Exploring the molecular mechanism of estrogen therapy effectiveness after TCRA in IUA patients at single-cell level.

Background: Intrauterine adhesion (IUA) is a common cause of clinically refractory infertility, and there exists significant heterogeneity in the treatment outcomes among IUA patients with the similar severity after transcervical resection of adhesion(TCRA). The underlying mechanism of different treatment outcomes occur remains elusive, and the precise contribution of various cell subtypes in this process remains uncertain.

Results: Here, we performed single-cell transcriptome sequencing on 10 human endometrial samples to establish a single-cell atlas differences between patients who responded to estrogen therapy and those who did not.

Interleukin-33 promotes intrauterine adhesion formation in mice through the mitogen-activated protein kinase signaling pathway.

IL-33 belongs to the inflammatory factor family and is closely associated with the inflammatory response. However, its role in the development of intrauterine adhesions (IUAs) remains unclear. In this study, the role of IL-33 in the formation of IUAs after endometrial injury was identified via RNA sequencing after mouse endometrial organoids were transplanted into an IUA mouse model.

NKD1 targeting PCM1 regulates the therapeutic effects of homoharringtonine on colorectal cancer.

Background: Colorectal cancer (CRC) is the most common primary malignancy. Recently, antineoplastic attributes of homoharringtonine (HHT) have attracted lots of attention. This study investigated the molecular target and underlying mechanism of HHT in the CRC process by using a cellular and animal models.

Corrigendum: Heme oxygenase-1 modulates ferroptosis by fine-tuning levels of intracellular iron and reactive oxygen species of macrophages in response to infection.

[This corrects the article DOI: 10.3389/fcimb.2022.

Heme oxygenase-1 modulates ferroptosis by fine-tuning levels of intracellular iron and reactive oxygen species of macrophages in response to infection.

Macrophages are the host cells and the frontline defense against (Mtb) infection, and the form of death of infected macrophages plays a pivotal role in the outcome of Mtb infections. Ferroptosis, a programmed necrotic cell death induced by overwhelming lipid peroxidation, was confirmed as one of the mechanisms of Mtb spread following infection and the pathogenesis of tuberculosis (TB). However, the mechanism underlying the macrophage ferroptosis induced by Mtb infection has not yet been fully understood.

Bone marrow mesenchymal stem cells combined with estrogen synergistically promote endometrial regeneration and reverse EMT via Wnt/β-catenin signaling pathway.

Background: Intrauterine adhesion (IUA) is a clinical disease characterized by the uterine cavity occlusion caused by the damage of the endometrial basal layer. Bone marrow mesenchymal stem cells (BMSCs) transplantation have the potential to promote endometrial regeneration mainly through paracrine ability. Estrogen is an indispensable and important factor in the repair of endometrial damage, which has been reported as a promising and adjunctive therapeutic application for stem cell transplantation therapy.

Exosomes derived from human placental mesenchymal stem cells ameliorate myocardial infarction via anti-inflammation and restoring gut dysbiosis.

Background: Myocardial infarction (MI) represents a severe cardiovascular disease with limited therapeutic agents. This study was aimed to elucidate the role of the exosomes derived from human placental mesenchymal stem cells (PMSCs-Exos) in MI.

Methods: PMSCs were isolated and cultured in vitro, with identification by both transmission electron microscopy (TEM) and nanoparticle tracking analysis (NTA).

Estrogen attenuates TGF-β1-induced EMT in intrauterine adhesion by activating Wnt/β-catenin signaling pathway.

Although estrogen has crucial functions for endometrium growth, the specific dose and underlying molecular mechanism in intrauterine adhesion (IUA) remain unclear. In this study, we aimed to investigate the effects of estrogen on epithelial-mesenchymal transition (EMT) in normal and fibrotic endometrium, and the role of estrogen and Wnt/β-catenin signaling in the formation of endometrial fibrosis. CCK-8 and immunofluorescence assay were performed to access the proliferation of different concentrations of estrogen on normal human endometrial epithelial cells (hEECs).

CircRNA hsa_circ_0004585 as a potential biomarker for colorectal cancer.

Circular RNAs (circRNAs) are involved in regulating of carcinogenesis of various cancer cells. However, the function of circRNAs in colorectal cancer (CRC) has remained largely unknown. This study investigated the characteristic expression of circRNAs in CRC and adjacent normal tissues, analyzed the miRNAs related to candidate circRNAs, and studied the correlation between circRNAs with clinical data of CRC.

Novel dual-color drug screening model for GLUT4 translocation in adipocytes.

Insulin-responsive glucose transporter type 4 (GLUT4) translocation plays a major role in controlling glucose uptake in adipose tissue and muscle, maintaining homeostasis and preventing hyperglycemia. Screening for chemicals enhancing GLUT4 translocation is an approach for identifying hits of drug development for type 2 diabetes. Here we developed a novel functional dual-color probe, pHluorin-GLUT4-mOrange2, and constructed 3T3-L1 adipocytes based screening system to simply and efficiently screen new compounds stimulating GLUT4 translocation.

EG-VEGF silencing inhibits cell proliferation and promotes cell apoptosis in pancreatic carcinoma via PI3K/AKT/mTOR signaling pathway.

Objective: Pancreatic carcinoma (PC), one of the most prevalent and malignant tumors, has a poor prognosis and a high mortality rate. EG-VEGF, a vascular endothelial growth factor from endocrine glands, also termed as PROK1, has a high positive expression rate in PC tissues and is involved in the pathogenesis of various tumors. However, the expression and potential role of EG-VEGF in PC has not been thoroughly explored.

Rapid pathogen identification using a novel microarray-based assay with purulent meningitis in cerebrospinal fluid.

In order to improve the diagnosis of pathogenic bacteria in cerebrospinal fluid (CSF) with purulent meningitis, we developed a DNA microarray technique for simultaneous detection and identification of seven target bacterium. DNA were extracted from 24 CSF samples with purulent meningitis (or suspected purulent meningitis). The specific genes of each pathogen were chosen as the amplification target, performed the polymerase chain reaction (PCR), labeled with a fluorescence dye, and hybridized to the oligonucleotide probes on the microarray.

Identification of microRNA-124 in regulation of Hepatocellular carcinoma through BIRC3 and the NF-κB pathway.

MicroRNAs (miRNAs) being proved to be involved in the carcinogenesis of numerous tumors. MicroRNA-124 (miR-124), identified as a tumor suppressor, has been demonstrated to exert pivotal roles in multiple processes of tumorigenesis. The present study demonstrated that miR-124 was low-expressed in human hepatocellular carcinoma (HCC) tissues and cell lines.

LncRNA AB209630 inhibits gemcitabine resistance cell proliferation by regulating PI3K/AKT signaling in pancreatic ductal adenocarcinoma.

Background: Recent study revealed that abnormal long noncoding RNAs (lncRNAs) expression are association with chemotherapy resistance of pancreatic ductal adenocarcinoma (PDAC).

Objective: The present study was aimed to investigate the effects of lncRNA AB209630 expression for gemcitabine resistance in PDAC cells.

Methods: In the study, increased expression of lncRNA AB209630 could suppress cell proliferation and cell colony formation ability in gemcitabine resistance cells of PDAC.

Clinical and genomic responses to ultra-short course chemotherapy in spinal tuberculosis.

Traditional treatments for spinal tuberculosis (TB) involve chemotherapy and surgery. In the present study, it has been identified that chemotherapy lasting <6 months [ultra-short course chemotherapy (UCCT)], rather than the 6-18 months of the traditional regimen, is effective in sustaining TB clearance following complete surgical debridement. This current study aims to compare the changes in peripheral blood gene expression prior to and following UCCT, subsequent to complete debridement of spinal TB lesions.