The role of N-glycosylation of CD200-CD200R1 interaction in classical microglial activation

Abstract Background Microglial inflammatory activation is the common feature of the central nervous system (CNS) diseases. Microglia can be activated and particularly polarized toward a dual role in the injured CNS. The CD200 receptor 1 (CD200R1) inhibits inflammatory microglia activation as illustrated by studies. Publications show abnormal activation of microglia secondary to the deficient inhibit of CD200-CD200R interaction. In the present study, we established a neuronal-microglia co-culture system to investigate the association between CD200R1 engagement and classical microglial activation. We analyzed the glycosylation of CD200R1 and the CD200 binding. Secretion of pro-inflammatory cytokines were measured. Results CD200R1 was N-glycosylated at Asparagine 44 (Asn44, N44). Mutation of this site disrupted CD200-CD200R1 interaction and up-regulated the expression of cytokines iNOS, CD86, IL-1β and TNF-α. Conclusion N44 of CD200R1 is a significant binding site for CD200-CD200R1 interaction and play a critical role in the maintenance of microglia. The N-glycosylation of CD200R1 could serve as a therapeutic agent for CNS inflammation

Innovation Input, Climate Change, and Energy-Environment-Growth Nexus: Evidence from OECD and Non-OECD Countries

With economic growth and rising incomes, increasing consumption of fossil energy is leading to environmental pollution and climate change, which requires increased innovative inputs to promote the efficiency of renewable energy use. Considering the important impact of innovation input and climate change on renewable energy consumption, greenhouse gas emissions, and green economic growth, this study uses simultaneous equation and sys-GMM model to explore the dynamic nexus of innovation input, climate change, and energy-environment-growth in OECD and non-OECD countries, with panel data covering 2000 to 2019. The empirical results show that renewable energy consumption in non-OECD countries significantly promoted green economic growth, while OECD countries did the opposite. Moreover, renewable energy consumption significantly reduces greenhouse gas emissions caused by climate change, especially for OECD countries. When the level of economic growth exceeds a certain inflection point, greenhouse gas emissions begin to turn from positive to negative, which further verifies the EKC hypothesis. In addition, this study found that innovation input has significantly increased renewable energy consumption, reduced greenhouse gas emissions, and promoted green economic growth in OECD countries. Finally, this study also found that the impact of innovation input in OECD and non-OECD countries on the energy-environment-growth nexus is greater in the short term and more significant in the medium and long term, while the impact of climate change on the energy-environment nexus in OECD and non-OECD countries is more significant in the medium and long term

Phomopsis longanae Chi-Induced Changes in Activities of Cell Wall-Degrading Enzymes and Contents of Cell Wall Components in Pericarp of Harvested Longan Fruit and Its Relation to Disease Development

The main goal of this study was to investigate the influences of Phomopsis longanae Chi infection on activities of cell wall-degrading enzymes (CWDEs), and contents of cell wall components in pericarp of harvested “Fuyan” longan (Dimocarpus longan Lour. cv. Fuyan) fruit and its relation to disease development. The results showed that, compared with the control samples, P. longanae-inoculated longans showed higher fruit disease index, lower content of pericarp cell wall materials (CWMs), as well as lower contents of pericarp cell wall components (chelate-soluble pectin (CSP), sodium carbonate-soluble pectin, hemicelluloses, and cellulose), but higher content of pericarp water-soluble pectin (WSP). In addition, the inoculation treatment with P. longanae significantly promoted the activities of CWDEs including pectinesterase, polygalacturonase, β-galactosidase, and cellulase. The results suggested that the P. longanae stimulated-disease development of harvested longans was due to increase in activities of pericarp CWDEs, which might accelerate the disassembly of pericarp cell wall components. In turn, resulting in the degradation of pericarp cell wall, reduction of pericarp mechanical strength, and subsequently leading to the breakdown of longan pericarp tissues. Eventually resulting in development of disease development and fruit decay in harvested longans during storage at 28°C

The role of NPY2R/NFATc1/DYRK1A regulatory axis in sebaceous glands for sebum synthesis

Abstract Background Sebaceous glands (SGs) synthesize and secret sebum to protect and moisturize the dermal system via the complicated endocrine modulation. Dysfunction of SG are usually implicated in a number of dermal and inflammatory diseases. However, the molecular mechanism behind the differentiation, development and proliferation of SGs is far away to fully understand. Methods Herein, the rat volar and mammary tissues with abundant SGs from female SD rats with (post-natal day (PND)-35) and without puberty onset (PND-25) were arrested, and conducted RNA sequencing. The protein complex of Neuropeptide Y receptor Y2 (NPY2R)/NPY5R/Nuclear factor of activated T cells 1 (NFATc1) was performed by immunoprecipitation, mass spectrum and gel filtration. Genome-wide occupancy of NFATc1 was measured by chromatin immunoprecipitation sequencing. Target proteins’ expression and localization was detected by western blot and immunofluorescence. Results NPY2R gene was significantly up-regulated in volar and mammary SGs of PND-25. A special protein complex of NPY2R/NPY5R/NFATc1 in PND-25. NFATc1 was dephosphorylated and activated, then localized into nucleus to exert as a transcription factor in volar SGs of PND-35. NFATc1 was especially binding at enhancer regions to facilitate the distal SG and sebum related genes’ transcription. Dual specificity tyrosine phosphorylation regulated kinase 1A (DYRK1A) contributed to NFATc1 phosphorylation in PND-25, and inactivated of DYRK1A resulted in NFATc1 dephosphorylation and nuclear localization in PND-35. Conclusions Our findings unmask the new role of NPY2R/NFATc1/DYRK1A in pubertal SG, and are of benefit to advanced understanding the molecular mechanism of SGs’ function after puberty, and provide some theoretical basis for the treatment of acne vulgaris from the perspective of hormone regulation. Graphical Abstrac