Hyperbaric oxygen treatment on keloid tumor immune gene expression / 中华医学杂志(英文版)

BACKGROUND@#Hyperbaric oxygen treatment (HBOT) has been demonstrated to influence the keloid recurrence rate after surgery and to relieve keloid symptoms and other pathological processes in keloids. To explore the mechanism of the effect of HBOT on keloids, tumor immune gene expression and immune cell infiltration were studied in this work.@*METHODS@#From February 2021 to April 2021, HBOT was carried out on keloid patients four times before surgery. Keloid tissue samples were collected and divided into an HBOT group (keloid with HBOT before surgery [HK] group, n = 6) and a non-HBOT group (K group, n = 6). Tumor gene expression was analyzed with an Oncomine Immune Response Research Assay kit. Data were mined with R package. The differentially expressed genes between the groups were compared. Hub genes between the groups were determined and verified with Quantitative Real-time PCR. Immune cell infiltration was analyzed based on CIBERSORT deconvolution algorithm analysis of gene expression and verified with immunohistochemistry (IHC).@*RESULTS@#Inflammatory cell infiltration was reduced in the HK group. There were 178 upregulated genes and 217 downregulated genes. Ten hub genes were identified, including Integrin Subunit Alpha M (ITGAM), interleukin (IL)-4, IL-6, IL-2, Protein Tyrosine Phosphatase Receptor Type C (PTPRC), CD86, transforming growth factor (TGF), CD80, CTLA4, and IL-10. CD80, ITGAM, IL-4, and PTPRC with significantly downregulated expression were identified. IL-10 and IL-2 were upregulated in the HK group but without a significant difference. Infiltration differences of CD8 lymphocyte T cells, CD4 lymphocyte T-activated memory cells, and dendritic resting cells were identified with gene CIBERSORT deconvolution algorithm analysis. Infiltration levels of CD4 lymphocyte T cell in the HK group were significantly higher than those of the K group in IHC verification.@*CONCLUSION@#HBOT affected tumor gene expression and immune cell infiltration in keloids. CD4 lymphocyte T cell, especially activated memory CD4+T, might be the key regulatory immune cell, and its related gene expression needs further study.

Pivotal micro factors associated with endothelial cells / 中华医学杂志(英文版)

Objective@#Recent studies have shown the important influence of various micro factors on the general biological activity and function of endothelial cells (ECs). Vascular endothelial growth factor (VEGF) and angiogenin (ANG) are classic micro factors that promote proliferation, differentiation, and migration of ECs. The underlying pathophysiological mechanisms and related pathways of these micro factors remain the focus of current research.@*Data sources@#An extensive search was undertaken in the PubMed database by using keywords including "micro factors" and "endothelial cell." This search covered relevant research articles published between January 1, 2007 and December 31, 2018.@*Study selection@#Original articles, reviews, and other articles were searched and reviewed for content on micro factors of ECs. Results: VEGF and ANG have critical functions in the occurrence, development, and status of the physiological pathology of ECs. Other EC-associated micro factors include interleukin 10, tumor protein P53, nuclear factor kappa B subunit, interleukin 6, and tumor necrosis factor. The results of Gene Ontology analysis revealed that variations were mainly enriched in positive regulation of transcription by the RNA polymerase II promoter, cellular response to lipopolysaccharides, negative regulation of apoptotic processes, external side of the plasma membrane, cytoplasm, extracellular regions, cytokine activity, growth factor activity, and identical protein binding. The results of the Kyoto Encyclopedia of Genes and Genomes analysis revealed that micro factors were predominantly enriched in inflammatory diseases.@*Conclusions@#In summary, the main mediators, factors, or genes associated with ECs include VEGF and ANG. The effect of micro factors on ECs is complex and multifaceted. This review summarizes the correlation between ECs and several micro factors.

Pivotal micro factors associated with endothelial cells / 中华医学杂志(英文版)

OBJECTIVE@#Recent studies have shown the important influence of various micro factors on the general biological activity and function of endothelial cells (ECs). Vascular endothelial growth factor (VEGF) and angiogenin (ANG) are classic micro factors that promote proliferation, differentiation, and migration of ECs. The underlying pathophysiological mechanisms and related pathways of these micro factors remain the focus of current research.@*DATA SOURCES@#An extensive search was undertaken in the PubMed database by using keywords including "micro factors" and "endothelial cell." This search covered relevant research articles published between January 1, 2007 and December 31, 2018.@*STUDY SELECTION@#Original articles, reviews, and other articles were searched and reviewed for content on micro factors of ECs.@*RESULTS@#VEGF and ANG have critical functions in the occurrence, development, and status of the physiological pathology of ECs. Other EC-associated micro factors include interleukin 10, tumor protein P53, nuclear factor kappa B subunit, interleukin 6, and tumor necrosis factor. The results of Gene Ontology analysis revealed that variations were mainly enriched in positive regulation of transcription by the RNA polymerase II promoter, cellular response to lipopolysaccharides, negative regulation of apoptotic processes, external side of the plasma membrane, cytoplasm, extracellular regions, cytokine activity, growth factor activity, and identical protein binding. The results of the Kyoto Encyclopedia of Genes and Genomes analysis revealed that micro factors were predominantly enriched in inflammatory diseases.@*CONCLUSIONS@#In summary, the main mediators, factors, or genes associated with ECs include VEGF and ANG. The effect of micro factors on ECs is complex and multifaceted. This review summarizes the correlation between ECs and several micro factors.