Epithelial cells and fibroblasts both express heat shock transcription factors, HSF1 and HSF4, yet they respond to heat shock differentially. For example, while HSP70 is induced in both cell types, the small heat shock protein, αB-crystallin gene (CRYAB) that contains a canonical heat shock promoter, is only induced in fibroblasts. A canonical heat shock promoter contains three or more inverted repeats of the pentanucleotide 5'-nGAAn-3' that make the heat shock element. It is known that, in vitro, promoter architecture (the order and spacing of these repeats) impacts the interaction of various heat shock transcription factors (HSFs) with the heat shock promoter, but in vivo relevance of these binding preferences so far as the expression is concerned is poorly understood. In this report, we first establish cell-type-dependent differential expression of CRYAB in four established cell lines and then working with adult human retinal pigment epithelial cells and NIH3T3 fibroblasts and employing chromatin immunoprecipitation, attempt to relate expression to promoter occupancy by HSF1 and HSF4. We show that HSF4 occupies only CRYAB and not HSP70 promoter in epithelial cells, while HSF1 occupies only HSP70 promoter in both cell types, and cryab promoter, only in heat shocked fibroblasts; HSF4, on the other hand, is never seen on these two promoters in NIH3T3 fibroblasts. This comparative analysis with CRYAB and HSP70 demonstrates that differential heat shock response is controlled by cell-type-dependent access of HSFs (HSF1 and HSF4) to specific promoters, independent of the promoter architecture.
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http://dx.doi.org/10.1007/s12192-012-0386-7 | DOI Listing |
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.
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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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December 2024
Rush University Medical Center, Chicago, IL, USA.
Background: Abnormal brain insulin signaling has been associated with Alzheimer's disease pathology and a faster rate of late-life cognitive decline. However, the underlying mechanisms remain unclear. In this study, we examined whether AD-related cortical proteins identified using targeted-proteomics play a role in the association of brain insulin signaling and cognitive decline.
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December 2024
Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, USA.
Background: Alzheimer's Disease (AD) presents complex molecular heterogeneity, influenced by a variety of factors including heterogeneous phenotypic, genetic, and neuropathologic presentations. Regulation of gene expression mechanisms is a primary interest of investigations aiming to uncover the underlying disease mechanisms and progression.
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