The heat shock response is a highly conserved process essential for surviving environmental stress, including extremes of temperature. To investigate whether heat shock has an impact on intracellular Zn(2+) homeostasis, cells were subjected to heat shock, and subsequently the intracellular free zinc concentration was investigated. Sublethal heat shock induced a temperature-dependent and transient intracellular Zn(2+) release that was repeatable after 24 h. The free zinc was localized in round-shaped nuclear bodies identified as nucleoli. Metallothionein, the main cellular zinc storing protein, was found to be not functionally essential for this heat-shock-induced effect. No significant oxidative stress within the cells was detected after heat shock. Cold shock and subsequent rewarming did not result in disturbed intracellular zinc homeostasis. These results show that heat shock and cold shock differ with respect to intracellular Zn(2+) release. A role for zinc as signaling ion during fever is conceivable.
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http://dx.doi.org/10.1002/jcp.22016 | DOI Listing |
J Med Chem
January 2025
The Center for Basic Research and Innovation of Medicine and Pharmacy (MOE), School of Pharmacy, Second Military Medical University (Naval Medical University), 325 Guohe Road, Shanghai 200433, China.
Invasive candidiasis has attracted global attention with a high incidence and mortality. Current antifungal drugs are limited by unfavorable therapeutic efficacy, significant hepatorenal toxicity, and the development of drug resistance. Herein, we designed the first generation of lanosterol 14α-demethylase (CYP51)/heat shock protein 90 (Hsp90) dual inhibitors on the basis of antifungal synergism.
View Article and Find Full Text PDFChin Med
January 2025
Department of Integrated Traditional Chinese and Western Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
Background: This research aims to explore the anti-obesity potential of Wu-Mei-Wan (WMW), particularly its effects on adipose tissue regulation in obese mice induced by a high-fat diet (HFD). The study focuses on understanding the role of heat shock factor 1 (HSF1) in mediating these effects.
Methods: HFD-induced obese mice were treated with WMW.
Funct Plant Biol
January 2025
Krishi Vigyan Kendra, Siwan, Dr. RPCAU, Pusa, Bihar, India.
Detrimental effects of terminal heat stress could be mitigated by exogenous application of synthetic compounds by preserving cell membrane integrity and protecting against oxidative damage. A field experiment was conducted to test the application of seven synthetic compounds on wheat growth traits: (1) thiourea (20 mM and 40mM); (2) potassium nitrate (1% and 2%); (3) sodium nitroprusside (400 μg mL-1 and 800μg mL-1 ); (4) dithiothreitol (25 ppm and 50ppm); (5) salicylic acid (100 ppm and 200ppm); (6) thioglycolic acid (200 ppm and 500ppm); and (7) putrescine (4 mM and 6mM). These compounds were applied at the anthesis and grain-filling stages to enhance physio-biochemical traits and yield attributes of wheat (Triticum aestivum ) cvs GW-11 and GW-496 under terminal heat stress.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Delaware State University, Dover, DE, USA.
Background: Aggregation of transactive response DNA binding protein 43 (TDP-43) is the major pathological feature of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Recently, in up to 50% of Alzheimer's disease (AD) cases TDP-43 pathology was discovered and this pathology has been referred to as limbic-predominant age-related TDP43 encephalopathy (LATE). Several studies reported that TDP-43 binds to heat shock protein family B (small) member 1 (HSPB1 or HSP27) but no functional evaluation of this interaction has been explored.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Ohio State University College of Medicine, Neurobiology of Aging & Resilience Center, Columbus, OH, USA.
Background: The cerebrovasculature is an essential component of brain homeostasis. Cerebrovascular disorders are associated with an increased risk for neurodegenerative diseases, including Alzheimer's disease (AD). However, the mechanisms by which cerebrovascular dysfunction contributes to neurodegeneration are poorly understood.
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