IL-10 mediates pleural remodeling in systemic lupus erythematosus.

Background: Interleukin-10 (IL-10), a pivotal anti-inflammatory cytokine, has gotten attention for its involvement in tissue remodeling and organ fibrosis. Pleurisy and subsequent pleural remodeling are recognized as quantifiable indicators of systemic lupus erythematosus (SLE) activity. However, the role of IL-10 in SLE-associated pleural remodeling remains unknown.

Synthesis and evaluation of L-quebrachitol derivatives against platelet aggregation.

Thrombosis plays an important role in the occurrence and development of cardiovascular and cerebrovascular diseases that contribute to high mortality and morbidity in patients. L-(-)-Quebrachitol (QCT), a natural product, was first isolated from quebracho bark. It can inhibit PAF receptor and decrease gastric damage induced by indomethacin, as a drug against platelet aggregation.

Aspirin enhances the sensitivity of hepatocellular carcinoma side population cells to doxorubicin via miR-491/ABCG2.

To explore whether aspirin (ASA) enhances the sensitivity of hepatocellular carcinoma (HCC) side population (SP) cells to doxorubicin (Doxo) via miR-491/ATP-binding cassette sub-family G member 2 (ABCG2). Non-SP and SP cells were isolated from MHCC-97L cell line using flow cytometry analysis and fluorescence-activated cell sorting. Colony formation assay was performed to determine the colony-formation ability of cells.

Interleukin-17A and -17F single nucleotide polymorphisms associate with susceptibility of asthma in Chinese Han population.

Interleukin 17 (IL-17) plays important roles in the progression of asthma. Genetic variants in the Il-17 may influence the immunopathogenesis of many diseases. Many studies have investigated the relevance of IL-17 polymorphism with cancers or immune diseases, including asthma.

IL-4-induced caveolin-1-containing lipid rafts aggregation contributes to MUC5AC synthesis in bronchial epithelial cells.

Background: Mucus overproduction is an important feature of asthma. Interleukin (IL)-4 is required for allergen-induced airway inflammation and mucus production. MUC5AC gene expression is regulated by transcript factors NF-κB.

miR-18a-5p Inhibits Sub-pleural Pulmonary Fibrosis by Targeting TGF-β Receptor II.

Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease that typically leads to respiratory failure and death within 3-5 years of diagnosis. Sub-pleural pulmonary fibrosis is a pathological hallmark of IPF. Bleomycin treatment of mice is a an established pulmonary fibrosis model.

Activation of calpain by renin-angiotensin system in pleural mesothelial cells mediates tuberculous pleural fibrosis.

Pleural fibrosis is defined as an excessive deposition of extracellular matrix (ECM) components that results in destruction of the normal pleural tissue architecture. It can result from diverse inflammatory conditions, especially tuberculous pleurisy. Pleural mesothelial cells (PMCs) play a pivotal role in pleural fibrosis.

Crosstalk between calpain activation and TGF-β1 augments collagen-I synthesis in pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease of unknown cause that typically leads to respiratory failure and death within 3-5years of diagnosis. TGF-β1 is considered a major profibrotic factor. However, TGF-β1 is necessary but not sufficient to the pathogenesis of fibrotic lesion of the lungs.

Bleomycin induced epithelial-mesenchymal transition (EMT) in pleural mesothelial cells.

Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease characterized by the development of subpleural foci of myofibroblasts that contribute to the exuberant fibrosis. Recent studies revealed that pleural mesothelial cells (PMCs) undergo epithelial-mesenchymal transition (EMT) and play a pivotal role in IPF. In animal model, bleomycin induces pulmonary fibrosis exhibiting subpleural fibrosis similar to what is seen in human IPF.

Clinical relevance of plasma miR-21 in new-onset systemic lupus erythematosus patients.

Background: Plasma miR-21 is widely investigated as biomarker in many diseases. Recent studies show that miR-21 participates in the development of systemic lupus erythematosus (SLE). The aim of this study was to evaluate the expression profile of miR-21 in the plasma of SLE patients.

Dissociation of FK506-binding protein 12.6 kD from ryanodine receptor in bronchial smooth muscle cells in airway hyperresponsiveness in asthma.

Airway hyperresponsiveness (AHR) in asthma is predominantly caused by increased sensitivity of bronchial smooth muscle cells (BSMCs) to stimuli. The sarcoplasmic reticulum (SR)-Ca(2+) release channel, known as ryanodine receptor (RyR), mediates the contractive response of BSMCs to stimuli. FK506-binding protein 12.

Reactive oxygen species and x-ray disrupted spontaneous [Ca²⁺]I oscillation in alveolar macrophages.

Radiation leads to a rapid burst of reactive oxygen species (ROS), which is considered to be one of the major causes of radiation-induced injury. ROS have previously been shown to induce changes in cytosolic Ca²⁺ ([Ca²⁺]i) including [Ca²⁺]i oscillation. However, the role of radiation in [Ca²⁺]i oscillation is poorly understood.

Exercise training attenuated chronic cigarette smoking-induced up-regulation of FIZZ1/RELMα in lung of rats.

FIZZ/RELM is a new gene family named "found in inflammatory zone" (FIZZ) or "resistin-like molecule" (RELM). FIZZ1/RELMα is specifically expressed in lung tissue and associated with pulmonary inflammation. Chronic cigarette smoking up-regulates FIZZ1/RELMα expression in rat lung tissues, the mechanism of which is related to cigarette smoking-induced airway hyperresponsiveness.

Polymorphisms of the T-cell immunoglobulin and mucin domain molecule-3 are not associated with autoimmune Graves' disease in a Chinese Han Population.

Objectives: This study aimed to investigate the association between polymorphisms of T-cell immunoglobulin and mucin domain molecule-3 (TIM-3) and Graves' disease (GD) in a Chinese population.

Design And Methods: Genomic DNA was extracted from peripheral blood cells of the 182 GD patients and 150 control subjects. The TIM-3 gene polymorphic sites were genotyped.

Transforming growth factor-β1 suppresses the up-regulation of matrix metalloproteinase-2 by lung fibroblasts in response to tumor necrosis factor-α.

Exposed to inflammatory factors or cytokines, fibroblasts appear to play additional roles beyond the deposition of extracellular matrix. It has been reported that tumor necrosis factor-α (TNF-α) induces the production of matrix metalloproteinase-2 (MMP-2) and transforming growth factor-β1 (TGF-β1) in fibroblasts. In this study, we demonstrated that the active MMP-2 secreted by lung fibroblasts reached the peak level at 12 hours after TNF-α treatment, whereas, by adding anti-TGF-β1 antibody in the culture medium, the MMP-2 production in response to TNF-α was maintained at high levels after 24 hours of treatment.

Family-based association study of Tim-1 and Tim-3 gene polymorphisms with childhood asthma in Chinese trios.

Background: Asthma is a complex genetic disease, caused by the interaction of multiple genetic and environmental factors. T cell immunoglobulin domain and mucin domain (Tim) genes are located in chromosome 5q31-33, a region repeatedly linked to asthma or asthma-related phenotypes in several populations. Two members of Tim families, Tim-1 and Tim-3, which are expressed on T cell surface and potentially involved in T cell proliferation and differentiation, are good candidate genes for asthma.

[Effects of transketolase-like gene TKTL1 on occurrence and metastasis of human nasopharyngeal carcinoma].

Objective: To investigate the effects of transketolase-like gene TKTL1 on the occurrence and metastasis of human nasopharyngeal carcinoma (NPC).

Methods: Real-time PCR was used to determine the mRNA expression levels of transketolase gene family (TKT, TKTL1, and TKTL2) in the 65 biopsy specimens of human nasopharyngeal carcinoma, 9 at stage I, 15 at stage II, 16 at stage III, 13 at stage IVA, and 12 at stage IVB, 42 with metastasis and 232 without metastasis, and 9 biopsy specimens of chronic nasopharyngitis.

Results: The TKL activity level of the NPC tissues was 21.

Overexpression of transketolase protein TKTL1 is associated with occurrence and progression in nasopharyngeal carcinoma: a potential therapeutic target in nasopharyngeal carcinoma.

Over 80 years ago, Warburg identified a particular metabolic pathway in carcinomas characterised by the anaerobic degradation of glucose even in the presence of oxygen that leads to the production of large amounts of lactate (known as the Warburg effect). Now, widespread clinical use of positron-emission tomography (PET) has confirmed that there exists enhanced glucose degradation in tumors. Recent research demonstrated that pentose phosphate pathway (PPP) was augmented in some tumors, especially non-oxidative part of PPP.

The TKTL1 gene influences total transketolase activity and cell proliferation in human colon cancer LoVo cells.

A plasmid carrying DNA to be transcribed into a small interfering RNA against transketolase-like-1 mRNA was constructed and transfected into a human colon cancer cell line. The mRNA expression of transketolase gene family in the human colon cell line was determined by real-time polymerase chain reaction. The effect of anti-transketolase-like-1 small interfering RNA on cell proliferation and cell cycle in the human colon cancer cell line cells was detected by flow cytometry and 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl tetrazolium bromide.

Gene silencing of TKTL1 by RNAi inhibits cell proliferation in human hepatoma cells.

We detected a strong upregulation of the mutated transketolase transcript (TKTL1) in human hepatoma cell line HepG2, whereas transketolase (TKT) and transketolase-like-2 (TKTL2) transcripts were not upregulated. We inhibited the expression of TKTL1 by RNAi in HepG2 cells. It was found that total transketolase activity was dramatically downregulated and the proliferation of cancer cells was significantly inhibited in HepG2 cells.