ArticleApoptosis : an international journal on programmed cell death2016
Heat stress prevents lipopolysaccharide-induced apoptosis in pulmonary microvascular endothelial cells by blocking calpain/p38 MAPK signalling.
Article in Apoptosis : an international journal on programmed cell death, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 46 citations in OpenAlex.
- Dietary curcumin supplementation does not alter peripheral blood mononuclear cell responses to exertional heat stress.European journal of applied physiology · 2018Trial
- Design and synthesis of novel sEH inhibitors for the treatment of acute lung injury.European journal of medicinal chemistry · 2026Article
- Heat therapy preserves myofibre size and SERCA-mediated CaPhysiological reports · 2025Article
- The relationship mammalian p38 with human health and its homolog Hog1 in response to environmental stresses inFrontiers in cell and developmental biology · 2025Review
- Transcriptomic Analysis Reveals Dynamics of Gene Expression in Liver Tissue of Spotted Sea Bass Under Acute Thermal Stress.Marine biotechnology (New York, N.Y.) · 2024Article
- Sepsis-Induced Endothelial Dysfunction: Permeability and Regulated Cell Death.Journal of inflammation research · 2024Review
- Hydrogen-rich saline alleviates cardiomyocyte apoptosis by reducing expression of calpain1 via miR-124-3p.ESC heart failure · 2023Article
- The key role of Calpain in COVID-19 as a therapeutic strategy.Inflammopharmacology · 2022Review
- Resveratrol inhibits cell apoptosis by suppressing long noncoding RNA (lncRNA) XLOC_014869 during lipopolysaccharide-induced acute lung injury in rats.Journal of thoracic disease · 2021Article
- NF‑κB/IκBα signaling pathways are essential for resistance to heat stress‑induced ROS production in pulmonary microvascular endothelial cells.Molecular medicine reports · 2021Article
- EGCG promotes PRKCA expression to alleviate LPS-induced acute lung injury and inflammatory response.Scientific reports · 2021Article
- Macrophages enhance lipopolysaccharide induced apoptosis via Ang1 and NF-κB pathways in human umbilical vein endothelial cells.Scientific reports · 2021Article
- Apelin‑36 protects against lipopolysaccharide‑induced acute lung injury by inhibiting the ASK1/MAPK signaling pathway.Molecular medicine reports · 2021Article
- Inhibitory Effect of Punicalagin on Inflammatory and Angiogenic Activation of Human Umbilical Vein Endothelial Cells.Frontiers in pharmacology · 2021Article
- ASK1-p38 cascaded signal mediates pulmonary microvascular endothelial barrier injury induced by the return of PHSML in rats.RSC advances · 2019Article
- Article
- Heat acclimation increases inflammatory and apoptotic responses to subsequent LPS challenge in C2C12 myotubes.Cell stress & chaperones · 2018Article
- Connexin 43 Hemichannel Activity Promoted by Pro-Inflammatory Cytokines and High Glucose Alters Endothelial Cell Function.Frontiers in immunology · 2018Article
- Ginkgolide B Suppresses TLR4-Mediated Inflammatory Response by Inhibiting the Phosphorylation of JAK2/STAT3 and p38 MAPK in High Glucose-Treated HUVECs.Oxidative medicine and cellular longevity · 2017Article
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
Abstract
Pulmonary microvascular endothelial cells (PMECs) injury including apoptosis plays an important role in the pathogenesis of acute lung injury during sepsis. Our recent study has demonstrated that calpain activation contributes to apoptosis in PMECs under septic conditions. This study investigated how calpain activation mediated apoptosis and whether heat stress regulated calpain activation in lipopolysaccharides (LPS)-stimulated PMECs. In cultured mouse primary PMECs, incubation with LPS (1 μg/ml, 24 h) increased active caspase-3 fragments and DNA fragmentation, indicative of apoptosis. These effects of LPS were abrogated by pre-treatment with heat stress (43 °C for 2 h). LPS also induced calpain activation and increased phosphorylation of p38 MAPK. Inhibition of calpain and p38 MAPK prevented apoptosis induced by LPS. Furthermore, inhibition of calpain blocked p38 MAPK phosphorylation in LPS-stimulated PMECs. Notably, heat stress decreased the protein levels of calpain-1/2 and calpain activities, and blocked p38 MAPK phosphorylation in response to LPS. Additionally, forced up-regulation of calpain-1 or calpain-2 sufficiently induced p38 MAPK phosphorylation and apoptosis in PMECs, both of which were inhibited by heat stress. In conclusion, heat stress prevents LPS-induced apoptosis in PMECs. This effect of heat stress is associated with down-regulation of calpain expression and activation, and subsequent blockage of p38 MAPK activation in response to LPS. Thus, blocking calpain/p38 MAPK pathway may be a novel mechanism underlying heat stress-mediated inhibition of apoptosis in LPS-stimulated endothelial cells.
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