Mechanical strain initiates a variety of responses in pulmonary epithelial cells. The signaling pathways and molecular alterations leading to these responses remain unclear To identify novel signal transduction pathways activated by strain, macroarray analysis was performed on strained pulmonary epithelial cells. Glutathione S-transferase (GST) pi, GST mu, and heat shock protein (HSP)-27 were increased by strain. Western blotting verified that increases in cDNA of these redox-related molecules resulted in an increase in protein. Phosphorylation of HSP-27 was increased after strain, further supporting the role of HSP-27 in strain-induced signal transduction. Strain-induced oxidative stress was verified with the oxidant-sensitive dye dichlorodihydrofluorescein diacetate.

Download full-text PDF

Source
http://dx.doi.org/10.1080/01902140490517782DOI Listing

Publication Analysis

Top Keywords

pulmonary epithelial
12
epithelial cells
12
macroarray analysis
8
signal transduction
8
hsp-27 increased
8
increased strain
8
analysis reveals
4
reveals strain-induced
4
strain-induced oxidant
4
oxidant response
4

Similar Publications

Improved Annotation of Asthma Gene Variants with Cell Type Deconvolution of Nasal and Lung Expression-Quantitative Trait Loci.

Am J Respir Cell Mol Biol

January 2025

University of Groningen, University Medical Center Groningen, Department of Pulmonology and Pediatric Allergy, Beatrix Children's Hospital, Groningen, Netherlands.

Asthma is a genetically complex inflammatory airway disease associated with over 200 Single nucleotide polymorphisms (SNPs). However, the functional effects of many asthma-associated SNPs in lung and airway epithelial samples are unknown. Here, we aimed to conduct expression quantitative trait loci (eQTL) analysis using a meta-analysis of nasal and lung samples.

View Article and Find Full Text PDF

COPD Airway Epithelial Cell-derived Extracellular Vesicles Spread Cellular Senescence via MicroRNA-34a.

Am J Respir Cell Mol Biol

January 2025

National Heart & Lung Institute, Imperial College London, Airway Disease Section, London, United Kingdom of Great Britain and Northern Ireland.

Chronic obstructive pulmonary disease (COPD) is associated with the acceleration of lung aging, and the accumulation of senescent cells in lung tissue. MicroRNA (miR)-34a induces senescence by suppressing the anti-aging molecule, sirtuin-1 (SIRT1). Senescent cells spread senescence to neighbouring and distant cells, favouring COPD progression and its comorbidities.

View Article and Find Full Text PDF

Secondhand vape exposure regulation of CFTR and immune function in cystic fibrosis.

Am J Physiol Lung Cell Mol Physiol

January 2025

Division of Pulmonology, Asthma, Cystic Fibrosis, and Sleep, Emory University School of Medicine, Atlanta, GA, USA.

Secondhand smoke exposure (SHSe) is a public health threat for people with cystic fibrosis (CF) and other lung diseases. Primary smoking reduces CFTR channel function, the causative defect in CF. We reported that SHSe worsens respiratory and nutritional outcomes in CF by disrupting immune responses and metabolic signaling.

View Article and Find Full Text PDF

Gemcitabine (GEM) is a first line chemotherapy drug for bladder cancer (BCa). GEM's lack of specificity has led to disadvantages, resulting in low efficiency, especially when combined with the targeted treatment of BCa stem cells (CSCs), which is considered the cause of BCa recurrence and progression. To enhance the anti-cancer effect and reduce the side effects of GEM targeting of BCa cells/CSCs, an aptamer drug conjugate (ApDC) targeted delivery system was used to improve the efficiency of GEM in BCa therapy using EpCAM aptamer-GEM conjugates based on the epithelial cell adhesion molecule (EpCAM), which is highly expressed on the cell membrane of BCa cells/CSCs.

View Article and Find Full Text PDF

Parkin deficiency aggravates inflammation-induced acute lung injury by promoting necroptosis in alveolar type II cells.

Chin Med J Pulm Crit Care Med

December 2024

Medical Research Center; The Zhejiang Key Laboratory of Intelligent Cancer, Biomarker Discovery and Translation, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, China.

Background: Necroptosis is a form of programmed cell death resulting in tissue inflammation due to the release of intracellular contents. Its role and regulatory mechanism in the context of acute lung injury (ALI) are unclear. Parkin (Prkn), an E3 ubiquitin ligase, has recently been implicated in the regulation of necroptosis.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!