Background: The myocardial protective role of heat shock protein (HSP) has been demonstrated. Recently, we reported that ischemia/reperfusion induced a significant activation of heat shock factor (HSF) 1 and an accumulation of mRNA for HSP70 and HSP90. We examined the role of reactive oxygen species (ROSs) in the induction of stress response in the ischemic-reperfused heart.
Methods And Results: Rat hearts were isolated and perfused with Krebs-Henseleit buffer by the Langendorff method. Whole-cell extracts were prepared for gel mobility shift assay using oligonucleotides containing the heat shock element. Induction of mRNA for HSP70 and HSP90 was examined by Northern blot analysis. Repetitive ischemia/reperfusion, which causes recurrent bursts of free radical generation, resulted in burst activation of HSF1, and this burst activation was significantly reduced with either allopurinol 1 mmol/L (an inhibitor of xanthine oxidase) or catalase 2x10(5) U/L (a scavenger of H2O2). Significant activation of HSF1 was observed on perfusion with buffer containing H2O2 150 micromol/L or xanthine 1 mmol/L plus xanthine oxidase 5 U/L. The accumulation of mRNA for HSP70 or HSP90 after repetitive ischemia/reperfusion was reduced with either allopurinol or catalase.
Conclusions: Our findings demonstrate that ROSs play an important role in the activation of HSF1 and the accumulation of mRNA for HSP70 and HSP90 in the ischemic-reperfused heart.
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http://dx.doi.org/10.1161/01.cir.99.7.934 | DOI Listing |
Mol Biol Rep
January 2025
Department of Biological Sciences, Sunandan Divatia School of Science, NMIMS Deemed to be University, Vile Parle (West), Mumbai, 400056, India.
Since the 1990s, fatty acids (FA) have drawn significant industrial attention due to their diverse applications creating a demand for biological systems capable of producing high FA titers. While various strategies have been explored to achieve this, many of the conventional approaches rely on extensive genetic manipulations, which often result in strain instability, thus limiting its potential to yield better FA titers. Moreover, stresses such as pH, osmotic, and oxidative imbalances generated during FA production aggravate these challenges, further limiting FA titers.
View Article and Find Full Text PDFEnviron Microbiol
February 2025
Marine Science Institute, University of the Philippines Diliman, Quezon City, Philippines.
Corals associate with a diverse community of prokaryotic symbionts that provide nutrition, antioxidants and other protective compounds to their host. However, the influence of microbes on coral thermotolerance remains understudied. Here, we examined the prokaryotic microbial communities associated with colonies of Acropora cf.
View Article and Find Full Text PDFFEBS J
January 2025
From the Department of Biological Sciences, Delaware State University, Dover, DE, USA.
Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disease that affects neurons in the brain and spinal cord, causing loss of muscle control, and eventually leads to death. Phosphorylated transactive response DNA binding protein-43 (TDP-43) is the major pathological protein in both sporadic and familial ALS, forming cytoplasmic aggregates in over 95% of cases. Of the 10-15% of ALS cases that are familial, mutations in TDP-43 represent about 5% of those with a family history.
View Article and Find Full Text PDFNew Phytol
January 2025
Shandong Provincial Key Laboratory of Plant Stress, College of Life Sciences, Shandong Normal University, Jinan, Shandong, 250014, China.
High temperature is one of several major abiotic stresses that can cause substantial loss of crop yields. Heat shock proteins (HSPs) are key components of heat stress resistance. Mutation of FES1A, an auxiliary molecular chaperone of HSP70, leads to defective acquired thermotolerance.
View Article and Find Full Text PDFMol Med Rep
March 2025
Department of Cardiology, The First Affiliated Hospital to Jiamusi University, Jiamusi, Heilongjiang 154000, P.R. China.
The present study aimed to investigate the cardioprotective effects of acteoside (AC) on myocardial ischemia‑reperfusion injury (MIRI). To meet this aim, a network pharmacological analysis was conducted to search for key genes and signaling pathways associated with AC and MIRI. The infarct size of the rat heart was evaluated using 2,3,5‑triphenyltetrazolium chloride staining, and the serum levels of creatine kinase MB isoenzyme, cardiac troponin I, malondialdehyde and superoxide dismutase were subsequently detected in an experiment.
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