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Journal articles on the topic 'Extracellular HSP27'

Author: Grafiati

Published: 1 June 2024

Last updated: 31 July 2025

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1

Stope, Matthias B., Gerd Klinkmann, Karoline Diesing, Dominique Koensgen, Martin Burchardt, and Alexander Mustea. "Heat Shock Protein HSP27 Secretion by Ovarian Cancer Cells Is Linked to Intracellular Expression Levels, Occurs Independently of the Endoplasmic Reticulum Pathway and HSP27’s Phosphorylation Status, and Is Mediated by Exosome Liberation." Disease Markers 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/1575374.

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The heat shock protein HSP27 has been correlated in ovarian cancer (OC) patients with aggressiveness and chemoresistance and, therefore, represents a promising potential biomarker for OC diagnosis, prognosis, and treatment response. Notably, secretion of soluble HSP27 has been described by a few cell types and may take place as well in OC cells. Therefore, we studied HSP27 secretion mechanisms under diverse cellular conditions in an OC cell model system. Secretion of HSP27 was characterized after overexpression of HSP27 by transfected plasmids and after heat shock. Intra- and extracellular HSP

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2

Winter, Julia, Elke Hammer, Jacqueline Heger, et al. "Adenine Nucleotide Translocase 1 Expression Is Coupled to the HSP27-Mediated TLR4 Signaling in Cardiomyocytes." Cells 8, no. 12 (2019): 1588. http://dx.doi.org/10.3390/cells8121588.

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The cardiac-specific overexpression of the adenine nucleotide translocase 1 (ANT1) has cardioprotective effects in various experimental heart disease models. Here, we analyzed the link between ANT1 expression and heat shock protein 27 (HSP27)-mediated toll-like receptor 4 (TLR4) signaling, which represents a novel communication pathway between mitochondria and the extracellular environment. The interaction between ANT1 and HSP27 was identified by co-immunoprecipitation from neonatal rat cardiomyocytes. ANT1 transgenic (ANT1-TG) cardiomyocytes demonstrated elevated HSP27 expression levels. Incr

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3

Gabai, Vladimir L., and Michael Y. Sherman. "Invited Review: Interplay between molecular chaperones and signaling pathways in survival of heat shock." Journal of Applied Physiology 92, no. 4 (2002): 1743–48. http://dx.doi.org/10.1152/japplphysiol.01101.2001.

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Heat shock of mammalian cells causes protein damage and activates a number of signaling pathways. Some of these pathways enhance the ability of cells to survive heat shock, e.g., induction of molecular chaperones [heat shock protein (HSP) HSP72 and HSP27], activation of the protein kinases extracellular signal-regulated kinase and Akt, and phosphorylation of HSP27. On the other hand, heat shock can activate a stress kinase, c-Jun NH2-terminal kinase, thus triggering both apoptotic and nonapoptotic cell death programs. Recent data indicate that kinases activated by heat shock can regulate synth

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4

Singer, Debora, Can Pascal Wulff, Matthias B. Stope, and Sander Bekeschus. "Extracellular Heat Shock Protein 27 Is Released by Plasma-Treated Ovarian Cancer Cells and Affects THP-1 Monocyte Activity." Plasma 5, no. 4 (2022): 569–78. http://dx.doi.org/10.3390/plasma5040040.

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Heat shock protein 27 (Hsp27) is a cytoprotective molecule and is inducible via oxidative stress. Anti-cancer therapies, such as the recently investigated gas plasma, subject tumor cells to a plethora of reactive oxygen species (ROS). In ovarian tumor microenvironments (TME), immune cells such as monocytes and macrophages can be found in large numbers and are often associated with cancer progression. Therefore, we quantified extracellular Hsp27 of OVCAR-3 and SK-OV-3 cells after gas plasma exposure in vitro. We found Hsp27 to be significantly increased. Following this, we investigated the effe

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Grotegut, Pia, Sandra Kuehn, H. Burkhard Dick, and Stephanie C. Joachim. "Destructive Effect of Intravitreal Heat Shock Protein 27 Application on Retinal Ganglion Cells and Neurofilament." International Journal of Molecular Sciences 21, no. 2 (2020): 549. http://dx.doi.org/10.3390/ijms21020549.

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Heat shock protein 27 (HSP27) is commonly involved in cellular stress. Increased levels of HSP27 as well as autoantibodies against this protein were previously detected in glaucoma patients. Moreover, systemic immunization with HSP27 induced glaucoma-like damage in rodents. Now, for the first time, the direct effects of an intravitreal HSP27 application were investigated. For this reason, HSP27 or phosphate buffered saline (PBS, controls) was applied intravitreally in rats (n = 12/group). The intraocular pressure (IOP) as well as the electroretinogram recordings were comparable in HSP27 and co

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Grotegut, Pia, Philipp Johannes Hoerdemann, Sabrina Reinehr, Nupur Gupta, H. Burkhard Dick, and Stephanie C. Joachim. "Heat Shock Protein 27 Injection Leads to Caspase Activation in the Visual Pathway and Retinal T-Cell Response." International Journal of Molecular Sciences 22, no. 2 (2021): 513. http://dx.doi.org/10.3390/ijms22020513.

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Heat shock protein 27 (HSP27) is one of the small molecular chaperones and is involved in many cell mechanisms. Besides the known protective and helpful functions of intracellular HSP27, very little is known about the mode of action of extracellular HSP27. In a previous study, we showed that intravitreal injection of HSP27 led to neuronal damage in the retina and optic nerve after 21 days. However, it was not clear which degenerative signaling pathways were induced by the injection. For this reason, the pathological mechanisms of intravitreal HSP27 injection after 14 days were investigated. Hi

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Bitar, K. N., A. Ibitayo та S. B. Patil. "HSP27 modulates agonist-induced association of translocated RhoA and PKC-α in muscle cells of the colon". Journal of Applied Physiology 92, № 1 (2002): 41–49. http://dx.doi.org/10.1152/jappl.2002.92.1.41.

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The recruitment of signal transduction molecules to the membrane is crucial for the efficient coupling of extracellular signals and contractile response. The trafficking is dynamic. We have investigated a possible cross talk between agonist-induced association of translocated RhoA and translocated protein kinase C-α (PKC-α) and a role for heat shock protein 27 (HSP27) in mediating this interaction. Immunoprecipitation with HSP27 monoclonal antibody followed by immunoblotting with either RhoA antibody or PKC-α antibody indicated that acetylcholine induced associations of HSP27-RhoA and HSP27-PK

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8

Sevin, Margaux, Nicolas Pernet, Franck Vitte, et al. "HSP27: A Therapeutic Target in Myelofibrosis." Blood 128, no. 22 (2016): 1963. http://dx.doi.org/10.1182/blood.v128.22.1963.1963.

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Abstract Myelofibrosis (MF) is the most aggressive myeloproliferative neoplasms (MPN) with the highest degree of morbidity and mortality, including progressive bone marrow fibrosis resulting into bone marrow failure. JAK2 kinase inhibitors have been successfully used for a few years in MPN and more particularly for MF treatment. Despite their beneficial effects on spleen size and symptoms, JAK2 inhibitors induce low molecular and survival responses underscoring the urgent need for other therapeutic approaches. Recently, heat shock protein 90 (HSP90) - known to stabilize JAK2 - has been reporte

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9

Hatakeyama, Daijiro, Osamu Kozawa, Masayuki Niwa, et al. "Inhibition by adenylyl cyclase-cAMP system of ET-1-induced HSP27 in osteoblasts." American Journal of Physiology-Endocrinology and Metabolism 281, no. 6 (2001): E1260—E1266. http://dx.doi.org/10.1152/ajpendo.2001.281.6.e1260.

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We have previously reported that endothelin-1 (ET-1) stimulates heat shock protein (HSP) 27 induction in osteoblast-like MC3T3-E1 cells and that p38 mitogen-activated protein (MAP) kinase acts at a point downstream from protein kinase C (PKC) in HSP27 induction. In the present study, we investigated the effect of the adenylyl cyclase-cAMP system on ET-1-stimulated induction of HSP27 in MC3T3-E1 cells. Dibutyryl-cAMP (DBcAMP) dose dependently inhibited the HSP27 accumulation stimulated by ET-1. Forskolin and cholera toxin significantly suppressed the ET-1-stimulated accumulation of HSP27. Howev

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10

Musiał, Kinga, and Danuta Zwolińska. "Extracellular Hsp27 in patients with chronic kidney disease." Kidney International 83, no. 5 (2013): 971. http://dx.doi.org/10.1038/ki.2013.33.

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11

Arslan, Badel, Nurcan Aras, Selma Yaman, and Ulku Comelekoglu. "Investigation of genetic stress parameters in brain tissues of rats exposed to 1.8 GHz cell phone radiofrequency electromagnetic field." Medicine Science | International Medical Journal 13, no. 1 (2024): 78. http://dx.doi.org/10.5455/medscience.2023.06.094.

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Heat Shock Proteins (HSPs) may induce various cellular processes, including replication, apoptosis, cell-cycle progression. Mitogen-activated protein kinase (MAPK) cascades are the primary mechanism that mediates the cellular stress response to extracellular stimuli and regulates transcriptional activity. It has been shown that mobile phone exposure can stimulate the Hsp27/p38MAPK stress pathway. In this study, twenty-seven mature female Wistar albino rats were exposed to 1.8 GHz radiofrequency electromagnetic field (RF-EMF) 2h/day for 8 weeks (SAR: 0.06 W/kg). Hsp27 and p38MAPK gene expressio

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12

Shi, Chunhua, Daiana Alvarez-Olmedo, Yuan Zhang, Badal S. B. Pattar, and Edward R. O’Brien. "The Heat Shock Protein 27 Immune Complex Enhances Exosomal Cholesterol Efflux." Biomedicines 8, no. 8 (2020): 290. http://dx.doi.org/10.3390/biomedicines8080290.

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Previously, we demonstrated that Heat Shock Protein 27 (HSP27) reduces the inflammatory stages of experimental atherogenesis, is released by macrophage (MΦ) exosomes and lowers cholesterol levels in atherosclerotic plaques. Recently, we discovered that natural autoantibodies directed against HSP27 enhance its signaling effects, as HSP27 immune complexes (IC) interact at the cell membrane to modulate signaling. We now seek to evaluate the potential role of the HSP27 IC on MΦ exosomal release and cholesterol export. First, in human blood samples, we show that healthy control subjects have 86% mo

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13

Singer, Debora, Verena Ressel, Matthias B. Stope, and Sander Bekeschus. "Heat Shock Protein 27 Affects Myeloid Cell Activation and Interaction with Prostate Cancer Cells." Biomedicines 10, no. 9 (2022): 2192. http://dx.doi.org/10.3390/biomedicines10092192.

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Heat shock proteins are cytoprotective molecules induced by environmental stresses. The small heat shock protein 27 (Hsp27) is highly expressed under oxidative stress conditions, mediating anti-oxidative effects and blocking apoptosis. Since medical gas plasma treatment subjects cancer cells to a multitude of reactive oxygen species (ROS), inducing apoptosis and immunomodulation, probable effects of Hsp27 should be investigated. To this end, we quantified the extracellular Hsp27 in two prostate cancer cell lines (LNCaP, PC-3) after gas plasma-induced oxidative stress, showing a significantly e

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Yamboliev, Ilia A., Jason C. Hedges, Jack L. M. Mutnick, Leonard P. Adam, and William T. Gerthoffer. "Evidence for modulation of smooth muscle force by the p38 MAP kinase/HSP27 pathway." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 6 (2000): H1899—H1907. http://dx.doi.org/10.1152/ajpheart.2000.278.6.h1899.

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Mitogen-activated protein (MAP) kinases signal to proteins that could modify smooth muscle contraction. Caldesmon is a substrate for extracellular signal-related kinases (ERK) and p38 MAP kinases in vitro and has been suggested to modulate actin-myosin interaction and contraction. Heat shock protein 27 (HSP27) is downstream of p38 MAP kinases presumably participating in the sustained phase of muscle contraction. We tested the role of caldesmon and HSP27 phosphorylation in the contractile response of vascular smooth muscle by using inhibitors of both MAP kinase pathways. In intact smooth muscle

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15

Hyväri, Laura, Sari Vanhatupa, Miina Ojansivu, et al. "Heat Shock Protein 27 Is Involved in the Bioactive Glass Induced Osteogenic Response of Human Mesenchymal Stem Cells." Cells 12, no. 2 (2023): 224. http://dx.doi.org/10.3390/cells12020224.

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Bioactive glass (BaG) materials are increasingly used in clinics, but their regulatory mechanisms on osteogenic differentiation remain understudied. In this study, we elucidated the currently unknown role of the p38 MAPK downstream target heat shock protein 27 (HSP27), in the osteogenic commitment of human mesenchymal stem cells (hMSCs), derived from adipose tissue (hASCs) and bone marrow (hBMSCs). Osteogenesis was induced with ionic extract of an experimental BaG in osteogenic medium (OM). Our results showed that BaG OM induced fast osteogenesis of hASCs and hBMSCs, demonstrated by enhanced a

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16

Thuringer, Dominique, Gaetan Jego, Guillaume Wettstein, et al. "Extracellular HSP27 mediates angiogenesis through Toll‐like receptor 3." FASEB Journal 27, no. 10 (2013): 4169–83. http://dx.doi.org/10.1096/fj.12-226977.

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17

Guay, J., H. Lambert, G. Gingras-Breton, J. N. Lavoie, J. Huot, and J. Landry. "Regulation of actin filament dynamics by p38 map kinase-mediated phosphorylation of heat shock protein 27." Journal of Cell Science 110, no. 3 (1997): 357–68. http://dx.doi.org/10.1242/jcs.110.3.357.

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We have studied the contribution of the individual kinases of the MAP (mitogen-activated protein) kinase family, including ERK (extracellular-signal regulated kinase), JNK/SAPK (c-JUN NH2-terminal kinase/stress-activated protein kinase) and p38, to activation of the HSP27 (heat shock protein 27) kinase MAPKAP kinase-2/3 and to HSP27 phosphorylation in Chinese hamster CCL39 cells stimulated by either growth factors, cytokines or stressing agents. In vitro assays using fractionated cell extracts or immunoprecipitates indicated that only fractions containing ERK or p38, and not those containing J

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18

Huot, Jacques, François Houle, Simon Rousseau, Réna G. Deschesnes, Girish M. Shah, and Jacques Landry. "SAPK2/p38-dependent F-Actin Reorganization Regulates Early Membrane Blebbing during Stress-induced Apoptosis." Journal of Cell Biology 143, no. 5 (1998): 1361–73. http://dx.doi.org/10.1083/jcb.143.5.1361.

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In endothelial cells, H2O2 induces the rapid formation of focal adhesion complexes at the ventral face of the cells and a major reorganization of the actin cytoskeleton into dense transcytoplasmic stress fibers. This change in actin dynamics results from the activation of the mitogen-activated protein (MAP) kinase stress-activated protein kinase-2/p38 (SAPK2/p38), which, via MAP kinase-activated protein (MAPKAP) kinase-2/3, leads to the phosphorylation of the actin polymerization modulator heat shock protein of 27 kD (HSP27). Here we show that the concomitant activation of the extracellular si

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Kim, Sung O., Christopher P. Baines, Stuart D. Critz, et al. "Ischemia induced activation of heat shock protein 27 kinases and casein kinase 2 in the preconditioned rabbit heart." Biochemistry and Cell Biology 77, no. 6 (1999): 559–67. http://dx.doi.org/10.1139/o99-065.

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Protein kinase C (PKC), p38 MAP kinase, and mitogen-activated protein kinase-activated kinases 2 and 3 (MAPKAPK2 and MAPKAPK3) have been implicated in ischemic preconditioning (PC) of the heart to reduce damage following a myocardial infarct. This study examined whether extracellular signal-regulated kinase (Erk) 1, p70 ribosomal S6 kinase (p70 S6K), casein kinase 2 (CK2), and other hsp27 kinases are also activated by PC, and if they are required for protection in rabbit hearts. CK2 and hsp27 kinase activities declined during global ischemia in control hearts, whereas PC with 5 min ischemia an

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20

Salari, Samira, Tara Seibert, Yong-Xiang Chen та ін. "Extracellular HSP27 acts as a signaling molecule to activate NF-κB in macrophages". Cell Stress and Chaperones 18, № 1 (2012): 53–63. http://dx.doi.org/10.1007/s12192-012-0356-0.

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21

Jin, Chunhua, Joseph C. Cleveland, Lihua Ao, et al. "Human Myocardium Releases Heat Shock Protein 27 (HSP27) after Global Ischemia: The Proinflammatory Effect of Extracellular HSP27 through Toll-like Receptor (TLR)-2 and TLR4." Molecular Medicine 20, no. 1 (2014): 280–89. http://dx.doi.org/10.2119/molmed.2014.00058.

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22

Abell, Amy N., Jaime A. Rivera-Perez, Bruce D. Cuevas, et al. "Ablation of MEKK4 Kinase Activity Causes Neurulation and Skeletal Patterning Defects in the Mouse Embryo." Molecular and Cellular Biology 25, no. 20 (2005): 8948–59. http://dx.doi.org/10.1128/mcb.25.20.8948-8959.2005.

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ABSTRACT Skeletal disorders and neural tube closure defects represent clinically significant human malformations. The signaling networks regulating normal skeletal patterning and neurulation are largely unknown. Targeted mutation of the active site lysine of MEK kinase 4 (MEKK4) produces a kinase-inactive MEKK4 protein (MEKK4K1361R). Embryos homozygous for this mutation die at birth as a result of skeletal malformations and neural tube defects. Hindbrains of exencephalic MEKK4K1361R embryos show a striking increase in neuroepithelial cell apoptosis and a dramatic loss of phosphorylation of MKK

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23

Zheng, Guopei, Zhijie Zhang, Hao Liu, et al. "HSP27-Mediated Extracellular and Intracellular Signaling Pathways Synergistically Confer Chemoresistance in Squamous Cell Carcinoma of Tongue." Clinical Cancer Research 24, no. 5 (2017): 1163–75. http://dx.doi.org/10.1158/1078-0432.ccr-17-2619.

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Solly, Françoise, Pascale Flandrin-Gresta, Carmen Aanei, et al. "High Levels of Heat Shock Proteins 90 and 27 in CD34-Positive Cells from Myelodysplastic Syndromes (MDS) Are Associated with Higher Expression and Activation of Focal Adhesion Kinase (FAK) and with Disease Progression." Blood 114, no. 22 (2009): 289. http://dx.doi.org/10.1182/blood.v114.22.289.289.

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Abstract Abstract 289 MDS are characterized by a high risk of evolution into acute myeloid leukemia (AML). The pathogenesis of this evolution is still unclear. Some studies indicate that aberrant activation of survival signaling pathways is involved. The 90-kDa heat shock protein (HSP90) is implicated in the conformational maturation and stabilization of protein kinases and has key roles in signal transduction, protein folding, and protein degradation. HSP90 levels are increased in AML cells, and associated with resistance to chemotherapy induced apoptosis. Moreover, HSP90 is involved in the f

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Joo, Jin Deok, Mihwa Kim, Patrick Horst, et al. "Acute and delayed renal protection against renal ischemia and reperfusion injury with A1 adenosine receptors." American Journal of Physiology-Renal Physiology 293, no. 6 (2007): F1847—F1857. http://dx.doi.org/10.1152/ajprenal.00336.2007.

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We showed previously that activation of A1 adenosine receptors (AR) protects against renal ischemia-reperfusion (IR) injury in rats and mice. In the heart, transient A1AR activation produces biphasic protective effects: acute protection wanes after several hours but protective effects return 24–72 h later (second window of protection). In this study, we determined whether A1AR activation produces delayed renal protection and elucidated the mechanisms of acute and delayed renal protection. A1AR wild-type mice were subjected to 30-min renal ischemia and 24 h of reperfusion to produce acute renal

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Ao, Lihua, Yufeng Zhai, Chunhua Jin, Joseph C. Cleveland, David A. Fullerton, and Xianzhong Meng. "Attenuated Recovery of Contractile Function in Aging Hearts Following Global Ischemia/Reperfusion: Role of Extracellular HSP27 and TLR4." Molecular Medicine 22, no. 1 (2016): 863–72. http://dx.doi.org/10.2119/molmed.2016.00204.

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Lee, J., J. Kim, J. Choi, J. Lee, B. Lee, and J. Park. "Abstract: P232 HSP27 MODULATES OXIDIZED LDL INDUCED DESTRUCTION AND SYNTHESIS OF EXTRACELLULAR MATRIX IN VASCULAR SMOOTH MUSCLE CELLS." Atherosclerosis Supplements 10, no. 2 (2009): e297. http://dx.doi.org/10.1016/s1567-5688(09)70297-1.

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Dave, Kandarp M., Donna B. Stolz, Venugopal R. Venna, et al. "Mitochondria-containing extracellular vesicles (EV) reduce mouse brain infarct sizes and EV/HSP27 protect ischemic brain endothelial cultures." Journal of Controlled Release 354 (February 2023): 368–93. http://dx.doi.org/10.1016/j.jconrel.2023.01.025.

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Dempsey, Nina C., Francesca Leoni, John H. H. Williams, and Christine Hoyle. "Heat Shock Protein Localisation in Chronic Lymphatic Leukaemia." Blood 112, no. 11 (2008): 2085. http://dx.doi.org/10.1182/blood.v112.11.2085.2085.

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Abstract Heat Shock Proteins (Hsps) are a highly conserved group of molecular chaperones, the over-expression of which has been well documented in many cancer types. However, the location of these proteins within the cancer cell appears to be crucial in terms of tumour progression. Intracellular Hsp70 expression in particular appears to confer resistance to apoptosis, while surface Hsp70 expression has been shown to aid immune recognition of the cancer cell by NK cells. High intracellular levels of Hsp90 and Hsp27 also contribute to cell survival, while surface Hsp90 and Hsp27 have been shown

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Nestorova, Gergana, Kristen Hutson, Guoting Qin, and Chengzhi Cai. "Abstract 1191 Mass Spectrometry Analysis of Hsp27 and EpCAM-Enriched Glioblastoma Extracellular Vesicles for Noninvasive Diagnostics and Biomarkers Discovery." Journal of Biological Chemistry 301, no. 5 (2025): 108640. https://doi.org/10.1016/j.jbc.2025.108640.

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Kostrzewa-Nowak, Dorota, Andrzej Ciechanowicz, Jeremy S. C. Clark, and Robert Nowak. "Damage-Associated Molecular Patterns and Th-Cell-Related Cytokines Released after Progressive Effort." Journal of Clinical Medicine 9, no. 3 (2020): 876. http://dx.doi.org/10.3390/jcm9030876.

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Inflammation-induced processes commence with the activation of signalling pathways at the cellular level, which mobilize inflammatory cells and stimulate the secretion of chemokines, cytokines, and damage-associated molecular pattern molecules (DAMPs). Physical effort stimulates inflammation, contributing to muscle repair and regeneration. We have examined the impact of different protocols of progressive-effort tests on T-cell DAMP levels, extracellular cleavage products (fibronectin and hyaluronan), and Th-cell-related cytokine levels among soccer players. Thirty male soccer players with a me

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Schwab, Melissa, Katharina Thunborg, Omid Azimzadeh, et al. "Targeting Cancer Metabolism Breaks Radioresistance by Impairing the Stress Response." Cancers 13, no. 15 (2021): 3762. http://dx.doi.org/10.3390/cancers13153762.

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The heightened energetic demand increases lactate dehydrogenase (LDH) activity, the corresponding oncometabolite lactate, expression of heat shock proteins (HSPs) and thereby promotes therapy resistance in many malignant tumor cell types. Therefore, we assessed the coregulation of LDH and the heat shock response with respect to radiation resistance in different tumor cells (B16F10 murine melanoma and LS174T human colorectal adenocarcinoma). The inhibition of LDH activity by oxamate or GNE-140, glucose deprivation and LDHA/B double knockout (LDH−/−) in B16F10 and LS174T cells significantly dimi

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An, Steven S., Corin M. Pennella, Achuta Gonnabathula, et al. "Hypoxia alters biophysical properties of endothelial cells via p38 MAPK- and Rho kinase-dependent pathways." American Journal of Physiology-Cell Physiology 289, no. 3 (2005): C521—C530. http://dx.doi.org/10.1152/ajpcell.00429.2004.

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Hypoxia alters the barrier function of the endothelial cells that line the pulmonary vasculature, but underlying biophysical mechanisms remain unclear. Using rat pulmonary microvascular endothelial cells (RPMEC) in culture, we report herein changes in biophysical properties, both in space and in time, that occur in response to hypoxia. We address also the molecular basis of these changes. At the level of the single cell, we measured cell stiffness, the distribution of traction forces exerted by the cell on its substrate, and spontaneous nanoscale motions of microbeads tightly bound to the cyto

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Timofeev, Yuriy S., Anton R. Kiselev, Olga N. Dzhioeva, and Oxana M. Drapkina. "Heat Shock Proteins (HSPs) and Cardiovascular Complications of Obesity: Searching for Potential Biomarkers." Current Issues in Molecular Biology 45, no. 12 (2023): 9378–89. http://dx.doi.org/10.3390/cimb45120588.

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Heat shock proteins (HSPs), a family of proteins that support cellular proteostasis and perform a protective function under various stress conditions, such as high temperature, intoxication, inflammation, or tissue hypoxia, constitute a promising group of possible biochemical markers for obesity and cardiovascular diseases. HSP27 is involved in essential cellular processes occurring in conditions of obesity and its cardiometabolic complications; it has protective properties, and its secretion may indicate a cellular response to stress. HSP40 plays a controversial role in the pathogenesis of ob

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Monda, Marcellino, Giovanni Messina, Ilaria Scognamiglio, et al. "Short-Term Diet and Moderate Exercise in Young Overweight Men Modulate Cardiocyte and Hepatocarcinoma Survival by Oxidative Stress." Oxidative Medicine and Cellular Longevity 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/131024.

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The present study was designed to evaluate the effects of diet lifestyle on extending lifespan and reducing liver cancer risk. Young overweight men(n=20), without metabolic syndrome, were placed in a 3-week residential program on a low-fat diet and moderate aerobic exercise. In each subject, pre- and postintervention fasting blood were collected for evaluating levels of serum lipids, and oxidative stress markers. Using subject sera and cardiomyocyte (H9C2) culture systems, we measured heat shock protein 27 and 90 expression, lipid accumulation, and oxidative stress marker levels. After 3-weeks

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Wantoch von Rekowski, Kathleen, Philipp König, Svenja Henze, et al. "Insight into Cisplatin-Resistance Signaling of W1 Ovarian Cancer Cells Emerges mTOR and HSP27 as Targets for Sensitization Strategies." International Journal of Molecular Sciences 21, no. 23 (2020): 9240. http://dx.doi.org/10.3390/ijms21239240.

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The microenvironment possesses a strong impact on the tumor chemoresistance when cells bind to components of the extracellular matrix. Here we elucidate the signaling pathways of cisplatin resistance in W1 ovarian cancer cells binding to collagen type 1 (COL1) and signaling interference with constitutive cisplatin resistance in W1CR cells to discover the targets for sensitization. Proteome kinase arrays and Western blots were used to identify the signaling components, their impact on cisplatin resistance was evaluated by inhibitory or knockdown approaches. W1 cell binding to COL1 upregulates i

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El-Yazbi, Ahmed, Khaled Abd-Elrahman, and Alejandro Moreno-Dominguez. "PKC-mediated cerebral vasoconstriction: Role of myosin light chain phosphorylation versus actin cytoskeleton reorganization." Biochemical Pharmacology 95, no. 2015 (2015): 263–78. https://doi.org/10.1016/j.bcp.2015.04.011.

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Defective protein kinase C (PKC) signaling has been suggested to contribute to abnormal vascular contraction in disease conditions including hypertension and diabetes. Our previous work on agonist and pressure-induced cerebral vasoconstriction implicated PKC as a major contributor to force production in a myosin light chain (LC20) phosphorylation-independent manner. Here, we used phorbol dibutyrate to selectively induce a PKC-dependent constriction in rat middle cerebral arteries and delineate the relative contribution of different contractile mechanisms involved. Specifically, we employed an

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Tanabe, Hiroki, Takuji Suzuki, Tomokazu Ohishi, Mamoru Isemura, Yoriyuki Nakamura, and Keiko Unno. "Effects of Epigallocatechin-3-Gallate on Matrix Metalloproteinases in Terms of Its Anticancer Activity." Molecules 28, no. 2 (2023): 525. http://dx.doi.org/10.3390/molecules28020525.

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Epidemiological studies have shown that the consumption of green tea has beneficial effects against cancer. Basic studies have provided evidence that epigallocatechin gallate (EGCG) is a major contributor to these effects. Matrix metalloproteinases (MMPs) are zinc-dependent metalloproteinases with the ability to degrade the extracellular matrix proteins and are involved in various diseases including cancer in which MMPs have a critical role in invasion and metastasis. In this review, we discuss the effects of EGCG on several types of MMPs in the context of its anticancer activity. In the promo

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Shi, Yu, Alexey Kotlyarov, Kathrin Laaß, et al. "Elimination of Protein Kinase MK5/PRAK Activity by Targeted Homologous Recombination." Molecular and Cellular Biology 23, no. 21 (2003): 7732–41. http://dx.doi.org/10.1128/mcb.23.21.7732-7741.2003.

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ABSTRACT MK5 (mitogen-activated protein kinase [MAPK]-activated protein kinase 5), also designated PRAK (p38-regulated and -activated kinase), was deleted from mice by homologous recombination. Although no MK5 full-length protein and kinase activity was detected in the MK5 knockout mice, the animals were viable and fertile and did not display abnormalities in tissue morphology or behavior. In addition, these mice did not show increased resistance to endotoxic shock or decreased lipopolysaccharide-induced cytokine production. Hence, MK5 deletion resulted in a phenotype very different from the c

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Weiss, Louis M., Yan Fen Ma, Peter M. Takvorian, Herbert B. Tanowitz, and Murray Wittner. "Bradyzoite Development in Toxoplasma gondii and the hsp70 Stress Response." Infection and Immunity 66, no. 7 (1998): 3295–302. http://dx.doi.org/10.1128/iai.66.7.3295-3302.1998.

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ABSTRACT Toxoplasma gondii is a well-described ubiquitous Apicomplexan protozoan parasite that is an important opportunistic pathogen. The factors affecting the transition of tachyzoites to the latent bradyzoite stage remain to be defined. The induction of bradyzoite development in vitro has been linked to temperature, pH, mitochondrial inhibitors, sodium arsenite, and many of the other stressors associated with heat shock protein (hsp) induction. There is evidence for other organisms that hsps are developmentally regulated. Therefore, we examined whether hsp induction is an early event in bra

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Voth, Daniel E., and Robert A. Heinzen. "Sustained Activation of Akt and Erk1/2 Is Required for Coxiella burnetii Antiapoptotic Activity." Infection and Immunity 77, no. 1 (2008): 205–13. http://dx.doi.org/10.1128/iai.01124-08.

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ABSTRACT Coxiella burnetii is an obligate intracellular bacterial pathogen that directs biogenesis of a lysosome-like, parasitophorous vacuole in mammalian cells. We recently reported that C. burnetii inhibits apoptotic cell death in macrophages, presumably as a mechanism to sustain the host for completion of its lengthy infectious cycle. In the current study, we further investigated C. burnetii manipulation of host cell signaling and apoptosis by examining the effect of C. burnetii infection on activation of 15 host proteins involved in stress responses, cytokine production, and apoptosis. C.

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Desjardins, Pascale, Rébecca Berthiaume, Camille Couture, et al. "Impact of Exosomes Released by Different Corneal Cell Types on the Wound Healing Properties of Human Corneal Epithelial Cells." International Journal of Molecular Sciences 23, no. 20 (2022): 12201. http://dx.doi.org/10.3390/ijms232012201.

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Corneal wound healing involves communication between the different cell types that constitute the three cellular layers of the cornea (epithelium, stroma and endothelium), a process ensured in part by a category of extracellular vesicles called exosomes. In the present study, we isolated exosomes released by primary cultured human corneal epithelial cells (hCECs), corneal fibroblasts (hCFs) and corneal endothelial cells (hCEnCs) and determined whether they have wound healing characteristics of their own and to which point they modify the genetic and proteomic pattern of these cell types. Exoso

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Johnson, John D., Jay Campisi, Craig M. Sharkey, Sarah L. Kennedy, Molly Nickerson, and Monika Fleshner. "Adrenergic receptors mediate stress-induced elevations in extracellular Hsp72." Journal of Applied Physiology 99, no. 5 (2005): 1789–95. http://dx.doi.org/10.1152/japplphysiol.00390.2005.

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Heat-shock protein concentrations in the blood increase after exposure to a variety of stressors, including trauma and psychological stress. Although the physiological function of extracellular heat shock protein remains controversial, there is evidence that extracellular heat shock protein 72 (Hsp72) can facilitate immunologic responses. The signal(s) that mediate(s) the in vivo elevation of extracellular Hsp72 in the blood after stressor exposure remain(s) unknown. Here we report that Hsp72 increases in the circulation via an α1-adrenergic receptor-mediated signaling pathway. Activation of α

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Ishida, Yoshihito, Hiroshi Kubota, Akitsugu Yamamoto, Akira Kitamura, Hans Peter Bächinger, and Kazuhiro Nagata. "Type I Collagen in Hsp47-null Cells Is Aggregated in Endoplasmic Reticulum and Deficient in N-Propeptide Processing and Fibrillogenesis." Molecular Biology of the Cell 17, no. 5 (2006): 2346–55. http://dx.doi.org/10.1091/mbc.e05-11-1065.

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Heat-shock protein of 47 kDa (Hsp47) is a molecular chaperone that recognizes collagen triple helices in the endoplasmic reticulum (ER). Hsp47-knockout mouse embryos are deficient in the maturation of collagen types I and IV, and collagen triple helices formed in the absence of Hsp47 show increased susceptibility to protease digestion. We show here that the fibrils of type I collagen produced by Hsp47-/- cells are abnormally thin and frequently branched. Type I collagen was highly accumulated in the ER of Hsp47-/- cells, and its secretion rate was much slower than that of Hsp47+/+ cells, leadi

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Zu, YL, Y. Ai, A. Gilchrist, ME Labadia, RI Sha'afi, and CK Huang. "Activation of MAP kinase-activated protein kinase 2 in human neutrophils after phorbol ester or fMLP peptide stimulation." Blood 87, no. 12 (1996): 5287–96. http://dx.doi.org/10.1182/blood.v87.12.5287.bloodjournal87125287.

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In response to extracellular stimulation, one of the earliest events in human neutrophils is protein phosphorylation, which mediates signal transduction and leads to the regulation of cellular functions. Mitogen- activated protein (MAP) kinases are rapidly activated by a variety of mitogens, cytokines, and stresses. The activated MAP kinases in turn regulate their substrate molecules by phosphorylation. MAP kinase- activated protein (MAPKAP) kinase 2, a Ser/Thr kinase, has been shown to be phosphorylated by p38 MAP kinase both in vivo and in vitro. Phosphorylation of the Thr-334 site of MAPKAP

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Osorio, Luis A., Mauricio Lozano, Paola Soto, et al. "Levels of Small Extracellular Vesicles Containing hERG-1 and Hsp47 as Potential Biomarkers for Cardiovascular Diseases." International Journal of Molecular Sciences 25, no. 9 (2024): 4913. http://dx.doi.org/10.3390/ijms25094913.

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The diagnosis of cardiovascular disease (CVD) is still limited. Therefore, this study demonstrates the presence of human ether-a-go-go-related gene 1 (hERG1) and heat shock protein 47 (Hsp47) on the surface of small extracellular vesicles (sEVs) in human peripheral blood and their association with CVD. In this research, 20 individuals with heart failure and 26 participants subjected to cardiac stress tests were enrolled. The associations between hERG1 and/or Hsp47 in sEVs and CVD were established using Western blot, flow cytometry, electron microscopy, ELISA, and nanoparticle tracking analysis

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Asea, Alexzander. "Initiation of the Immune Response by Extracellular Hsp72: Chaperokine Activity of Hsp72." Current Immunology Reviews 2, no. 3 (2006): 209–15. http://dx.doi.org/10.2174/157339506778018514.

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Ganter, Michael T., Lorraine B. Ware, Marybeth Howard, et al. "Extracellular heat shock protein 72 is a marker of the stress protein response in acute lung injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 291, no. 3 (2006): L354—L361. http://dx.doi.org/10.1152/ajplung.00405.2005.

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Previous studies have shown that heat shock protein 72 (Hsp72) is found in the extracellular space (eHsp72) and that eHsp72 has potent immunomodulatory effects. However, whether eHsp72 is present in the distal air spaces and whether eHsp72 could modulate removal of alveolar edema is unknown. The first objective was to determine whether Hsp72 is released within air spaces and whether Hsp72 levels in pulmonary edema fluid would correlate with the capacity of the alveolar epithelium to remove alveolar edema fluid in patients with ALI/ARDS. Patients with hydrostatic edema served as controls. The s

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Yamada, Paulette M., Fabiano T. Amorim, Pope Moseley, Robert Robergs, and Suzanne M. Schneider. "Effect of heat acclimation on heat shock protein 72 and interleukin-10 in humans." Journal of Applied Physiology 103, no. 4 (2007): 1196–204. http://dx.doi.org/10.1152/japplphysiol.00242.2007.

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Heat acclimation (HA) results in whole body adaptations that increase heat tolerance, and in addition, HA may also result in protective cellular adaptations. We hypothesized that, after HA, basal intracellular heat shock protein (HSP) 72 and extracellular IL-10 levels would increase, while extracellular HSP72 levels decrease. Ten male and two female subjects completed a 10-day exercise/HA protocol (100-min exercise bout at 56% of maximum O2 uptake in a 42.5°C DB, 27.9% RH environment); subjects exhibited classic adaptations that accompany HA. Peripheral blood mononuclear cells (PBMCs) were iso

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Beck, Franz-X., Wolfgang Neuhofer, and Eva Müller. "Molecular chaperones in the kidney: distribution, putative roles, and regulation." American Journal of Physiology-Renal Physiology 279, no. 2 (2000): F203—F215. http://dx.doi.org/10.1152/ajprenal.2000.279.2.f203.

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Molecular chaperones are intracellular proteins that prevent inappropriate intra- and intermolecular interactions of polypetide chains. A specific group of highly conserved molecular chaperones are the heat shock proteins (HSPs), many of which are constitutively expressed but most of which are inducible by diverse (in some cases specific) stress factors. HSPs, either alone or in cooperation with “partner” chaperones, are involved in cellular processes as disparate as correct folding and assembly of proteins, transport of proteins to specific intracellular locations, protein degradation, and pr

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