ROS Scavenging Mitigates TNFα Induced Endoplasmic Reticulum Stress and Mitochondrial Fragmentation in Human Airway Smooth Muscle
Clicks: 3
ID: 327453
2026
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This
article has not been analysed, so there is no overall score —
reader engagement is measured and shown alongside.
Reader Engagement
Emerging Content
0.6
/100
3 views
2 readers
AI Quality Assessment
Not analyzed
Readership in this journal
EmergingRanked #55 of 55 articles by views in Food & function
Most read
Least read
Bar heights use a square-root scale.
Mint this article as an NFT
Not yet mintedCreate a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.
5
SUSD
one-off · no wallet required
Abstract
The pro-inflammatory cytokine tumor necrosis factor alpha (TNFα) mediates airway responses to acute inflammation. Previously we demonstrated that, in human airway smooth muscle (hASM) cells, TNFα increases reactive oxygen species (ROS) formation. TNFα also selectively activates the inositol-requiring enzyme 1α (pIRE1α S724 autophosphorylation) endoplasmic reticulum (ER) stress pathway involving splicing of X-box binding protein 1 (XBP1s) and transcriptionally activates cyclin-dependent kinases 1 and 5 (CDK1 and CDK5), promoting dynamin-related protein 1 (DRP1) phosphorylation at serine 616 (pDRP1 S616 ) and mitochondrial fragmentation. In the present study, we hypothesized that in hASM, TNFα-induced ROS triggers pIRE1α S724 /XBP1s ER stress pathway. To test this hypothesis, we examined the impact of the ROS scavenger Tempol on TNFα-induced pIRE1α S724 /XBP1s ER stress pathway and downstream signaling mediating mitochondrial fragmentation. Bronchiolar tissue samples were obtained from 6 patients with no history of smoking or chronic pulmonary disease. The smooth muscle layer was dissected, and hASM cells were dissociated and randomly assigned to four treatment groups: 1) Vehicle, 2) Vehicle + TNFα (20 ng/mL, 6 h), 3) Tempol (500 μM) only, and 4) Tempol (500 μM) + TNFα (20 ng/mL, 6 h). ROS formation was determined by confocal imaging using MitoSOX™ Red. Mitochondria were labeled with MitoTracker Red and imaged using confocal microscopy. Using Western blot, we demonstrated that Tempol reduced cellular ROS formation and mitigated the TNFα-induced increase in pIRE1α S724 , XBP1s, CDK1/5, pDRP1 S616 protein levels and reduced mitochondrial fragmentation. These findings support our hypothesis and indicate a role of ROS in mediating TNFα-induced ER stress and mitochondrial fragmentation.
| Reference Key |
openalex_W7207646463
Use this key to autocite in the manuscript while using
SciMatic Manuscript Manager or Thesis Manager
|
|---|---|
| Authors | Debanjali Dasgupta, Sanjana Mahadev Bhat, G C Sieck |
| Journal | Food & function |
| Year | 2026 |
| DOI |
10.1152/function.036.2026
|
| URL | |
| Keywords | Keywords not found |
Citations
No citations found. To add a citation, contact the admin at info@scimatic.org
Comments
No comments yet. Be the first to comment on this article.