YTHDF1-mediated m6A modification of GBP4 promotes M1 macrophage polarization in acute lung injury.

Background: Acute lung injury (ALI) is a severe condition with multifaceted causes, including inflammation and oxidative stress. This research investigates the influence of m6A (N6-methyladenosine) modification on GBP4, a protein pivotal for macrophage polarization, a critical immune response in ALI.

Methods: Utilizing a mouse model to induce ALI, the study analyzed GBP4 expression in alveolar macrophages.

Risk factors of in-hospital mortality in patients with pneumocystis pneumonia diagnosed by metagenomics next-generation sequencing.

Objectives: The metagenomic next-generation sequencing (mNGS) test is useful for rapid and accurate detection and identification of pathogenic microorganisms. The aim of the present study was to investigate the factors associated with in-hospital mortality in pneumocystis pneumonia (PCP) patients with mNGS-assisted diagnosis.

Methods: Our study enrolled 154 patients with mNGS-positive PCP from August 2018 to February 2022 at the First Affiliated Hospital of Zhengzhou University respectively.

TGFβ1-Smad Signaling Pathway Participates in Interleukin-33 Induced Epithelial-to-Mesenchymal Transition of A549 Cells.

Backgrounds/aims: Epithelial-to-mesenchymal transition (EMT) has been proven to be involved in development and progression of pulmonary fibrosis. This study aims to investigate the role of transforming growth factor β1 (TGFβ1)-smad signaling pathway in the interleukin-33 (IL-33) induced EMT.

Methods: The human type II alveolar epithelial cell line, A549, and small airway epithelial cells (SAEC) were cultured and divided into 4 groups including Control, LY-2109761 (TGFβ receptor inhibitor), IL-33 and IL-33+LY-2109761 group.

Calpain 1 regulates TGF-β1-induced epithelial-mesenchymal transition in human lung epithelial cells via PI3K/Akt signaling pathway.

Cell proliferation, transformation, and epithelial-mesenchymal transition (EMT) are key processes involved in the development of idiopathic pulmonary fibrosis (IPF). This study investigated the regulatory factors and signaling pathways that mediate EMT in the human type II alveolar epithelial A549 cell line. A549 cells were cultured in RPMI-1640 medium and allocated to the following four groups: blank control group or treated with transforming growth factor-β1 (TGF-β1), TGF-β1 + PD 150606 (a calpain 1 inhibitor), or PD 150606.

Cigarette smoke induces the expression of Notch3, not Notch1, protein in lung adenocarcinoma.

The aim of the present study was to determine the effect of cigarette smoke on the expression of Notch proteins in lung adenocarcinoma (LAC). Protein expression levels of Notch1 and Notch3 were analyzed using immunohistochemistry in 102 human LAC specimens. Of these, 52 were obtained from smokers and 50 from non-smokers.

[Transforming growth factor-β1 induces epithelial-mesenchymal transition in A549 cells by up-regulating expression of calpain].

Objective: To investigate the effect of transforming growth factor-β1 (TGF-β1) on epithelial-mesenchymal transition in type II alveolar epithelial cells and the relationship with Calpain.

Methods: The type II alveolar epithelial cell line-A549 cells cultured in vitro were divided into 4 groups: the control group, the TGF-βl group, the TGF-β1 + PD150606 group, the PD150606 group. Given the corresponding processing,Western-blot and RT-PCR were utilized to evaluate the expression of Calpain- 1,E-cad and α-SMA.

Beneficial Impact of bFGF Antisense Therapy in a Rat Model of Pulmonary Fibrosis.

Objectives: This study aims to explore basic fibroblast growth factor (bFGF)'s role in the development of pulmonary fibrosis through applying bFGF antisense oligonucleotide therapy in a rat model of pulmonary fibrosis.

Methods: Thirty rats were randomly divided into five groups: bFGF sense-transfected, bFGF antisense-transfected, null vector-transfected, pulmonary fibrosis (PF), and control groups. Sense, antisense, null, and PF groups were administered bleomycin to induce pulmonary fibrosis.

Lack of association between ACE insertion/deletion polymorphism and lung cancer: A meta-analysis.

Objective: Previous case-control studies on the relation between the angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and lung cancer were controversial. In this study, we aimed to further evaluate the relation between the ACE gene I/D polymorphism and lung cancer.

Methods: We selected eight case-control studies related to the ACE gene I/D polymorphism and lung cancer by searching PubMed, EMBase, Chinese Biomedical Literature Database, and Wanfang database.