Background: CCAAT/enhancer binding proteins (C/EBPs) are key regulators of cell differentiation and linked processes such as proliferation, apoptosis, and gene expression in several organs. C/EBPs are also central for inflammatory responses and infectious defenses, but so far little is known of their role in lung diseases. Chronic bronchitis (CB) and COPD are common smoking-associated lung diseases involving the airway epithelium.
Methods: Gelshifts were used to study C/EBP transcription factor activity in airway epithelial cells obtained by bronchial brush biopsy in four groups: healthy never-smokers (n = 10), asymptomatic smokers (n = 7), and smokers with CB and recurrent infectious exacerbations without COPD (n = 23) and with COPD (n = 13).
Results: C/EBP-binding activity was increased 4.6-fold in airway epithelial cells of healthy smokers compared with never-smokers. In contrast, C/EBP binding activity was not increased in the epithelium of smokers with CB or COPD. C/EBP-beta was the dominant C/EBP in the airway epithelium in all groups.
Conclusions: We hypothesize that this lack of increase in C/EBP-beta activity renders the epithelium incompetent of efficient regeneration and more sensitive to infection, suggesting a previously unknown role for C/EBPs in the pathogenesis of CB and COPD.
Introduction: Macrophages abundantly express liver X receptors (LXRs), which are ligand-dependent transcription factors and sensors of several cholesterol metabolites. In response to agonists, LXRs induce the expression of key lipid homeostasis regulators. Crosstalk between LXRs and inflammatory signals exist in a cell type- and gene-specific manner.
State Key Laboratory of Membrane Biology, School of Basic Medical Sciencese, Institute of Precision Medicine, Tsinghua University, Beijing, 100084, China.
Background: Idiopathic Pulmonary Fibrosis (IPF) is a type of interstitial lung disease characterized by chronic inflammation due to persistent lung damage. Mesenchymal stem cells (MSCs), including those derived from the umbilical cord (UCMSCs) and placenta (PLMSCs), have been utilized in clinical trials for IPF treatment. However, the varying therapeutic effectiveness between these two MSC types remains unclear.
Matrix Gla protein (MGP) is a vitamin K-dependent γ-carboxylated protein that was initially identified as a physiological inhibitor of ectopic calcification, primarily affecting cartilage and the vascular system. Mutations in the gene were found to be responsible for the Keutel syndrome, a condition characterized by abnormal calcifications in the cartilage, lungs, brain, and vascular system. has been shown to be dysregulated in several tumors, including cervical, ovarian, urogenital, and breast cancers.
Department of Physiology, Obesity-mediated Disease Research Center, Keimyung University School of Medicine, 1095 Dalgubeoldae-ro, Dalseo-gu, Daegu, 42601, Republic of Korea. Electronic address:
Type 2 diabetes increases the risk of developing obesity. Although fulvic acid alleviates back fat thickness in pigs, the mechanism underlying its anti-obesity effect remains unclear. Therefore, we investigated the anti-obesity mechanism of fulvic acid using 3T3-L1 adipocytes.
4-(2-Aminoethyl)-benzenesulfonyl fluoride (AEBSF) is a serine protease inhibitor that may alleviate endoplasmic reticulum (ER) stress, a significant contributing factor to cerebral ischemia/reperfusion injury. The molecular crosstalk between ER stress, oxidative stress and autophagy represents a vicious cycle that can be pharmacologically targeted to minimize neuronal death after acute injuries to the central nervous system. However, the neuroprotective effects of AEBSF in the context of cerebral ischemia/reperfusion injury remain unknown.
