The adiponectin paralog CORS-26 (collagenous repeat-containing sequence of 26kDa protein) is a member of the C1q/TNF-alpha molecular superfamily. CORS-26 is a secreted protein and baculovirus-produced CORS-26 released in the supernatant of insect cells forms stable trimers. Adiponectin exerts anti-inflammatory effects in LPS-treated monocytic cells and CORS-26 also reduces IL-6 and TNF-alpha secretion but does not increase IL-10. Suppression of NFkappaB signalling may explain the anti-inflammatory actions of CORS-26. Furthermore CORS-26 protein was detected in human monocytic and dendritic cells. The present data demonstrate for the first time that CORS-26 forms trimers, exerts anti-inflammatory properties and that it is expressed in monocytic cells. Therefore CORS-26 may provide a new target for pharmacological drugs in inflammatory diseases like the metabolic syndrome.
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http://dx.doi.org/10.1016/j.febslet.2005.09.022 | DOI Listing |
Sci Rep
January 2025
Department of Biomedical Engineering, University of Rochester, Rochester, NY, USA.
The aberrant vascular response associated with tendon injury results in circulating immune cell infiltration and a chronic inflammatory feedback loop leading to poor healing outcomes. Studying this dysregulated tendon repair response in human pathophysiology has been historically challenging due to the reliance on animal models. To address this, our group developed the human tendon-on-a-chip (hToC) to model cellular interactions in the injured tendon microenvironment; however, this model lacked the key element of physiological flow in the vascular compartment.
View Article and Find Full Text PDFCell Death Dis
January 2025
NHC Key Laboratory of Advanced Reproductive Medicine and Fertility (China Medical University), National Health Commission, Shenyang, 110004, China.
Metabolic rewiring underlies effective macrophages defense to respond disease microenvironment. However, the underlying mechanisms driving metabolic rewiring to enhance macrophage effector functions remain unclear. Here, we demonstrated that the metabolic reprogramming in inflammatory macrophages depended on the acetylation of CLYBL, a citramalyl-CoA lyase, at lysine 154 (K154), and blocking CLYBL-K154 acetylation restricted the release of pro-inflammatory factors.
View Article and Find Full Text PDFSpectrochim Acta A Mol Biomol Spectrosc
January 2025
Department of Analytical Chemistry, University of Valencia, Dr. Moliner 50, 46100 Burjassot, Spain. Electronic address:
The presence of cells in urine and in particular White Blood Cells (WBCs) is often associated with Urinary Tract Infections (UTIs) and other diseases. Non-invasive screening of WBCs requires the development of cost-effective point of care diagnostic tools. Infrared (IR) spectroscopy has the potential to identify and quantify cells in urine.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Health Science Center, Ningbo University, Ningbo, China. Electronic address:
Myasthenia gravis (MG) is a T cell-dependent, B cell-mediated disorder strongly associated with antigen presentation by dendritic cells (DCs). In MG, mucosal tolerance is linked to increased expression of TGF-β mRNA in monocytes. Additionally, monocytic myeloid-derived suppressor cells (M-MDSCs) exhibit negative immunomodulatory effects by suppressing autoreactive T and B cells.
View Article and Find Full Text PDFInflamm Res
January 2025
Department of Pathology and Laboratory Medicine, Medical University of South Carolina, 173 Ashley Ave, Charleston, SC, 29425, USA.
Background: Sepsis-associated encephalopathy (SAE) often results from neuroinflammation. Recent studies have shown that brain platelet-derived growth factor receptor β (PDGFRβ) cells, including pericytes, may act as early sensors of infection by secreting monocyte chemoattractant protein-1 (MCP-1), which transmits inflammatory signals to the central nervous system. The erythroblast transformation-specific (ETS) transcription factor Friend leukemia virus integration 1 (Fli-1) plays a critical role in inflammation by regulating the expression of key cytokines, including MCP-1.
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