OSGIN1 regulates PM-induced fibrosis via mediating autophagy in an in vitro model of COPD.

Fine particulate matter (PM) has been identified as a significant contributing factor to the exacerbation of chronic obstructive pulmonary disease (COPD). It has been observed that PM may induce lung fibrosis in COPD, although the precise molecular mechanism behind this remains unclear. In a previous study, we demonstrated that PM upregulates oxidative stress induced growth inhibitor 1 (OSGIN1), which in turn leads to injury in airway epithelial cells, thereby, suggesting a potential link between PM exposure and COPD.

Reactive Oxygen Species-Triggered Curcumin Release from Hollow Mesoporous Silica Nanoparticles for PM-Induced Acute Lung Injury Treatment.

Exposure to fine particulate matter with a diameter ≤2.5 μm (PM) can result in serious inflammation and oxidative stress in lung tissue. However, there is presently very few effective treatments for PM-induced many pulmonary diseases, such as acute lung injury (ALI).

LncRNA BCLET variant confers bladder cancer susceptibility through alternative splicing of MSANTD2 exon 1.

Background: Alternative splicing (AS)-related single nucleotide polymorphisms (SNPs) are associated with risk of cancers, but the potential mechanism has not been fully elucidated.

Methods: Two-stage case-control studies comprising 1630 cases and 2504 controls were conducted to investigate the association between the AS-SNPs and bladder cancer susceptibility. A series of assays were used to evaluate the functional effect of AS-SNPs on bladder cancer risk.

linc01515 regulates PM-induced oxidative stress via targeting NRF2 in airway epithelial cells.

Dysregulation of long non-coding RNAs (lncRNAs) is involved in the adverse effects caused by fine particulate matter (PM). However, the molecular mechanism is not fully clarified. In this study, we performed lncRNA sequencing on PM-treated human bronchial epithelial (HBE) cells to identify vital lncRNAs, and verified the differential expression of the lncRNAs by RT-qPCR in HBE and human normal lung epithelial (BEAS-2B) cells.

Biomineralized MnO Nanoplatforms Mediated Delivery of Immune Checkpoint Inhibitors with STING Pathway Activation to Potentiate Cancer Radio-Immunotherapy.

Radiotherapy (RT), as one of the main methods in the clinical treatment of various malignant tumors, would induce systemic immunotherapeutic effects by triggering immunogenic cell death (ICD) of cancer cells. However, the antitumor immune responses produced by RT-induced ICD alone usually are not robust enough to eliminate distant tumors and thus ineffective against cancer metastases. Herein, a biomimetic mineralization method for facile synthesis of MnO nanoparticles with high anti-programmed death ligand 1 (αPDL1) encapsulation efficiency (αPDL1@MnO) is proposed to reinforce RT-induced systemic antitumor immune responses.

Chlorinated Organophosphate Flame Retardants Impair the Lung Function via the IL-6/JAK/STAT Signaling Pathway.

Toxicological studies have revealed the adverse impacts of organophosphate flame retardants (OPFRs) on the respiratory system, while there is a lack of epidemiological evidence, and information for risk assessment remains insufficient. Herein, we investigated the associations of urinary metabolites of OPFRs with the lung function in 987 adults participating in the U.S.