China
Africa
Explore chapters and articles related to this topic
Mother and Embryo Cross Communication during Conception
Published in Carlos Simón, Carmen Rubio, Handbook of Genetic Diagnostic Technologies in Reproductive Medicine, 2022
Anna Idelevich, Andrea Peralta, Felipe Vilella
The placental interface mediates interaction between the mother and fetus, and efforts were made to analyze changes in placental gene expression [135]. A recent study carried out single-cell transcriptomics on the villous tissue from two human term placentas, obtaining 87 single-cell transcriptomes. These transcriptomes were grouped into three large clusters. The data were further complemented by two transcriptomes of a syncytiotrophoblast, collected from a single placenta by laser microdissection, the transcriptomes of primary undifferentiated endometrial stromal fibroblast (ESF), and the transcriptome of in vitro primary differentiated decidual cells. Single-cell data were aligned with tissue-level data to estimate cell origin and the top 25% (2108) most highly expressed genes were found to comprise 80% of the total aligned placental mRNAs. Trophoblast cells at term were concluded to be the most abundant cell type. Single-cell gene expression profiles were segregated into five clusters, based on combinations of known trophoblast markers (KRT7, KRT8, GCM1, and CYP19A1) and diagnostic genes with > 10-fold higher expression than in uterine and immune cells.
Germ Cell Tumors of the Central Nervous System
Published in David A. Walker, Giorgio Perilongo, Roger E. Taylor, Ian F. Pollack, Brain and Spinal Tumors of Childhood, 2020
Matthew J. Murray, Ute Bartels, James C. Nicholson
At a transcriptomic level, histological subtypes of GCT display distinct gene expression profiles and patterns of cellular pathway activation.36,37 For example, germinomas express pluripotency genes (NANOG, POU5F1 (OCT3/4), TFAP2C, and UTF)37 whereas YSTs express genes relevant to differentiation (KRT8, KRT19) and lipid metabolism (APOA1, APOA2).37 In addition, YSTs/NGGCTs have activation of the BMP/Wnt38 and EGFR/mTOR39 proliferation pathways. These biological variances may account for differences in the observed natural history between germinomas and NGGCTs.
Single-cell profiling of infiltrating B cells and tertiary lymphoid structures in the TME of gastric adenocarcinomas
Published in OncoImmunology, 2021
Lizhou Jia, Tengqi Wang, Youcai Zhao, Shuyu Zhang, Teer Ba, Xingwang Kuai, Bin Wang, Ning Zhang, Wei Zhao, Zhiping Yang, Haishi Qiao
We selected cell group 8, 9, 22, 23, and 26 for epithelial cell cluster analysis. Nine sub-clusters (5,036 epithelial cells) were obtained (Figure 5a), and the most highly expressed genes in each subgroup are shown in the Supplementary Figure S6. We divided the epithelial cells into benign and malignant cells by analyzing the proportion of sub-cluster in different samples. We found that subclusters 1, 2, 5, 6, 8, and 9 mainly existed in tumor samples, while sub-clusters 3, 4, and 3 are mainly present in non-tumor samples (Figure 5b). InferCNV is a relatively effective tool to determine changes in intracellular chromosome copy number variation (CNV). Therefore, InferCNV was used to explore tumor RNA-seq data to analyze somatic large-scale copy number alterations (CNA), such as the gain or loss of whole chromosomes and large segments of chromosomes.22 In general, tumor cells are prone to be CNV mutations, and genes in the regions with CNV changes occurring are always characterized with over-expressed or down-expressed compared with normal cells (Figure 5c). We selected the cell population previously defined as epithelial cells, and inferred malignant cells and nonmalignant cells of cell population according to the expression matrix by InferCNV. Finally, we employed the average expression levels of “KRT14”, “KRT17”, “KRT6A”, “KRT5”, “KRT8”, “KRT18”, “KRT15”, “KRT6C”, “KRTCAP3”, “SFN”, “EpCAM”, and other genes as Epithelial scores between malignant tumor and cancer-adjacent tissue. Significant differences were found between the two groups (t-test, P < .001) (Figure 5d).
Gut commensal derived-valeric acid protects against radiation injuries
Published in Gut Microbes, 2020
Yuan Li, Jiali Dong, Huiwen Xiao, Shuqin Zhang, Bin Wang, Ming Cui, Saijun Fan
Keratins (KRTs) have yet been discovered consist of more than 20 members. A major role fulfilled by KRTs is to protect epithelial cells from mechanical and non-mechanical stresses. Additional functions of KRTs manifests including the regulation of cell signaling and stress responses.14,15 Dysfunction of KRT may cause various diseases. For example, epidermolysis bullosa simplex (EBS) is related to the mutation of KRT5 and KRT14.16 KRT8/KRT18 variants could be a risk factor for liver fibrosis progression.17 In addition, diffuse expression of KRT7 and KRT19 in the end-stage kidney could increase the risk of tumor development.18 Importantly, clinical and laboratory researches have demonstrated the significant role for KRTs in the protection of the epithelial integrity in the small intestine,19,20 and the down-regulation of KRT1 is correlated with the progression of inflammatory bowel disease (IBD).21 Our previous studies have shown that radiation could cause intestinal injury, covering elevated levels of inflammation and the destruction of intestinal integrity. However, whether KRT1 contributes to radioprotection remains an enigma.
Systemic inflammation is associated with circulating cell death released keratin 18 fragments in colorectal cancer
Published in OncoImmunology, 2020
Päivi Sirniö, Juha P. Väyrynen, Shivaprakash J. Mutt, Karl-Heinz Herzig, Jaroslaw Walkowiak, Kai Klintrup, Jyrki Mäkelä, Tuomo J. Karttunen, Markus J. Mäkinen, Anne Tuomisto
In particular, the liver is a potential source of the KRT18 fragments. KRT8/KRT18 represents the characteristic and only keratin pair of normal hepatocytes.40 Indeed, an increase in KRT18 fragment levels is an established marker of liver injury.41 Potential mechanism leading to liver injury in CRC may be related to changes in the extra-tumoral intestinal mucosa or tumor secreted or induced mediators, or metastasis. When the intestinal epithelial barrier is disrupted, and intestinal permeability is increased, bacteria or bacterial components can enter the liver via the portal circulation. Animal CRC models have shown a strong association between circulating IL6 levels and intestinal permeability.42,43 In the liver, gut-derived endotoxin, lipopolysaccharide (LPS) of gram-negative bacteria, induces Kupffer cell activation and liver injury that is reflected to circulating aKRT18 and tKRT18 and nKRT18 levels.44 Thus, part of serum KRT18 in CRC patients may originate from the liver, representing a consequence rather than cause of systemic inflammation. Moreover, liver is the most common site of metastasis in CRC patients, and metastatic spread may result in cell damage in the metastatic site. Accordingly, in patients with metastatic CRC, alkaline phosphatase, and aspartate transaminase levels, markers of liver injury have been shown to correlate with tKRT18 and aKRT18.20 All in all, multiple tissues may contribute to circulating KRT18 levels, and the potential sources besides necrotic tumor cells in CRC remain hypothetical.