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Journal articles on the topic 'Heat-mediated release'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

Cantet, Juan M., Zhantao Yu, and Agustín G. Ríus. "Heat Stress-Mediated Activation of Immune–Inflammatory Pathways." Antibiotics 10, no. 11 (2021): 1285. http://dx.doi.org/10.3390/antibiotics10111285.

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Physiological changes in animals exposed to elevated ambient temperature are characterized by the redistribution of blood toward the periphery to dissipate heat, with a consequent decline in blood flow and oxygen and nutrient supply to splanchnic tissues. Metabolic adaptations and gut dysfunction lead to oxidative stress, translocation of lumen contents, and release of proinflammatory mediators, activating a systemic inflammatory response. This review discusses the activation and development of the inflammatory response in heat-stressed models.

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2

Zhang, W., and P. J. Lachmann. "Neutrophil lactoferrin release induced by IgA immune complexes can be mediated either by Fc alpha receptors or by complement receptors through different pathways." Journal of Immunology 156, no. 7 (1996): 2599–606. http://dx.doi.org/10.4049/jimmunol.156.7.2599.

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Abstract Our previous results showed that neutrophil secondary granule release, indicated by release of lactoferrin, was a slow process when induced by IgA immune complexes (IC) formed in heat-inactivated serum, but became very fast if IgA IC were formed in normal human serum. This phenomenon did not apply to the IC of other Ab isotypes. In this paper, we demonstrate that the fast lactoferrin release is caused by complement, mainly due to the deposition of C3b and iC3b on IgA IC. Either CR1 or CR3 can mediate the response and both receptors have to be blocked to prevent it. Complement also inf

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Obi, Syotaro, Toshiaki Nakajima, Takaaki Hasegawa, et al. "Heat induces interleukin-6 in skeletal muscle cells via TRPV1/PKC/CREB pathways." Journal of Applied Physiology 122, no. 3 (2017): 683–94. http://dx.doi.org/10.1152/japplphysiol.00139.2016.

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Interleukin-6 (IL-6) is released from skeletal muscle cells and induced by exercise, heat, catecholamine, glucose, lipopolysaccharide, reactive oxygen species, and inflammation. However, the mechanism that induces release of IL-6 from skeletal muscle cells remains unknown. Thermosensitive transient receptor potential (TRP) proteins such as TRPV1–4 play vital roles in cellular functions. In this study we hypothesized that TRPV1 senses heat, transmits a signal into the nucleus, and produces IL-6. The purpose of the present study is to investigate the underlying mechanisms whereby skeletal muscle

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Saikia, Nabanita, Anupam Nath Jha, and Ramesh Ch Deka. "Dynamics of Fullerene-Mediated Heat-Driven Release of Drug Molecules from Carbon Nanotubes." Journal of Physical Chemistry Letters 4, no. 23 (2013): 4126–32. http://dx.doi.org/10.1021/jz402231p.

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Iga, Katsumi, Naoru Hamaguchi, Yasutaka Igari, Yasuaki Ogawa, Hajime Toguchi, and Tsugio Shimamoto. "Heat-specific drug release of large unilamellar vesicle as hyperthermia-mediated targeting delivery." International Journal of Pharmaceutics 57, no. 3 (1989): 241–51. http://dx.doi.org/10.1016/0378-5173(89)90214-7.

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Coaxum, Sonya D., Tina M. Griffin, Jody L. Martin та Ruben Mestril. "Influence of PKC-α overexpression on HSP70 and cardioprotection". American Journal of Physiology-Heart and Circulatory Physiology 292, № 5 (2007): H2220—H2226. http://dx.doi.org/10.1152/ajpheart.01080.2006.

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Recent research has indicated that the protein kinase C (PKC) isoforms and the heat shock proteins (HSPs) are involved in cardioprotection. We have investigated the possible interaction between these two protein families. We have found that adenoviral-mediated expression of PKC-α in neonatal rat ventricular myocytes (NRVM) not only increases the expression of HSP70 but also protects against simulated ischemia-reperfusion. In addition, Western blots of PKC-α-infected NRVM indicated that other HSPs are not induced in the same manner as HSP70. In an effort to determine the mechanism of induction

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Crane, John K., Shilpa S. Choudhari, Tonniele M. Naeher, and Michael E. Duffey. "Mutual Enhancement of Virulence by Enterotoxigenic and Enteropathogenic Escherichia coli." Infection and Immunity 74, no. 3 (2006): 1505–15. http://dx.doi.org/10.1128/iai.74.3.1505-1515.2006.

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ABSTRACT Enterotoxigenic Escherichia coli (ETEC) and enteropathogenic E. coli (EPEC) are common causes of diarrhea in children in developing countries. Dual infections with both pathogens have been noted fairly frequently in studies of diarrhea around the world. In previous laboratory work, we noted that cholera toxin and forskolin markedly potentiated EPEC-induced ATP release from the host cell, and this potentiated release was found to be mediated by the cystic fibrosis transmembrane conductance regulator. In this study, we examined whether the ETEC heat-labile toxin (LT) or the heat-stable

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Takagi, Satoshi, Yuki Sasaki, Sumie Koike, et al. "Platelet-derived lysophosphatidic acid mediated LPAR1 activation as a therapeutic target for osteosarcoma metastasis." Oncogene 40, no. 36 (2021): 5548–58. http://dx.doi.org/10.1038/s41388-021-01956-6.

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AbstractOsteosarcoma is the most common primary malignant bone cancer, with high rates of pulmonary metastasis. Osteosarcoma patients with pulmonary metastasis have worse prognosis than those with localized disease, leading to dramatically reduced survival rates. Therefore, understanding the biological characteristics of metastatic osteosarcoma and the molecular mechanisms of invasion and metastasis of osteosarcoma cells will lead to the development of innovative therapeutic intervention for advanced osteosarcoma. Here, we identified that osteosarcoma cells commonly exhibit high platelet activ

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Gupta, Sanjiv, and A. A. Knowlton. "HSP60 trafficking in adult cardiac myocytes: role of the exosomal pathway." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 6 (2007): H3052—H3056. http://dx.doi.org/10.1152/ajpheart.01355.2006.

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The heat shock proteins (HSP) are a highly conserved family of proteins with critical functions in protein folding, protein trafficking, and cell signaling. These proteins also protect the cell against injury. HSP60 has been found in the extracellular space and has been identified in the plasma of some individuals. HSP60 is thought to be a “danger signal” to the immune system and is also highly immunogenic. Thus extracellular HSP60 is possibly toxic to the cell. The mechanism by which HSP60 is released into the extracellular space is unknown, as is whether it is released by cardiac myocytes. W

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Kelly, Ryan M., Jianmin Chen, Lauren E. Yauch, and Stuart M. Levitz. "Opsonic Requirements for Dendritic Cell-Mediated Responses to Cryptococcus neoformans." Infection and Immunity 73, no. 1 (2005): 592–98. http://dx.doi.org/10.1128/iai.73.1.592-598.2005.

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ABSTRACT The encapsulated pathogenic yeast Cryptococcus neoformans is poorly recognized by phagocytic cells in the absence of opsonins. Macrophages will bind and internalize complement- or antibody-opsonized C. neoformans; however, less is known about the role of opsonins in dendritic cell (DC)-mediated recognition of the organism. Thus, we studied the opsonic requirements for binding to C. neoformans by cultured human monocyte-derived and murine bone marrow-derived DCs and whether binding leads to antifungal activity and cytokine release. Binding of unopsonized C. neoformans to human and muri

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Lee, S. C., and P. A. Pappone. "Effects of P2 purinergic receptor stimulation in brown adipocytes." American Journal of Physiology-Cell Physiology 273, no. 2 (1997): C679—C686. http://dx.doi.org/10.1152/ajpcell.1997.273.2.c679.

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Sympathetic stimulation of brown adipocytes plays a major role in body energy homeostasis by activating energy-wasting pathways. Sympathetic neuronal input initiates a variety of metabolic, developmental, and membrane responses in brown fat cells. Many of these actions are mediated by adrenergic pathways mobilized by released norepinephrine. However, since sympathetic stimulation may also release vesicular ATP, we tested brown fat cells for ATP responses. Micromolar concentrations of extracellular ATP had a number of effects on brown adipocytes. We have shown previously that ATP elicits substa

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Garello, Francesca, Rachele Stefania, Silvio Aime, Enzo Terreno, and Castelli Daniela Delli. "Successful Entrapping of Liposomes in Glucan Particles: An Innovative Micron-Sized Carrier to Deliver Water-Soluble Molecules." Mol Pharm. 11, no. 10 (2014): 3760–5. https://doi.org/10.1021/mp500374f.

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Glucan particles (GPs) are monodisperse microspheres derived from baker's yeast and represent an interesting class of microcarriers for theranostic applications as they show a high affinity toward immune system cells. The typical loading strategy was to harness the ability of the molecule to be loaded to interact with nano-/microassembled systems through electrostatic or hydrophobic forces. However, small water-soluble chemicals could not be steadily retained by the leaky shell of GPs. In this work, we propose an alternative loading approach for small water-soluble compounds that is based

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Giesbrecht, Gordon G., and Magdy Younes. "Exercise- and Cold-Induced Asthma." Canadian Journal of Applied Physiology 20, no. 3 (1995): 300–314. http://dx.doi.org/10.1139/h95-023.

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Exercise- and cold-induced asthma are commonly recognized respiratory disorders. The asthmatic response includes several factors contributing to airway narrowing, and thus increased airway resistance. These include airway smooth muscle contraction, mucus accumulation, and bronchial vascular congestion as well as epithelial damage and vascular leakage. The etiology for these disorders is nonantigenic. The primary stimulus is probably a combination of airway cooling and drying (leading to hypertonicity of airway lining fluid). Symptoms generally do not occur during the stimulus period (e.g., exe

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Bagchi, M. K., S. Y. Tsai, M. J. Tsai, and B. W. O'Malley. "Progesterone enhances target gene transcription by receptor free of heat shock proteins hsp90, hsp56, and hsp70." Molecular and Cellular Biology 11, no. 10 (1991): 4998–5004. http://dx.doi.org/10.1128/mcb.11.10.4998-5004.1991.

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Steroid receptors regulate transcription of target genes in vivo and in vitro in a steroid hormone-dependent manner. Unoccupied progesterone receptor exists in the low-salt homogenates of target cells as a functionally inactive 8 to 10S complex with several nonreceptor components such as two molecules of 90-kDa heat shock protein (hsp90), a 70-kDa heat shock protein (hsp70), and a 56-kDa heat shock protein (hsp56). Ligand-induced dissociation of receptor-associated proteins such as hsp90 has been proposed as the mechanism of receptor activation. Nevertheless, it has not been established whethe

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Bagchi, M. K., S. Y. Tsai, M. J. Tsai, and B. W. O'Malley. "Progesterone enhances target gene transcription by receptor free of heat shock proteins hsp90, hsp56, and hsp70." Molecular and Cellular Biology 11, no. 10 (1991): 4998–5004. http://dx.doi.org/10.1128/mcb.11.10.4998.

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Steroid receptors regulate transcription of target genes in vivo and in vitro in a steroid hormone-dependent manner. Unoccupied progesterone receptor exists in the low-salt homogenates of target cells as a functionally inactive 8 to 10S complex with several nonreceptor components such as two molecules of 90-kDa heat shock protein (hsp90), a 70-kDa heat shock protein (hsp70), and a 56-kDa heat shock protein (hsp56). Ligand-induced dissociation of receptor-associated proteins such as hsp90 has been proposed as the mechanism of receptor activation. Nevertheless, it has not been established whethe

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Hosoya, Hitomi, Andrey S. Dobroff, Wouter H. P. Driessen, et al. "Integrated nanotechnology platform for tumor-targeted multimodal imaging and therapeutic cargo release." Proceedings of the National Academy of Sciences 113, no. 7 (2016): 1877–82. http://dx.doi.org/10.1073/pnas.1525796113.

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A major challenge of targeted molecular imaging and drug delivery in cancer is establishing a functional combination of ligand-directed cargo with a triggered release system. Here we develop a hydrogel-based nanotechnology platform that integrates tumor targeting, photon-to-heat conversion, and triggered drug delivery within a single nanostructure to enable multimodal imaging and controlled release of therapeutic cargo. In proof-of-concept experiments, we show a broad range of ligand peptide-based applications with phage particles, heat-sensitive liposomes, or mesoporous silica nanoparticles t

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Atkins, E., and L. Francis. "Suppression of Ag-induced release of EP (IL 1) by spleen cells of specifically desensitized donors: evidence for the role of a suppressor cell." Journal of Immunology 134, no. 4 (1985): 2436–43. http://dx.doi.org/10.4049/jimmunol.134.4.2436.

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Abstract Monocytes or macrophages may be induced to produce IL 1 by activators (e.g., lipopolysaccharide endotoxin) that act directly or by antigens/mitogens (e.g., Con A) that stimulate inducer lymphocytes to release a lymphokine that stimulates macrophages. Using guinea pigs (GP) rendered delayed hypersensitive to ovalbumin (OVA), we investigated the role of spleen cells from normal, sensitized, and specifically desensitized GP in suppressing release of IL 1, measured as endogenous pyrogen (EP), from peritoneal exudates of sensitized GP when incubated with OVA in vitro. Co-cultivation of all

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Wolf, J. E., V. Kerchberger, G. S. Kobayashi, and J. R. Little. "Modulation of the macrophage oxidative burst by Histoplasma capsulatum." Journal of Immunology 138, no. 2 (1987): 582–86. http://dx.doi.org/10.4049/jimmunol.138.2.582.

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Abstract The production of reactive oxygen species by phagocytic cells is an important host defense against invading microorganisms. Because pathogens that achieve intracellular survival escape destruction by reactive oxidants, we investigated the relationship between the intracellular survival of H. capsulatum and the macrophage oxidative burst. H. capsulatum yeast failed to stimulate the release of reactive oxygen metabolites in unprimed murine macrophages despite extensive phagocytosis of the microorganisms. This effect was observed with live as well as heat-killed fungi over a wide range o

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Charbonneau, Marie-Ève, Frédéric Berthiaume, and Michael Mourez. "Proteolytic Processing Is Not Essential for Multiple Functions of the Escherichia coli Autotransporter Adhesin Involved in Diffuse Adherence (AIDA-I)." Journal of Bacteriology 188, no. 24 (2006): 8504–12. http://dx.doi.org/10.1128/jb.00864-06.

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ABSTRACT The Escherichia coli adhesin involved in diffuse adherence (AIDA-I), like many other autotransporter proteins, is released in the periplasm as a proprotein undergoing proteolytic processing after its translocation across the outer membrane. The proprotein is cleaved into a membrane-embedded fragment, AIDAc, and an extracellular fragment, the mature AIDA-I adhesin. The latter remains noncovalently associated with the outer membrane and can be released by heat treatment. The mechanism of cleavage of the proprotein and its role in the functionality of AIDA-I are not understood. Here, we

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Pawaria, Sudesh. "Role of inflammasome in HSP-mediated innate immunity (114.5)." Journal of Immunology 188, no. 1_Supplement (2012): 114.5. http://dx.doi.org/10.4049/jimmunol.188.supp.114.5.

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Abstract The immunogenic heat shock proteins gp96, hsp70 and calreticulin stimulate antigen presenting cells to provide co-stimulation in the form of cytokines and co-stimulatory molecules. The unique pattern of co-stimulation is dependent on the type of antigen presenting cell and the HSP that is used as the stimulant. The pattern of co-stimulation also determines the T helper response that is primed. A cytokine that is routinely released by HSP-stimulated APCs is IL-1beta. Here we investigate the role of (components of) the inflammasome pathway in HSP-mediated IL-1beta release. Our results s

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Chauhan, Dharminder, Guilan Li, Teru Hideshima, et al. "Hsp27 inhibits release of mitochondrial protein Smac in multiple myeloma cells and confers dexamethasone resistance." Blood 102, no. 9 (2003): 3379–86. http://dx.doi.org/10.1182/blood-2003-05-1417.

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AbstractSmac, second mitochondria-derived activator of caspases, promotes apoptosis via activation of caspases. Heat shock protein 27 (Hsp27) negatively regulates another mitochondrial protein, cytochrome c, during apoptosis; however, the role of Hsp27 in modulating Smac release is unknown. Here we show that Hsp27 is overexpressed in both dexamethasone (Dex)-resistant multiple myeloma (MM) cell lines (MM.1R, U266, RPMI-8226) and primary patient cells. Blocking Hsp27 by an antisense (AS) strategy restores the apoptotic response to Dex in Dex-resistant MM cells by triggering the release of mitoc

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Faught, Erin, Lynsi Henrickson, and Mathilakath M. Vijayan. "Plasma exosomes are enriched in Hsp70 and modulated by stress and cortisol in rainbow trout." Journal of Endocrinology 232, no. 2 (2017): 237–46. http://dx.doi.org/10.1530/joe-16-0427.

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Exosomes are endosomally derived vesicles that are secreted from cells and contain a suite of molecules, including proteins and nucleic acids. Recent studies suggest the possibility that exosomes in circulation may be affecting recipient target cell function, but the modes of action are unclear. Here, we tested the hypothesis that exosomes are in circulation in fish plasma and that these vesicles are enriched with heat shock protein 70 (Hsp70). Exosomes were isolated from rainbow trout (Oncorhynchus mykiss) plasma using differential centrifugation, and their presence was confirmed by transmiss

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Groom, Linda, Sheila M. Muldoon, Zhen Zhi Tang, et al. "Identical de novo Mutation in the Type 1 Ryanodine Receptor Gene Associated with Fatal, Stress-induced Malignant Hyperthermia in Two Unrelated Families." Anesthesiology 115, no. 5 (2011): 938–45. http://dx.doi.org/10.1097/aln.0b013e3182320068.

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Background Mutations in the type 1 ryanodine receptor gene (RYR1) result in malignant hyperthermia, a pharmacogenetic disorder typically triggered by administration of anesthetics. However, cases of sudden death during exertion, heat challenge, and febrile illness in the absence of triggering drugs have been reported. The underlying causes of such drug-free fatal "awake" episodes are unknown. Methods De novo R3983C variant in RYR1 was identified in two unrelated children who experienced fatal, nonanesthetic awake episodes associated with febrile illness and heat stress. One of the children als

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Barcelos, Júlia Muniz, Tácio Gonçalves Hayasaki, Ricardo Costa de Santana, Eliana Martins Lima, Sebastião Antonio Mendanha, and Andris Figueiroa Bakuzis. "Photothermal Properties of IR-780-Based Nanoparticles Depend on Nanocarrier Design: A Comparative Study on Synthetic Liposomes and Cell Membrane and Hybrid Biomimetic Vesicles." Pharmaceutics 15, no. 2 (2023): 444. http://dx.doi.org/10.3390/pharmaceutics15020444.

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Biomimetic nanoparticles hold great promise for photonic-mediated nanomedicine due to the association of the biological functionality of the membrane with the physical/chemical goals of organic/inorganic structures, but studies involving fluorescent biomimetic vesicles are still scarce. The purpose of this article is to determine how photothermal therapy (PTT) with theranostic IR-780-based nanoparticles depends on the dye content, cholesterol content, lipid bilayer phase and cell membrane type. The photophysical responses of synthetic liposomes, cell membrane vesicles and hybrid nanoparticles

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Morrison, Ewan E., Yi-Fen Wang, and David M. Meredith. "Phosphorylation of Structural Components Promotes Dissociation of the Herpes Simplex Virus Type 1 Tegument." Journal of Virology 72, no. 9 (1998): 7108–14. http://dx.doi.org/10.1128/jvi.72.9.7108-7114.1998.

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ABSTRACT The role of phosphorylation in the dissociation of structural components of the herpes simplex virus type 1 (HSV-1) tegument was investigated, using an in vitro assay. Addition of physiological concentrations of ATP and magnesium to wild-type virions in the presence of detergent promoted the release of VP13/14 and VP22. VP1/2 and the UL13 protein kinase were not significantly solubilized. However, using a virus with an inactivated UL13 protein, we found that the release of VP22 was severely impaired. Addition of casein kinase II (CKII) to UL13 mutant virions promoted VP22 release. Hea

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Mun, Hye-Seong, Fumie Aosai, Kazumi Norose, et al. "Toll-Like Receptor 4 Mediates Tolerance in Macrophages Stimulated with Toxoplasma gondii-Derived Heat Shock Protein 70." Infection and Immunity 73, no. 8 (2005): 4634–42. http://dx.doi.org/10.1128/iai.73.8.4634-4642.2005.

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ABSTRACT Peritoneal macrophages (PMs) from toll-like receptor 4 (TLR4)-deficient and wild-type (WT) mice were responsive to recombinant Toxoplasma gondii-derived heat shock protein 70 (rTgHSP70) and natural TgHSP70 (nTgHSP70) in NO release, but those from TLR2-, myeloid differentiation factor 88 (MyD88)-, and interleukin-1R-associated kinase 4 (IRAK4)-deficient mice were not. Polymyxin B did not inhibit PM activation by TgHSP70 and nTgHSP70 from WT and TLR4-deficient mice, while it inhibited PM activation by lipopolysaccharide. Pretreatment of PMs from WT but not from TLR4-deficient mice with

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Geng, Cunzhen, Zhihui Zhao, Zhixin Xue, Peilong Xu, and Yanzhi Xia. "Preparation of Ion-Exchanged TEMPO-Oxidized Celluloses as Flame Retardant Products." Molecules 24, no. 10 (2019): 1947. http://dx.doi.org/10.3390/molecules24101947.

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Cellulose, as one of the most abundant natural biopolymers, has been widely used in textile industry. However, owing to its drawbacks of flammability and ignitability, the large-scale commercial application of neat cellulose is limited. This study investigated some TEMPO-oxidized cellulose (TOC) which was prepared by selective TEMPO-mediated oxidation and ion exchange. The prepared TOC was characterized by Fourier transform infrared (FT-IR) spectroscopy and solid-state 13C-nuclear magnetic resonance (13C-NMR) spectroscopy. The thermal stability and combustion performance of TOC were investigat

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Feldstein, J. B., R. A. Gonzales, S. P. Baker, C. Sumners, F. T. Crews, and M. K. Raizada. "Decreased alpha 1-adrenergic receptor-mediated inositide hydrolysis in neurons from hypertensive rat brain." American Journal of Physiology-Cell Physiology 251, no. 2 (1986): C230—C237. http://dx.doi.org/10.1152/ajpcell.1986.251.2.c230.

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The expression of alpha 1-adrenergic receptors and norepinephrine (NE)-stimulated hydrolysis of inositol phospholipid has been studied in neuronal cultures from the brains of normotensive (Wistar-Kyoto, WKY) and spontaneously hypertensive (SH) rats. Binding of 125I-2-[beta-(4-hydroxyphenyl)-ethyl-aminomethyl] tetralone (HEAT) to neuronal membranes was 68-85% specific and was rapid. Competition-inhibition experiments with various agonists and antagonists suggested that 125I-HEAT bound selectively to alpha 1-adrenergic receptors. Specific binding of 125I-HEAT to neuronal membranes from SH rat br

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Okada, Takayuki, Hajime Otani, Yue Wu, et al. "Role of F-actin organization in p38 MAP kinase-mediated apoptosis and necrosis in neonatal rat cardiomyocytes subjected to simulated ischemia and reoxygenation." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 6 (2005): H2310—H2318. http://dx.doi.org/10.1152/ajpheart.00462.2005.

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Activation of p38 mitogen-activated protein (MAP) kinase (MAPK) has been implicated in the mechanism of cardiomyocyte (CMC) protection and injury. The p38 MAPK controversy may be related to differential effects of this kinase on apoptosis and necrosis. We have hypothesized that p38 MAPK-mediated F-actin reorganization promotes apoptotic cell death, whereas it protects from osmotic stress-induced necrotic cell death. Cultured neonatal rat CMCs were subjected to 2 h of simulated ischemia followed by reoxygenation. p38 MAPK activity measured by phosphorylation of MAP kinase-activated protein (MAP

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Tsuchiya, Daisuke, Shwuhuey Hong, Yasuhiko Matsumori, et al. "Overexpression of Rat Heat Shock Protein 70 is Associated with Reduction of Early Mitochondrial Cytochrome c Release and Subsequent DNA Fragmentation after Permanent Focal Ischemia." Journal of Cerebral Blood Flow & Metabolism 23, no. 6 (2003): 718–27. http://dx.doi.org/10.1097/01.wcb.0000054756.97390.f7.

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Although protective effects of heat shock protein 70 (HSP70) overproduction after ischemic injury have been shown both in vitro and in vivo in neurons, the mechanisms are not fully understood. The hypothesis of this study is that transgenic mice overexpressing HSP70 (HSP70 Tg) show reduced mitochondrial cytochrome c release into cytosol and diminished apoptotic cell death after permanent focal ischemia in comparison to wild-type (Wt) mice. Permanent middle cerebral artery occlusion (pMCAO) was produced by intraluminal suture cannulation in HSP70 Tg and Wt mice. DNA fragmentation was evaluated

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Lippoldt, Erika K., Serra Ongun, Geoffrey K. Kusaka та David D. McKemy. "Inflammatory and neuropathic cold allodynia are selectively mediated by the neurotrophic factor receptor GFRα3". Proceedings of the National Academy of Sciences 113, № 16 (2016): 4506–11. http://dx.doi.org/10.1073/pnas.1603294113.

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Tissue injury prompts the release of a number of proalgesic molecules that induce acute and chronic pain by sensitizing pain-sensing neurons (nociceptors) to heat and mechanical stimuli. In contrast, many proalgesics have no effect on cold sensitivity or can inhibit cold-sensitive neurons and diminish cooling-mediated pain relief (analgesia). Nonetheless, cold pain (allodynia) is prevalent in many inflammatory and neuropathic pain settings, with little known of the mechanisms promoting pain vs. those dampening analgesia. Here, we show that cold allodynia induced by inflammation, nerve injury,

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Blackburn, Warren D., Louis W. Heck, William J. Koopman, and Hattie D. Gresham. "A low molecular weight, heat-labile factor enhances neutrophil fc receptor–mediated lysosomal enzyme release and phagocytosis." Arthritis & Rheumatism 30, no. 9 (1987): 1006–14. http://dx.doi.org/10.1002/art.1780300907.

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Magee, D. M., and E. J. Wing. "Cloned L3T4+ T lymphocytes protect mice against Listeria monocytogenes by secreting IFN-gamma." Journal of Immunology 141, no. 9 (1988): 3203–7. http://dx.doi.org/10.4049/jimmunol.141.9.3203.

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Abstract Murine T lymphocyte clones sensitized to Listeria monocytogenes were developed to investigate specific mechanisms of T cell-mediated immunity. The clones were of the Thy-1.2+, L3T4+, Lyt-2- phenotype and proliferated in a dose response fashion to heat-killed Listeria. Cloned T lymphocytes injected intravenously protected nonimmune mice against L. monocytogenes challenge as determined by spleen and liver bacterial numbers. Supernatants, produced by stimulating clones with heat-killed Listeria for 48 h, also afforded protection against L. monocytogenes. The clonal supernatants contained

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Duval, Martine, Fabrice Le Bœuf, Jacques Huot, and Jean-Philippe Gratton. "Src-mediated Phosphorylation of Hsp90 in Response to Vascular Endothelial Growth Factor (VEGF) Is Required for VEGF Receptor-2 Signaling to Endothelial NO Synthase." Molecular Biology of the Cell 18, no. 11 (2007): 4659–68. http://dx.doi.org/10.1091/mbc.e07-05-0467.

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Nitric oxide (NO) release from endothelial cells, via endothelial NO synthase (eNOS) activation, is central to the proangiogenic actions of vascular endothelial growth factor (VEGF). VEGF signaling to eNOS is principally mediated by an Akt-dependent phosphorylation of eNOS and by increased association of eNOS to the molecular chaperone, heat-shock protein 90 kDa (Hsp90). Herein, we report that VEGFR-2 activation induces tyrosine phosphorylation of VEGF receptor 2 (VEGFR-2)-associated Hsp90β. Tyrosine phosphorylation of Hsp90β in response to VEGF is dependent on internalization of the VEGFR-2 a

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Odegard, Amy L., Maggie H. Kwan, Hanna E. Walukiewicz, Manidipa Banerjee, Anette Schneemann, and John E. Johnson. "Low Endocytic pH and Capsid Protein Autocleavage Are Critical Components of Flock House Virus Cell Entry." Journal of Virology 83, no. 17 (2009): 8628–37. http://dx.doi.org/10.1128/jvi.00873-09.

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ABSTRACT The process by which nonenveloped viruses cross cell membranes during host cell entry remains poorly defined; however, common themes are emerging. Here, we use correlated in vivo and in vitro studies to understand the mechanism of Flock House virus (FHV) entry and membrane penetration. We demonstrate that low endocytic pH is required for FHV infection, that exposure to acidic pH promotes FHV-mediated disruption of model membranes (liposomes), and particles exposed to low pH in vitro exhibit increased hydrophobicity. In addition, FHV particles perturbed by heating displayed a marked in

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Hoeppner, Luke H., Kathryn N. Phoenix, Karl J. Clark та ін. "Revealing the role of phospholipase Cβ3 in the regulation of VEGF-induced vascular permeability". Blood 120, № 11 (2012): 2167–73. http://dx.doi.org/10.1182/blood-2012-03-417824.

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AbstractVEGF induces vascular permeability (VP) in ischemic diseases and cancer, leading to many pathophysiological consequences. The molecular mechanisms by which VEGF acts to induce hyperpermeability are poorly understood and in vivo models that easily facilitate real-time, genetic studies of VP do not exist. In the present study, we report a heat-inducible VEGF transgenic zebrafish (Danio rerio) model through which VP can be monitored in real time. Using this approach with morpholino-mediated gene knock-down and knockout mice, we describe a novel role of phospholipase Cβ3 as a negative regu

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Neri, Giulia, Salvatore Spadaro, Francesco Barreca, Saveria Santangelo, Fortunato Neri, and Enza Fazio. "Electrospun Ag/PMA Nanofibrous Scaffold as a Drug Delivery System." Current Nanomaterials 4, no. 1 (2019): 32–38. http://dx.doi.org/10.2174/2405461504666190416144047.

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Background: Polymers play a key-role in the drug delivery technology. They allow for the controlled release of therapeutic agents under an external stimulus if a sensitive segment is suitable incorporated in the polymer matrix. Actually, polymer capsules containing noble metal nanostructures are regarded as promising light-responsive drug carriers. Among polymers, poly(methacrylic acid), PMA, offers manifold advantages: i) solubility in water, ii) coordination ability for Ag-Au nanoparticles, and iii) ability to act as capping agent. However, the preparation of Ag/PMA nanocolloids involves com

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Veuthey, Tania, Jeremy T. Florman, Sebastián Giunti, et al. "The neurohormone tyramine stimulates the secretion of an insulin-like peptide from the Caenorhabditis elegans intestine to modulate the systemic stress response." PLOS Biology 23, no. 1 (2025): e3002997. https://doi.org/10.1371/journal.pbio.3002997.

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The DAF-2/insulin/insulin-like growth factor signaling (IIS) pathway plays an evolutionarily conserved role in regulating reproductive development, life span, and stress resistance. In Caenorhabditis elegans, DAF-2/IIS signaling is modulated by an extensive array of insulin-like peptides (ILPs) with diverse spatial and temporal expression patterns. However, the release dynamics and specific functions of these ILPs in adapting to different environmental conditions remain poorly understood. Here, we show that the ILP, insulin-3 (INS-3), plays a crucial role in modulating the response to various

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Peters, Isabel, Sylvia Müller, Claudia Küchler, Ute Jäger, and Sebastian Drube. "The Heat Shock Protein 90 (HSP90) Is Required for the IL-33-Induced Cytokine Production in Mast Cells (MCs)." International Journal of Molecular Sciences 23, no. 18 (2022): 10855. http://dx.doi.org/10.3390/ijms231810855.

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The alarmin interleukin-33 (IL-33) is released upon cell stress and damage in peripheral tissues. The receptor for IL-33 is the Toll/Interleukin-1 receptor (TIR)-family member T1/ST2 (the IL-33R), which is highly and constitutively expressed on MCs. The sensing of IL-33 by MCs induces the MyD88−TAK1−IKK2-dependent activation of p65/RelA and MAP-kinases, which mediate the production of pro-inflammatory cytokines and amplify FcεRI-mediated MC-effector functions and the resulting allergic reactions. Therefore, the investigation of IL-33-induced signaling is of interest for developing therapeutic

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Tan, Yanan, Yun Zhu, Lijuan Wen, et al. "Mitochondria-Responsive Drug Release along with Heat Shock Mediated by Multifunctional Glycolipid Micelles for Precise Cancer Chemo-Phototherapy." Theranostics 9, no. 3 (2019): 691–707. http://dx.doi.org/10.7150/thno.31022.

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Wischmeyer, P. E., M. W. Musch, M. B. Madonna, R. Thisted, and E. B. Chang. "Glutamine protects intestinal epithelial cells: role of inducible HSP70." American Journal of Physiology-Gastrointestinal and Liver Physiology 272, no. 4 (1997): G879—G884. http://dx.doi.org/10.1152/ajpgi.1997.272.4.g879.

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Glutamine (Gln) protects gut mucosa against injury and promotes mucosal healing. Because the induction of heat shock proteins (HSP) protects cells under conditions of stress, we determined whether Gln conferred protection against stress in an intestinal epithelial cell line through HSP induction. Gln added to IEC-18 cells induces an increase in HSP70, a concentration-dependent effect also seen with mRNA. Two forms of injury, lethal heat (49 degrees C) and oxidant, were used, and viability was determined by 51Cr release. Gln-treated cells were significantly more resistant to injury. Treatment w

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Wang, Qiushi, Ruijun He, Qi Zhang, Jin Shan, Yanmei Zhao, and Xia Wang. "Released ATP Mediates Spermatozoa Chemotaxis Promoted by Uterus-Derived Factor (UDF) in Ascaris suum." International Journal of Molecular Sciences 23, no. 7 (2022): 4069. http://dx.doi.org/10.3390/ijms23074069.

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Fertilization requires sperm migration toward oocytes and subsequent fusion. Sperm chemotaxis, a process in which motile sperm are attracted by factors released from oocytes or associated structures, plays a key role in sperm migration to oocytes. Here, we studied sperm chemotaxis in the nematode Ascaris suum. Our data show that uterus-derived factor (UDF), the protein fraction of uterine extracts, can attract spermatozoa. UDF is heat resistant, but its activity is attenuated by certain proteinases. UDF binds to the surface of spermatozoa but not spermatids, and this process is mediated by mem

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Muraoka, Rina, Keisuke Nakano, and Toshiyuki Kawakami. "Heat Shock Protein Overexpression-Mediated Periodontal Ligament Regeneration: A Fundamental Approach to Generate a Potential Biomaterial." Materials 15, no. 3 (2022): 809. http://dx.doi.org/10.3390/ma15030809.

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The periodontal ligament (PDL) is a cell-rich fibrous connective tissue supporting the tooth roots. The tissue helps to maintain homeostasis and exhibits regenerative and repairing ability, which is mediated by the heat shock protein (HSP). Here, we experimentally created PDL tissue with notable ability to regenerate hard tissue and evaluated it as a potential biomaterial. We immunohistochemically examined the mechanical load-induced HSP overexpression in mouse PDL. Following mechanical load application and release, HSP70 localization in the PDL was altered immediately, suggesting that the HSP

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Lou, Qiang, Yanzhong Hu, Yuanfang Ma та Zheng Dong. "Heat shock factor 1 induces crystallin-αB to protect against cisplatin nephrotoxicity". American Journal of Physiology-Renal Physiology 311, № 1 (2016): F94—F102. http://dx.doi.org/10.1152/ajprenal.00201.2016.

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Cisplatin, a wildly used chemotherapy drug, induces nephrotoxicity that is characterized by renal tubular cell apoptosis. In response to toxicity, tubular cells can activate cytoprotective mechanisms, such as the heat shock response. However, the role and regulation of the heat shock response in cisplatin-induced nephrotoxicity remain largely unclear. In the present study, we demonstrated the induction of heat shock factor (Hsf)1 and the small heat shock protein crystallin-αB (CryAB) during cisplatin nephrotoxicity in mice. Consistently, cisplatin induced Hsf1 and CryAB in a cultured renal pro

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Dillmann, W. H. "Heat Shock Proteins and Protection Against Ischemic Injury." Infectious Diseases in Obstetrics and Gynecology 7, no. 1-2 (1999): 55–57. http://dx.doi.org/10.1155/s1064744999000113.

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Heat shock proteins present a complex family of proteins exerting chaperone-like activities that are classified according to their molecular weight. We especially explored protective functions of inducible heat shock protein 70, the mitochondrial heat shock protein 60 and 10, and the small heat shock proteins HSP27 and αB-crystallin against ischemic, reoxygenation-mediated injury using transgenic animals and hearts under in vivo conditions and in isolated cardiac myocyte-derived cells using adenoviral vectors. We noted with great interest that differential protective effects are exerted by spe

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Lydan, M. A., and D. A. Cotter. "The role of Ca2+ during spore germination in Dictyostelium: autoactivation is mediated by the mobilization of Ca2+ while amoebal emergence requires entry of external Ca2+." Journal of Cell Science 108, no. 5 (1995): 1921–30. http://dx.doi.org/10.1242/jcs.108.5.1921.

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One of the developmental pathways used by the social amoeba Dictyostelium discoideum produces dormant spores. As with any temporary resistant stage, these spores must be able to germinate rapidly in response to positive environmental stimuli. One such stimulus is the autoactivator, an endogenous, diffusible molecule that is secreted by spores. Previous work has shown that three phases of germination, autoactivation, spore swelling and amoebal emergence, require the activity of the Ca(2+)-dependent, regulatory protein calmodulin, implicating Ca2+ as an essential cation during germination. In th

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Ueda, N., B. Guidet, and S. V. Shah. "Gentamicin-induced mobilization of iron from renal cortical mitochondria." American Journal of Physiology-Renal Physiology 265, no. 3 (1993): F435—F439. http://dx.doi.org/10.1152/ajprenal.1993.265.3.f435.

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Iron, presumably by participating in generation of hydroxyl radical or other oxidant species or initiation of lipid peroxidation, has been shown to play an important role in several models of tissue injury, including acute renal failure induced by the antibiotic gentamicin. However, the sources of iron remain unknown. Rat renal mitochondria incubated at 37 degrees C with gentamicin resulted in a time- (15-60 min) and a dose-dependent (0.01-5 mM) iron release as measured by formation of iron-bathophenanthroline sulfonate complex FeII-(BPS)3 [at 60 min, control: 1.2 +/- 0.1 nmol/mg protein, n =

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Cotton, Mark E. "SENSITIVE DETECTION AND EARLY PROGNOSTIC SIGNIFICANCE OF p24 ANTIGEN IN HEAT-DENATURED PLASMA OF HUMAN IMMUNODEFICIENCY VIRUS TYPE 1-INFECTED INFANTS." Pediatrics 96, no. 2 (1995): 406–7. http://dx.doi.org/10.1542/peds.96.2.406a.

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Purpose of Study. To investigate the effect of heat-dissociated release of complexed antigen on the sensitivity of commercial p24 antigen assays, to compare it with polymerase chain reaction (PCR) and viral culture, and to examine its prognostic utility in HIV-1 infected infants. Acid-mediated release of antigen from immune complexes is inefficient in the presence of high titers of antibody to p24 antigen. Study Population. Six hundred ninety banked serum or plasma samples from 305 patients of a cohort were studied (median age, 11 months), including 142 samples from 53 infected patients. In ad

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Walker, Faye, Lays Martin Sobral, Etienne Danis, et al. "XRT-06. RAPID PTEFB-DEPENDENT TRANSCRIPTIONAL REORGANIZATION UNDERPINS THE GLIOMA ADAPTIVE RESPONSE TO RADIOTHERAPY." Neuro-Oncology 25, Supplement_1 (2023): i78. http://dx.doi.org/10.1093/neuonc/noad073.302.

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Abstract Dynamic regulation of gene expression is fundamental for cellular adaptation to exogenous stressors. PTEFb-mediated pause-release of RNA polymerase II (Pol II) is a conserved regulatory mechanism for synchronous transcriptional induction in response to heat shock, but this pro-survival role has not been examined in the applied context of cancer therapy. Using a combination of ChIP-, ATAC-, and RNA-seq in model systems of diffuse intrinsic pontine glioma and other pediatric high-grade gliomas, we observe a rapid genome-wide reorganization of active chromatin within hours of exposure to

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Honing, S., G. Kreimer, H. Robenek, and B. M. Jockusch. "Receptor-mediated endocytosis is sensitive to antibodies against the uncoating ATPase (hsc70)." Journal of Cell Science 107, no. 5 (1994): 1185–96. http://dx.doi.org/10.1242/jcs.107.5.1185.

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We have investigated the functional role of the coated vesicle-uncoating ATPase (UA), a cognate heat shock protein (hsc70), in receptor-mediated endocytosis. A monoclonal antibody against bovine brain UA/hsc70 was generated that recognizes a 26 kDa proteolytic fragment harbouring the putative clathrin-binding site. In vitro, this antibody blocked the UA/hsc70-mediated release of clathrin from isolated coated vesicles (CVs). Upon microinjection into tissue culture cells, it specifically inhibited the heat shock-induced nuclear migration of UA/hsc70. This antibody also interfered with endocytosi

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