自噬的免疫调节作用和机制

Autophagy is a major pathway for degradation of cellular components and it contributes to the survival, differentiation, development, and dynamic homeostasis of organisms. Recent studies have demonstrated that autophagic mechanisms act as the effectors of immune systems, pattern recognition receptors and cy-tokines to clean the invasive pathogens in the cells. It was also found that immune systems recognize the invasive pathogens via monitoring the autophagic products. This pathway delivers the cytoplasmic material for lysosomal hydrolysis and presents the antigens to MHC Ⅱ molecules so as to activate the CD4 + T cells. Importantly, autophagy can couple with signaling for stress responses of cells and/or inflammatory responses to function as a defense. This paper reviewed the advance of rapidly developing research field and introduced the molecular mechanisms that autophagy regulates innate and adaptive immunity. These studies will deepen our understanding the mechanisms of immune responses and may provide a novel therapeutic strategy for autophage-associated diseases.     

自噬的免疫调节作用和机制

Autophagy is a major pathway for degradation of cellular components and it contributes to the survival, differentiation, development, and dynamic homeostasis of organisms. Recent studies have demonstrated that autophagic mechanisms act as the effectors of immune systems, pattern recognition receptors and cy-tokines to clean the invasive pathogens in the cells. It was also found that immune systems recognize the invasive pathogens via monitoring the autophagic products. This pathway delivers the cytoplasmic material for lysosomal hydrolysis and presents the antigens to MHC Ⅱ molecules so as to activate the CD4 + T cells. Importantly, autophagy can couple with signaling for stress responses of cells and/or inflammatory responses to function as a defense. This paper reviewed the advance of rapidly developing research field and introduced the molecular mechanisms that autophagy regulates innate and adaptive immunity. These studies will deepen our understanding the mechanisms of immune responses and may provide a novel therapeutic strategy for autophage-associated diseases.     

凋亡与肿瘤及其治疗进展

Apoptosis, a common and evolutionarily conserved property of all metazoan, is an essential part of life. The loss of cellular homeostasis balance is a character of tumor. The mitochondria (the intrinsic pathway) and the death receptors (the extrinsic pathway) are two major signal transduction pathways. With elucidation of the apoptotic molecular mechanism, some key proteins and genes related with apoptosis had been as the molecular targets for anticancer new drugs. There is the fundamental signficance to research further both apoptotic molecular mechanism and tumor therapy.     

热休克蛋白60的研究进展

The family of HSP60 belongs to heat shock proteins with highly species conservatism and some important biologic functions. It can help other proteins for their assembling, folding and translocating, and plays a role in protecting cells against injuries and other types of stress. In addition, HSP60 is frequently recognized by the immune system as predominant antigens during infections and the progression of certain autoimmune diseases and might provide a novel strategy for the development of immunotherapeutics. This review focuses on distribution, molecular chaperone mechanism, function and gene expression regulation of HSP60.     

Communicating clocks shape circadian homeostasis

Circadian clocks temporally coordinate physiology and align it with geophysical time,which enables diverse life-forms to anticipate daily environmental cycles.In complex organisms,clock function originates from the molecular oscillator within each cell and builds upward anatomically into an organism-wide system.Recent advances have transformed our understanding of how clocks are connected to achieve coherence across tissues.Circadian misalignment,often imposed in modern society,disrupts coordination among clocks and has been linked to diseases ranging from metabolic syndrome to cancer.     

Research of the Effect of the Shear Stress on Endothelial Cells

1 IntroductionCellular mechanism is one of the foundations of regenerating medicine and tissue engineering, which is also an advanced subject in cell mechanism in recent years~([1]). The form and function of a cell, and the growing, reproducing and death, even canceration are related to the characteristics of cell mechanism. While the research of the shear stress on endothelial cells is an important field in cell mechanism. The main bio-functions of endothelial cells are as follows: anti-cruor…     

自噬在肥胖中的研究进展

Obesity is a harmful nutritional metabolic disorder to human health. Autophagy is a catabolic mechanism whereby cells degrade intracellular substances. Recent studies show that autophagy was closely correlated with insulin resistance, fat composing, and lipid droplet and triglyceride accumulation. Here, we review the association between autophagy and obesity, which may provide theoretical and experimental evidence for prevention of obesity and related diseases.     

自噬及铁死亡相关靶点与慢性肾病肾功能损伤的进展：生物信息学分析及实验验证

BACKGROUND: Autophagy and ferroptosis play important roles in the development of chronic kidney disease, but the molecular mechanisms and gene targets related to autophagy and ferroptosis in renal tissue of chronic kidney disease are still unclear. OBJECTIVE: To screen differentially expressed genes in chronic kidney disease-related datasets based on bioinformatics, and to explore potential key biomarkers suitable for screening renal function progression in patients with chronic kidney disease. METHODS: (1) The GSE137570 dataset was obtained from GEO database to screen the differentially expressed genes by Networkanalyst database analysis. Ferroptosis and autophagy related targets were obtained by OMIM, GENECARD, FerrDb and HAMdb databases. The respective data were intersected to obtain autophagy-ferroptosis related differentially expressed genes in chronic kidney disease for parallel enrichment analysis. The STRING website was used to construct the protein-protein interaction network of differentially expressed genes, which was imported into Cytoscape software and analyzed by MCODE and Cytohubba plug-in to screen potential core targets. Enrichment analysis was performed to obtain the functions of these potential core targets. (2) In the in vitro experiment, mouse renal tubular epithelial cells were divided into two groups: the control group received no intervention, while the model group was stimulated with 5 ng/mL transforming growth factor β1 for 24 hours to induce mesenchymal transformation of renal tubular epithelial cells. Flow cytometry was used to measure the levels of reactive oxygen species and changes in mitochondrial membrane potential in the cells. RT-PCR was employed to assess ferroptosis, autophagy-related markers, and the mRNA expression of potential core targets in the cells. RESULTS AND CONCLUSION: After screening the GSE137570 dataset, a total of 480 differentially expressed genes were obtained, including 104 upregulated genes and 376 downregulated genes (log2| (FC) | > 1, P < 0.05). There were 562 ferroptosis-related targets and 1 266 autophagy-related targets obtained from the OMIM, GENECARD, FerrDb, and HAMdb databases. Intersection of differentially expressed genes with ferroptosis- and autophagy-related targets yielded 15 ferroptosis-related targets and 18 autophagy-related targets, respectively. The enrichment analysis results indicate that ferroptosis-related differentially expressed genes are primarily involved in biological processes such as sulfur amino acid metabolism, neutrophil degranulation, and ferroptosis signaling pathways. Autophagy-related differentially expressed genes are mainly enriched in biological processes such as platelet degranulation, extracellular matrix degradation, and receptor tyrosine kinase signaling. After screened by MCODE and CytoHubba, key genes were identified in the protein-protein interaction network, including CD44, ALB, TIMP1, PLG, CCL2, and DPP4. Immune infiltration analysis results indicate that immune cells such as B cells, CD4+ T cells, NK cells, and monocytes show significant differential expression in renal tissue after chronic kidney disease, and the core targets are also significantly correlated with these immune cells (P < 0.05). The results of receiver operator characteristic curve analysis further demonstrate that the pathological progression of chronic kidney disease can be effectively diagnosed by CD44, ALB, TIMP1, PLG, CCL2, and DPP4. Single-cell sequencing results show that, except for PLG, the expression of target genes in the renal tissue of mice in each model group is generally consistent with the results of this experiment. RT-PCR results demonstrate that, for the validation of autophagy and ferroptosis phenotypes, compared with the control group, the model group shows a significant decrease in mRNA expression of LC3B, Nrf2, and SLC7A11 (P < 0.05), and a significant increase in P62 mRNA expression (P < 0.05). Regarding the validation of potential core targets, compared with the control group, the model group exhibits a significant decrease in mRNA expression of ALB and PLG (P < 0.05), and a significant increase in TIMP1 and CCL2 mRNA expression (P < 0.05). Overall, these findings indicate that, through bioinformatics analysis and experimental validation, CD44, ALB, TIMP1, PLG, and CCL2 are abnormally expressed in the renal tissue of patients with chronic kidney disease, closely correlated with estimated glomerular filtration rate and tubulointerstitial fibrosis, and maybe play a predictive role in the progression of chronic kidney disease. © 2024, Chinese Journal of Tissue Engineering Research. All rights reserved.     

内皮抑素及其在肿瘤治疗中的应用研究进展

Endostatin as an endogenous angiogenesis inhibitor can inhibit the tumor angiogenesis through the inhibition of vascular endothelial cell migration by variety of mechanisms, thereby inhibiting the growth of tumor. The effect of combination of endostatin, radiotherapy and chemotherapy is remarkable. In addition, endostatin as a tumor marker with special drug delivery systems has brought a breakthrough in treatment of tumor. Injection of recombinant human endostatin can enhance the anti-tumor effect greatly, and it has entered Phase Ⅲ experimental study. Small molecular endostatin can be purified easily by using the technology of site-directed mutagenesis. Not only can it low the cost of mass production, but also it can provide a broad prospect in the treatment of cancer. In this paper, we provide a review of the progress in the structure of endostatin,anti-tumnor mechanism and the application in cancer therapy.     

神经干细胞的研究

Neural stem cells(NSCs)maintain the potential of proliferation and differentiation in nerve system.The research and application of NSCs have developed into a frontier of neuroscience in recent ysars.This review describes the specificity,contribution,regulation mechanism and application of NSCs.Neural stem cells play an important role in the nervous system of growth and reparation.     

瘦素（leptin）与肥胖

Obesity is a severely public health problem the whole society faces, and it is correlated closely with many diseases, such as diabetesⅡ, hypertension, coronary heart disease,gallqtone, and so on.Therefore it threatens people‘ s survival quality severely. Obesity is a multiple - factor disease including genetic, metabolic and behavioral factor, and the gene is the main determining factor. With the development of molecular biology technique, people have founded several genes involved in obesity. Among these genes, the research on obese gene is the most profound. The protein leptin is the expression product of the obese gene.This review elucidates the structure, the main biological function, the mechanism of leptin and it‘‘s relationship with obesity.     

MicroRNAs,immune cells and pregnancy

MicroRNAs （miRNAs） are a recently discovered class of non-coding RNAs that are expressed in many cell types, where they regulate the expression of complementary RNAs, thus modulating the stability and translation of mRNAs, miRNAs are predicted to regulate the expression of -50% of all protein coding genes in mammals. Therefore, they participate in virtually all cellular processes investigated so far. Altered miRNAs expressions are associated with both physiological （pregnancy） and pathological processes （cancer）. As the dynamic maternal-fetal interface plays a critical role in the maintenance of successful pregnancy, it is not surprising that the miRNAs that are unique to reproductive tissues are abundantly expressed. Research in this field has demonstrated the presence and dysregulation of a distinct set of pregnancy-associated miRNAs; however, most studies have centered on localizing various miRNAs in reproductive microdomains associated with normal or complicated pregnancies. Although several independent miRNA regulatory mechanisms associated with endometrial receptivity, immune cells, angiogenesis and placental development have been studied, miRNA-mediated regulation of pregnancy remains poorly understood. This review provides a summary of the current data on miRNA regulation as well as functional profiles of miRNAs that are found in the uterus, in immune cells associated with maternal tolerance to the fetus, and those involved in angiogenesis and placental development.     

Virus-Encoded microRNAs： Future Therapeutic Targets？

The discovery of microRNAs （miRNAs） is a remarkable breakthrough in the field of molecular genetics, as miRNAs are key actors which regulate gene expression in diverse cellular processes from unicellular yeast to human. The recent discovery of virus-encoded miRNAs indicates that viruses also use this fundamental mode of gene regulation. Research into viral miRNAs function demonstrates that some miRNAs play an important role in regulating both the viral life cycle and the interaction between viruses and their hosts. The first in vivo ＂antagomir＂ study provides an exciting first step towards miRNA therapy, and the potential for ultimately designing molecular medicines based on the modulation of miRNAs seems good.