Gax suppresses chemerin/CMKLR1-induced preadipocyte biofunctions through the inhibition of Akt/mTOR and ERK signaling pathways.

Adipose tissue is closely associated with angiogenesis and vascular remodeling. Chemerin is involved in inflammatory reaction and vascular dysfunction. However, the mechanisms of chemerin participating in vascular remodeling and whether Growth arrest-specific homeobox (Gax) can effectively intervene it remain obscured. Here, 3T3-F442A preadipocytes were cultured, injected into athymic mice to model fat pads, and treated respectively with Ad-chemerin, Ad-Gax, or specific inhibitors in vitro and in vivo. MTT, flow cytometry, Western blotting, and imunohisto(cyto)-chemistry analyses showed that chemerin enhanced the expression of FABP4 and VEGF, activated Akt/mTOR and ERK pathways, increased the cell percent of S phase, decreased the percent of G0-G1 phase and apoptotic cells, and augmented neovascular density in fat pads. Inversely, Gax suppressed the expression of these adipogenic and vasifactive markers and these signaling proteins, decreased the percent of S phase cells, and increased those of G0-G1 phase and apoptotic cells, and reduced the neovascular density. Our results indicate that chemerin-CMKLR1 activates Akt/mTOR and ERK pathways and facilitates preadipocyte proliferation, adipogenesis, and angiogenesis. Contrarily, Gax weakens the effect of chemerin on preadipocyte biofunctions.

Analysis of internal heat recovery capability in air-cooled indirect fired GAX-based absorption chiller in part-load operation.

Single-effect absorption chillers are the most popular because of their low cost, despite their low COP. Among them, GAX-based AirCooled absorption chillers are very interesting because they have improved COP because of their ability to recover internal heat at low thermal lifts. This workshop analysed the ability of these types of chillers to recover internal heat at high thermal lifts by changing the pressure drop of an extra valve, a feature of the Robur absorption chiller when operating in subzero applications. The complete differential mathematical model analyses the components involved in heat supply and recovery and provides information on their operation. A thorough assessment of exergy destruction in the absorption refrigeration system was carried out. The main results show that when the chiller is driven at a temperature of 210 °C and an ambient temperature of 40 °C, a rise in the pressure drop of the additional valve, ΔPval1, from 175 to 700 kPa causes the extension of the vapour purification process to be reduced by 13.7% in the column of distillation and by 70.6% in the rectifier. Despite the adverse effect of ΔPval1 increase on the cooling capacity, there is no risk that the distillation column operates in weeping mode. However, this adjustment increases the internal thermal load of the generator by 26.9%. Furthermore, the mass fraction of the refrigerant flow is very similar. In addition, the occurrence of a two-phase solution flow at the input of a solution cooling absorber is the practical upper limit of ΔPval1. The refrigerant flow in the solution cooling absorber is reduced by 21.3%. Finally, the contribution of the heat recovery loop to the total exergy destruction in the refrigeration system rises slightly by 2.7% when ΔPval1 increases due to the contribution of the vapour purification system, which increases at the expense of that of the re-boiler and the SolutionCooled absorber. The results of this study show to what extent the modified GAX-based cycle can function effectively at high thermal lifts.

An update on xylan structure, biosynthesis, and potential commercial applications.

•Xylan is an abundant carbohydrate component of plant cell walls that is vital for proper cell wall structure and vascular tissue development.•Xylan structure is known to vary between different tissues and species.•The role of xylan in the plant cell wall is to interact with cellulose, lignin, and hemicelluloses.•Xylan synthesis is directed by several types of Golgi-localized enzymes.•Xylan is being explored as an eco-friendly resource for diverse commercial applications.

Practical Enhancements in Current Density and Power Generation of Bifacial Semitransparent Ultrathin CIGSe Solar Cells via Utilization of Wide Bandgap Zn-Based Buffer.

Among many building-integrated semitransparent photovoltaics (BISTPVs), semitransparent ultrathin (STUT) Cu(Inx ,Ga1-x )Se2 (CIGSe) solar cells are distinguishable due to their potential high power conversion efficiency (PCE) among other thin-film solar cells, versatile applicability based on thin film deposition processes, high stability consisting of all inorganic compositions, and practical expandability to bifacial applications. However, the fundamental trade-off relationship between PCE and transparency limits the performance of BISTPV because implementing a higher semitransparency lowers the optical budget of incoming light. To expand the available optical budget and to enhance the PCE while maintaining a suitable transparency in STUT CIGSe solar cell with single-stage coevaporated 500-nm-thick absorber, an atomic layer deposited wide bandgap Zn(O,S) buffer is introduced as the replacement of conventional CdS buffer, which partially limits incoming light less than 520 nm in wavelength. As a replacement result, more incoming light becomes valid for power conversion, and the short circuit current density (Jsc ) has increased comparatively by 17%, which has directly lead to a large increase in PCE up to 12.41%. Furthermore, Zn(O,S) buffer in the STUT CIGSe solar cell also has enhanced the bifacial compatible efficiency (BCE), which has increased to 14.44% at 1.3 sun and 19.42% at 2.0 sun.

Tumor-derived exosomal miRNA-141 promote angiogenesis and malignant progression of lung cancer by targeting growth arrest-specific homeobox gene (GAX).

Previous researches have suggested that exosomal miRNA-141 has association with metastatic lung cancer, however, its role and regulatory mechanism require further study. In this study, exosomes were isolated from lung cancer patients and normal human serum and identified. We found that the expression of miRNA-141 was up-regulated in the lung cancer serum exosomes compared with the normal serum exosomes. When the exosomes were extracted for co-culture with HUVECs, they were absorbed and distributed around the nucleus by confocal microscopy. Moreover, exosomal miRNA-141 from A549 significantly not only promoted the migration and invasion of A549 but also increased the cell proliferation, tube formation of HUVECs. In order to reveal the mechanism of exosomal miRNA-141, bioinformatics analysis revealed that miRNA-141 targeted the binding of Growth arrest-specific homeobox gene (GAX) in the 3'UTR region, and confirmed by MS2-RIP assay and dual-luciferase assay. Exosome miRNA-141 could down-regulate the expression of GAX. Taken together, our results demonstrate that tumor-derived exosomal miRNA-141 promote angiogenesis and malignant progression of lung cancer by targeting GAX. It provides a new possibility for the treatment of lung cancer.

Gax regulates human vascular smooth muscle cell phenotypic modulation and vascular remodeling.

Abnormal phenotypic modulation of vascular smooth muscle cells (VSMCs) is a hallmark of cardiovascular diseases such as atherosclerosis, hypertension and restenosis after angioplasty. Transcription factors have emerged as critical regulators for VSMCs function, and recently we verified inhibiting transcription factor Gax was important for controlling VSMCs proliferation and migration. This study aimed to determine its role in phenotypic modulation of VSMCs. Western blot revealed that overexpression of Gax increased expression of VSMCs differentiation marker genes such as calponin and SM-MHC 11. Then, Gax overexpression potently suppressed proliferation and migration of VSMCs with or without platelet-derived growth factor-induced-BB (PDGF-BB) stimuli whereas Gax silencing inhibited these processes. Furthermore, cDNA array analysis indicated that Rap1A gene was the downstream target of Gax in human VSMCs. And overexpression of Gax significantly inhibited expression of Rap1A in VSMCs with or without PDGF-BB stimuli. Moreover, overexpression of Rap1A decreased expression of VSMCs differentiation marker genes and increased proliferation and migration of VSMCs with or without PDGF-BB stimuli. Finally, Gax overexpression significantly inhibited the neointimal formation in carotid artery injury of mouse models, specifically through maintaining VSMCs contractile phenotype by decreasing Rap1A expression. In conclusion, these results indicated that Gax was a regulator of human VSMCs phenotypic modulation by targeting Rap1A gene, which suggested that targeting Gax or its downstream targets in human VSMCs may provide an attractive approach for the prevention and treatment of cardiovascular diseases.

Gax inhibits perivascular preadipocyte biofunction mediated by IGF-1 induced FAK/Pyk2 and ERK2 cooperative pathways.

Perivascular adipocyte (PVAC) biofunctions were closely related to cardiovascular diseases; its specific biological mechanisms remained unclear. How to adjust PVAC functions of vascular cells is an important topic. The present study was designed to investigate whether FAK/Pyk2 and ERK1/2 MAPK signaling pathways participate in PVAC functions, which is activated by insulin-like growth factor 1(IGF-1) and inhibited by Gax. PVACs isolated from perivascular adipocyte were cultured, dedifferentiated, and stimulated with 10nM IGF-I. Cellular function experiments showed that IGF-1 promoted PVAC proliferation, adhesion, and migration. However Gax weakened IGF-1-mediated these function. Flow cytometry demonstrated that IGF-1 increased PVACs percent of S phase and decreased the percent of G0/G1 phase and apoptotic cells. While, Gax decreased the percent of S phase cells and increased those of G0-G1 phase and apoptotic cells. Western blotting and RT-PCR revealed that IGF-1 activated FAK/Pyk2 and ERK1/2 signaling pathways, upregulated the mRNA and protein expression of FAK, Pyk2, and ERK1/2, and suppressed p53 expression. Reversely, Gax lowered the expression of these signaling proteins and increased p53 expression. Therefore, IGF-1 mediated FAK/Pyk2 and ERK1/2 pathways to augment PVAC functions; Gax effectively counteracted these effects of IGF-1, repressed PVAC activities, and increased the cell apoptosis. Our findings suggested that FAK/Pyk2 and ERK1/2 cooperative activation mediated by IGF-1 is essential for PVAC functions, and Gax is a promising candidate gene to interfere with these signaling pathways and inhibit PVAC functions.