide microfluidic based biomaterials into four kinds. According to the material dimensionality, it includes: 0D (particulate materials), 1D (fibrous materials), 2D (sheet materials), and 3D (construct forms of materials). In particular, micro/nano-particles and micro/nano-fibers are introduced respectively. This classification standard could include all of the microfluidic biomaterials, and we envision introducing a comprehensive and overall evaluation and presentation of microfluidic based biomaterials and their applications.

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Combinations of 3D bioprinting and microfluidics could complement each other to create artificial tissues and organs with complex architectures.

Glutamate excitotoxicity has been implicated as one of the pathological mechanisms contributing to neuronal cell death and is involved in many neurological disorders. Stem cell transplantation is a promising approach for the treatment of nervous system damage or diseases. Previous studies have shown that mesenchymal stem cells (MSCs) have important therapeutic effects in experimental animal and preclinical disease model of central nervous system pathology. However, it is not well understood whether neurogenesis of MSCs or MSC conditioned-medium (CM) containing microparticles mediates therapeutic effects. Here, we investigated the neuroprotective effects of human adipose-derived MSCs (AMSCs) on cortical neurons using models of glutamate excitotoxicity. Following exposure to glutamate (100 μM, 15 min), cortical neurons were co-cultured with either AMSCs separated by a semiporous membrane (prohibiting direct cell-cell contact) or with AMSC-CM for 18 h. Compared to untreated control groups, AMSCs and AMSC-CM partially and similarly reduced neuronal cell damages, as indicated by reduced LDH release, a decreased number of trypan-positive cells and a decline in the number of apoptotic nuclei. Protection by CM was associated with increased GAP-43 expression and an elevated number of GAP-43-positive neurites. Furthermore, CM increased levels of ATP, NAD+ and NADH and the ratio of NAD+/NADH, while preventing a glutamate-induced decline in mitochondrial membrane potential. These results demonstrate that AMSC-CM mediates direct neuroprotection by inhibiting neuronal cell damage/apoptosis, promoting nerve regeneration and repair, and restoring bioenergy following energy depletion caused by glutamate excitotoxicity.

In this work, manganese well-dispersed on Fe3O4 microsphere (Mn–Fe3O4) catalyst was synthesized. It exhibited excellent catalytic performance for the direct conversion of carbon dioxide (CO2) into light olefins. A CO2 conversion of 44.7% with high selectivity of light olefin (46.2%, yield of 18.7%), high O/P ratio (6.5), and low selectivity of CO (9.4%) was obtained over the 10Mn–Fe3O4 catalyst. The Mn–Fe3O4 catalyst was studied by XRD, SEM, (HR)­TEM, STEM–EDS, H2-TPR, and CO2-TPD. The result indicated that the manganese promoter could facilitate the adsorption of CO2 and the activation of CO bonds as well as inhibit the secondary hydrogenation. This work offered a novel Fe-based catalyst system to the utilization of CO2 and an understanding in promoting CO bond activation in the first step of CO2 hydrogenation to hydrocarbon reaction.

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