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Toxic Effects and Biodistribution of Ultrasmall Gold Nanoparticles *
Published in Valerio Voliani, Nanomaterials and Neoplasms, 2021
Gunter Schmid, Wolfgang G. Kreyling, Ulrich Simon
Following the initial growth response, heat shock and stress-related genes were upregulated after 6 h and strongly upregulated after 12 h in Au1.4MS-treated but not in Au15MS-treated or untreated HeLa cells. This group of genes (HSPA1A, DNAJA4, CHAC1, HSPA1A, DDIT3, GEM, LOC387763, PGF, HSPA6, SESN2, LOC284561, PPP1R15A, HMOX1, C16orf81, LOC344887, NGF, OSGIN1, FOSL1, CXCL2, IL8) suggested that a robust stress response had occurred in the Au1.4MS-treated cells. Highly elevated expression of heat shock proteins has been demonstrated to inhibit apoptosis at several stages including blocking of cytochrome c release from mitochondria, thus preventing the formation of an apoptosome and the activation of caspase-3, ultimately forcing cells into necrosis instead of apoptosis.
Pyrrolizidine Alkaloids
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
As PA clivorine is shown to induce apoptotic cell death and oxidative stress injury in human normal liver L-02 cells, a plant-derived flavonoid called quercetin is being trialed for preventing clivorine-induced apoptotic cell death. Through upregulation of oxidative or metabolic stress-related genes (e.g., Fmo5, Polr2k, Sod2, Ephx2, Sod1, Hmox2, Hmox1, Cyp2b10, Cyp1b1, Cyp2a5, Cyp3a11, and Cyp7a1) and heat shock–related genes (e.g., Hspa5, Hspa1 l, Hspa1b, Dnaja1, and Hspe1), quercetin works to increase the level of liver GSH (which is an important endogenous antioxidant), and to ameliorate clivorine-induced oxidative stress [34].
Ménière's Disease
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
While Ménière’s disease is sporadic in the majority of cases, an estimated 5–15% of cases are familial.5 Several candidate genes have been proposed for Ménière’s disease, including AQP2, KCNE1, KCNE3, HCFC1, COCH, ADD, HSPA1A, PTPTN22 and IL1. Many of them are linked to inner ear ion and water transportation. AQP2 is one of the aquaporin water channel genes,6KCNE1 and KCNE3 are potassium channel genes7 and ADD1 is linked to a sodium–potassium pump activity regulator.3COCH is linked to cochlin protein production, which is part of the extracellular matrix of the inner ear.8COCH gene is also known as DFNA9 and leads to progressive non-syndromic deafness and bilateral vestibular areflexia.9HCFC1 is associated with the host cell factor C1 which has been involved in cell cycle control and transcriptional regulation during herpes simplex virus infection.10HSPA1A is related to single nucleotide polymorphisms of the heat-shock protein 70 gene,11PTPN22 encodes a lymphoid protein phosphatase12 and the interleukin-1 gene (IL1).13 A higher prevalence of autoimmune diseases and longer spells of vertigo have been reported in patients affected by a familial form of Ménière’s disease.14,15 The familial form is more prone to present bilaterally during a lifetime.16
Housing of A350V IQSEC2 pups at 37 °C ambient temperature prevents seizures and permits the development of social vocalizations in adulthood
Published in International Journal of Hyperthermia, 2021
Reem Jada, Liron Zag, Veronika Borisov, Nina S. Levy, Shai Netser, Renad Jabarin, Shlomo Wagner, Kinneret Schragenheim-Rozales, Reut Shalgi, Andrew P. Levy
In order to demonstrate that the housing of 15–20 day old mice at an ambient temperature of 37 °C induced a physiologically relevant increase in temperature in brain tissue, we measured the production of heat shock Hspa1a mRNA in the hippocampus after this exposure. Hspa1a is the major Hsp70 in mice and is known to be induced by an increase in temperature in vitro and in vivo [15]. We assessed if the fever range hyperthermia protocol was associated with an increase in Hspa1a in the hippocampus which is the major site of production of IQSEC2 in the brain [16,17] and where IQSEC2 mutation mediated pathology has been shown to be prominent [6,18–20]. Compared to A350V IQSEC2 mice housed at room temperature (22 °C), we observed that A350V mice housed for 5 days at 37 °C demonstrated a significant induction of Hspa1a mRNA by qRT-PCR (2.7-fold increase 3.9 ± 0.6 vs 1.5 ± 0.2 normalized to HPRT, p = 0.007, n = 5 for each group) (Figure 2).
Encounters with adenovirus
Published in Upsala Journal of Medical Sciences, 2019
Most proteins, uniquely altered at 12 hpi, are up-regulated, and several different pathways are overrepresented by them. Remodeling the cytoskeleton stands out, and many up-regulated proteins are involved in cytoskeletal regulation by Rho GTPase as well as inflammation mediated by chemokine and cytokine signaling, and integrin signaling. The toll receptor signaling pathway is deregulated at this time, although the activation increases at 24 hpi. Toll-like receptors play critical roles in the innate immune system by recognizing pathogen-associated molecular patterns derived from various microbes (69,70). Other altered proteins are involved in the regulation of the glutathione metabolism and detoxification processes, in the organization of the proteasome system, and in signaling pathways such as TGF-beta, Rho, and NFκB. The stress response proteins HSPA1A/B are mildly altered at 12 hpi before becoming the most highly up-regulated protein at 24 hpi. Another deregulated pathway is fructose galactose metabolism. This makes sense as proteins in this pathway are involved in the production of precursors to be used in the glycolysis cycle for energy production.
Microanatomy of the metabolic associated fatty liver disease (MAFLD) by single-cell transcriptomics
Published in Journal of Drug Targeting, 2023
Lijun Wang, Kebing Zhou, Qing Wu, Lingping Zhu, Yang Hu, Xuefeng Yang, Duo Li
In the constructed molecular interaction network, the genes closely related to four key protein-coding genes were: hspa1a, cd63, cd9, and ago2. HSPA1A (Heat Shock Protein Family A (Hsp70) Member 1A) is a gene associated with transient cerebral ischaemia and carotid artery occlusion [25]. Among its related pathways are the HIV Life Cycle and the Proteolysis Role of Parkin in the Ubiquitin-Proteasomal Pathway [26]. Significantly enriched GO terms related to this gene include RNA binding and ubiquitin protein ligase binding. An important paralog of this gene is HSPA1B. CD63 is also a protein-coding gene associated with diseases, including Hermansky-Pudlak Syndrome and Storage Pool Platelet Disease [27]. Among its related pathways are the innate immune system and response to elevated platelet cytosolic Ca2 + [28]. An important paralog of this gene is TSPAN3. CD9 is associated with Diphtheria and Human Immunodeficiency Virus [29]. Among its related pathways are a6b1 and a6b4 Integrin signalling and HIV Life Cycle [30], while enriched GO terms include integrin binding. An important paralog of this gene is TSPAN2. Moreover, AGO2 (Argonaute RISC Catalytic Component 2) is associated with AGO2 include Lessel-Kreienkamp Syndrome and Non-Specific Syndromic Intellectual Disability [31], related pathways include Pre-NOTCH Expression and Processing and Mitotic Prophase [32], GO annotations include nucleic acid binding and RNA binding and an important paralog is AGO1. These related genes have hitherto not been reported to be associated with MAFLD, which is inconsistent with the four key genes found in this single-cell sequencing bioinformatics analysis, indicating the innovative nature of our research.