Nicotinic acetylcholine receptor (nAChR) of subtypes said "neuronal" are expressed in epithelial and immune system cells and participate in acetylcholine signaling by neural or non-neural pathways. It has been shown in macrophages that activation of type α7 nAChRs inhibits the release of pro-inflammatory cytokines, but the ion channel function has not been recorded in these cells. The objective of this work was to clarify what are the molecular mechanisms of transduction of α7 nAChRs in macrophages. To this end, RAW 264.7 cells, mouse peritoneal macrophages and rat hippocampal neurons were used. Cells were submitted to electrophysiological studies and stimulated with brief applications of the agonists acetylcholine, choline and nicotine, associated or not with the allosteric modulator PNU-120596. Responses to ATP were recorded as a reference. Furthermore, macrophages were submitted to cytokine quantitation. The electrophysiological results showed that macrophages responded to ATP but did not show whole-cell current by stimulation with nicotinic agonists. However, hippocampal neurons stimulated in the same pharmacological conditions of the macrophages showed ionic currents typical of the α7 nicotinic receptors. No effect of nicotine was observed in the lipopolysaccharide-induced TNF-α release. These results suggest that the α7 nAChR in macrophages do not work as ion channels similar to those expressed in neurons.

Background: Hepatocellular carcinoma (HCC) faces significant challenges in early diagnosis and prognostic assessment, necessitating novel molecular biomarkers. The role of GCN1 in tumorigenesis remains unclear, warranting systematic investigation of its clinical value. Methods: Utilizing multi-omics data from 164 HCC patients in the TCGA database, we comprehensively evaluated the diagnostic and prognostic value of GCN1 through differential expression analysis, Cox proportional hazards regression, and gene set enrichment analysis (GSEA). Results: GCN1 expression was significantly upregulated in tumor tissues (P<0.001), with ROC analysis demonstrating an AUC of 0.921 (95% CI: 0.893-0.950) for discriminating tumor from normal tissue. Clinical correlation analysis revealed that high GCN1 expression significantly associated with advanced T stage (OR=1.941, P=0.002) and AFP levels >400 ng/ml (OR=3.697, P<0.001). Multivariate survival analysis confirmed its independent prognostic value (HR=1.454, P=0.038). Functional analysis indicated GCN1 promotes tumor progression by regulating cell cycle (NES=2.385) and axon guidance (NES=2.307) pathways. Conclusion: This study first elucidates the dual clinical value of GCN1 in HCC, providing a theoretical foundation for developing novel diagnostic biomarkers and prognostic evaluation systems. Future research should validate its molecular mechanisms and explore potential targeted therapies.

Objective: The study investigated the biological effects and molecular mechanisms of platelet-rich plasma (PRP) on periodontal bone regeneration. Methods: Electronic and manual searches were searched up to 1 October 2022 in the following databases: Pubmed, Scopus, Cochrane Library and Embase. [Platelet rich plasma or platelet or growth factors] and [periodontal] or [bone regeneration or bone defect or bone reconstruction] were used for searching. This study reviewed and analyzed published papers associated with PRP and periodontal bone defect restoration or bone regeneration or bone reconstruction. Results: Different growth factors exhibited varied biological characteristics and function. In-vitro studies, animal experiments and clinical studies confirmed that PRP displayed assorted role in periodontal bone defects repair. The growth factors secreted from PRP can promote new bone formation, soft tissue regeneration and wound healing. The fiber three-dimensional structure in PRP is conducive to the growth and migration of cells and provides strong support for the regeneration of periodontal soft and hard tissues. The anti-inflammatory characteristics of PRP are also closely related to the repair of periodontal bone defects. Conclusion: PRP played an important biological effect on periodontal bone regeneration. The mechanism is closely related to PRP promoting the growth, proliferation, differentiation and migration of periodontal ligament cells and osteoblasts, and the fiber stereo configuration of PRP and the anti-inflammatory effect of leukocytes.