NCF4 regulates antigen presentation of cysteine peptides by intracellular oxidative response and restricts activation of autoreactive and arthritogenic T cells.

Autoimmune diseases, such as rheumatoid arthritis (RA) and systemic lupus erythematous, are regulated by polymorphisms in genes contributing to the NOX2 complex. Mutations in both Ncf1 and Ncf4 affect development of arthritis in experimental models of RA, but the different regulatory pathways mediated by NOX2-derived reactive oxygen species (ROS) have not yet been clarified. Here we address the possibility that intracellular ROS, regulated by the NCF4 protein (earlier often denoted p40phox) which interacts with endosomal membranes, could play an important role in the oxidation of cysteine peptides in mononuclear phagocytic cells, thereby regulating antigen presentation and activation of arthritogenic T cells.

Critical Roles of Protein Arginine Methylation in the Central Nervous System.

A remarkable post-transitional modification of both histones and non-histone proteins is arginine methylation. Methylation of arginine residues is crucial for a wide range of cellular process, including signal transduction, DNA repair, gene expression, mRNA splicing, and protein interaction. Arginine methylation is modulated by arginine methyltransferases and demethylases, like protein arginine methyltransferase (PRMTs) and Jumonji C (JmjC) domain containing (JMJD) proteins.

LncRNA WDR11-AS1 Promotes Extracellular Matrix Synthesis in Osteoarthritis by Directly Interacting with RNA-Binding Protein PABPC1 to Stabilize SOX9 Expression.

Osteoarthritis (OA) is a degenerative disease of articular cartilage that is mainly characterized by chronic and mild inflammation of the joints. Recently, many studies have reported the crucial roles of long noncoding RNAs (lncRNAs) in OA as gene transcriptional regulatory factors, diagnostic biomarkers, or therapeutic targets. However, the exact mechanisms of lncRNAs in the regulation of OA progression remain unclear.

Retracted Article: CircRNA PVT1 modulates cell metastasis the miR-181a-5p/NEK7 axis and cisplatin chemoresistance through miR-181a-5p-mediated autophagy in non-small cell lung cancer.

In the initiation and evolution of human cancers, circular RNAs (circRNAs) act as crucial regulators. The aim of this report was to ascertain the functional mechanisms of circRNA plasmacytoma variant translocation 1 (circPVT1) in the metastasis and chemoresistance of non-small cell lung cancer (NSCLC). The levels of circPVT1, microRNA-181a-5p (miR-181a-5p) and non-inherited maternal antigens-related kinase 7 (NEK7) were examined quantitative real-time polymerase chain reaction (qRT-PCR).

Interpreting the MicroRNA-15/107 family: interaction identification by combining network based and experiment supported approach.

Background: The highly conservative miR-15/107 family (also named as miR-15/107 gene group) including ten miRNA members is currently recognized strongly implicated in multiple human disorders. Some studies focus on the entire family rather than individual miRNA for a bigger picture, while there is also certain signature dysregulation for some of the individual miRNA implicated even in the same disorder.

Methods: Faced with the exponential growth of experimental evidence, our study tries to analyze their function and target interactions using various bioinformatics tools.

miR-497 Is Implicated in the Process of Chondrogenesis and Inhibits IHH Gene Expression in Human Chondrocytes.

Objective: The aim of this study was to examine differences in microRNA-497 (miR-497) expression during cartilage tissue formation and to test whether miR-497 directly interferes with Indian hedgehog (IHH) gene and inhibits IHH expression in human chondrocytes.

Design: At different cartilage development stages and different time points in bone matrix gelatin-induced endochondral ossification (BMG-ECO) rat models, the expression of miR-497 and the Ihh gene was monitored at the mRNA level. Bioinformatic analysis, gene mutation, dual luciferase reporter gene assays and gene expression assays at both the mRNA and protein levels in human chondrocytes were subsequently performed to validate the interaction between miR-497 and the IHH gene.

Downregulation of HS6ST2 by miR-23b-3p enhances matrix degradation through p38 MAPK pathway in osteoarthritis.

Osteoarthritis (OA) is the most common form of arthritis involving major structural changes of peripheral joints and local or systemic inflammation and in lack of therapeutic approaches because of complexity of underlying molecular basis. Our previous work showed that HS6ST2, an enzyme involved in the transfer of sulfate, is downregulated in cartilage tissues of OA patients compared with normal donors, but little is known about its regulatory mechanism. In this study, we demonstrated that the expression of HS6ST2 was lower in OA-damaged cartilage than smooth cartilage from the same patient.

GPx1 knockdown suppresses chondrogenic differentiation of ATDC5 cells through induction of reductive stress.

Glutathione peroxidase 1 (GPx1) is a selenium (Se)-containing protein and is induced in cartilage formation. GPx1 eliminates reactive oxygen species (ROS), which are required for chondrogenic induction. The physiological properties of GPx1 in cartilage and the redox mechanisms involved are not known.

Selenoprotein O deficiencies suppress chondrogenic differentiation of ATDC5 cells.

Selenoprotein O (Sel O) is a selenium-containing protein, but its function is still unclear. In the present study, we observed that the mRNA and protein expression levels of Sel O increased during chondrogenic induction of ATDC5 cells. The effects of Sel O on chondrocyte differentiation were then examined through shRNA-mediated gene silencing technique.

TrxR2 deficiencies promote chondrogenic differentiation and induce apoptosis of chondrocytes through mitochondrial reactive oxygen species.

Thioredoxin reductase 2 (TrxR2) is a selenium (Se) containing protein. Se deficiency is associated with an endemic osteoarthropathy characterized by impaired cartilage formation. It is unclear whether TrxR2 have roles in cartilage function.

A novel long noncoding RNA Lnc-HC binds hnRNPA2B1 to regulate expressions of Cyp7a1 and Abca1 in hepatocytic cholesterol metabolism.

Unlabelled: Cholesterol metabolism disorder in hepatocytes predicts a higher risk of metabolic syndrome (MetS). Long noncoding RNAs (lncRNAs) have emerged as critical players in cellular cholesterol metabolism, but their functions are not systematically clarified. Here, we have identified a novel lncRNA named lnc-HC negatively regulating cholesterol metabolism within hepatocytes through physical interaction with hnRNPA2B1.

Non-Epstein-Barr virus-associated double primary lymphoepithelioma-like carcinoma of the esophagus and stomach: a case report and literature review.

A 55-year-old Chinese male was admitted to the hospital for epigastralgia and dysphagia with a two month history, and hematemesis and melena with a two-day history. Two lesions were found in the esophagus and stomach by esophago--gastroduodenoscopy and computed tomography. The patient underwent subtotal esophagectomy and gastrectomy, esophagogastric anastomosis above the aortic arch, and thoracic-abdominal two-field lymph node dissection.

Upregulation of miR-497 induces hepatic insulin resistance in E3 rats with HFD-MetS by targeting insulin receptor.

Objective: The study aims to find regulatory microRNA(s) responsible for down-regulated insulin receptor (InsR) in the liver of HFD-MetS E3 rats with insulin resistance.

Methods: Firstly, hepatic insulin resistance in HFD-MetS E3 rats was evaluated by RT-qPCR, western blotting, immunohistochemistry and PAS staining. Secondly, the candidate miRNAs targeting rat InsR were predicted through online softwares and detected in the liver of HFD-MetS E3 rats with insulin resistance.

Abnormality of epiphyseal plate induced by selenium deficiency diet in two generation DA rats.

This study aimed to observe the effects of Se deficiency on epiphyseal plates of two generation DA rats fed with artificial total synthetic low Se diet. All F0 and F1 DA rats were fed with synthetic low Se diet (SeD group) and low Se diet supplied with Se (SeS group). The levels of selenium and enzyme activities of GPx were detected in plasma of the rats.

Expression and prognostic significance of VEGFR-2 in breast cancer.

Breast cancer is one of the most common cancers among women in the world. Vascular endothelial growth factor receptor 2 (VEGFR-2) was not only found to play a key role in the development of tumor angiogenesis, but has also been located in tumor cells of a variety of tumors. This study investigated the expression pattern of VEGFR-2 in breast cancer tissue specimens in order to evaluate the role of VEGFR-2 in the prognosis of breast cancer.

Primary malignant melanoma of esophagus: a case report and review of literature.

Primary malignant melanoma of esophagus is a rare but highly aggressive neoplasm, with an incidence less than 0.2% of all primary esophagus neoplasms. There are no clinical differences from other forms of esophagus cancer.

Expression and significance of transforming growth factor-β receptor type II and DPC4/Smad4 in non-small cell lung cancer.

The aim of the present study was to investigate the expression levels of transforming growth factor-β (TGF-β) receptor type II (TβRII) and DPC4/Smad4 in the TGF-β signaling pathway and the importance of these expression levels in non-small cell lung cancer (NSCLC). The mRNA and protein expression levels of TβRII and DPC4/Smad4 were detected by reverse transcription-quantitative polymerase chain reaction and western blotting, respectively, in NSCLC and control nonlesional lung tissues of 60 patients. The protein expression levels of DPC4/Smad4 were detected by immunohistochemistry in paraffin-embedded samples of NSCLC.

Giant neurogenic tumors of mediastinum: report of two cases and literature review.

Neurogenic tumors are commonly found in the mediastinum, especially in the posterior mediastinum or in the chest wall, neurogenic tumors may reach large size before becoming symptomatic. If the neurogenic tumor occupied more than half size of the chest wall accompanied by mediastinal shift, tracheal compression, or superior vena reflux disorder, it may be called giant intrathoracic neurogenic tumors. Giant intrathoracic neurogenic tumors are relatively rare.

Selenium effect on selenoprotein transcriptome in chondrocytes.

Selenium is an essential micronutrient and exerts its biological functions predominantly through selenoproteins. Selenium deficiency is associated with cartilage function. This study demonstrated that all 24 selenoprotein transcripts in mouse genome were detectable in ATDC5 chondrocytes except deiodinase 1 (DIO1), DIO2, and selenoprotein V (Sel V), while all 25 selenoprotein transcripts in human genome were detectable in C28/I2 chondrocytes except glutathione peroxidase 6 (GPx6) and DIO1.

Further evidence for the association of genetic variants of ZNF804A with schizophrenia and a meta-analysis for genome-wide significance variant rs1344706.

Recent accumulating evidence has indicated that ZNF804A (zinc finger protein 804A) may be one of the most robustly implicated genes in schizophrenia. In this report, we examined ZNF804A single nucleotide polymorphisms (SNPs) encompassing exon 4 by performing an association study that used a Han Chinese sample comprised of 492 schizophrenia patients and 516 healthy control subjects. A meta-analysis based on previous studies was also performed.

T-2 toxin enhances catabolic activity of hypertrophic chondrocytes through ROS-NF-κB-HIF-2α pathway.

T-2 toxin (T-2), one of the most important and toxic trichothecene mycotoxins, can cause many medical problems, such as diarrhea, nervous disorders, immunodepression and death, and is also believed as an etiological factor of Kashin-Beck disease, an endemic osteochondropathy prevailing in North China. However, the molecular mechanisms underlying T-2 effects on tissue damage remain elusive. We differentiated ATDC5 chondrogenic cells into hypertrophic chondrocytes, and found that T-2 reduced the expression of anabolic genes, and increased the expression of catabolic genes.

Selenium promotes proliferation of chondrogenic cell ATDC5 by increment of intracellular ATP content under serum deprivation.

Selenium (Se) is an essential micronutrient, and low Se intake in Se-deficient areas plays roles in an endemic osteochondropathy characterized by chondronecrosis in growth plate and articular cartilage. However, the biological activities of Se on cartilage are largely unknown. In this study, we examined the effects of Se on chondrogenic cell ATDC5 and the possible mechanisms involved.

PTHrP inhibits BMP-6 expression through the PKA signaling pathway in breast cancer cells.

Background: PTHrP, a mediator of humoral hypercalcemia of malignancy, is considered as a potential activator to induce breast cancer cells metastasizing to bone. However, recent clinical evidences and basal research results prove that PTHrP expression in primary tumors indicates good prognosis. BMP-6, as a member of TGF-β superfamily, is closely correlated with tumor differentiation and skeletal metastasis.

DeltaEF1 promotes breast cancer cell proliferation through down-regulating p21 expression.

Although the zinc finger-homeodomain transcription factor deltaEF1 is implied as a regulatory factor at the crossroad between proliferation and differentiation in carcinogenesis, its potential effect in the regulation of cell cycle progression has not been well elucidated. In our present study, we provide novel finding that, in breast cancer, the ectopic expression of deltaEF1 in MDA-MB-231 cells significantly promoted cell proliferation by increasing the cell number in S phase of the cell cycle. In contrast, deltaEF1 knockdown by RNA interference exhibited an opposite effect, highlighting a potent role of deltaEF1 to promote G1-S transition of breast cancer cells.