Indomethacin and ibuprofen induce Hsc70 nuclear localization and activation of the heat shock response in HeLa cells

Lagunas, Lucio; Bradbury, C. Matthew; Laszlo, Andrei; Hunt, Clayton R.; Gius, David

doi:10.1016/j.bbrc.2003.12.018

Cited by 19 publications

(12 citation statements)

References 32 publications

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“…Since Hsc70 is a cytoplasmic chaperone protein and oxidative stress but not apoptosis induces its translocation into the nucleus [38, 39], it is more likely that Ipr1 tends to bind with MYBBP1A in the nuclear. And furthermore, MYBBP1A could promote the apoptosis through regulation of its interacting proteins: Ahr and Myb, which were reported to mediate cells apoptosis [40, 41].…”

Section: Resultsmentioning

confidence: 99%

MYBBP1A: a new Ipr1’s binding protein in mice

et al. 2010

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Infection with mycobacterium tuberculosis (MTB) can cause different outcomes in hosts with variant genetic backgrounds. Previously, we identified an intracellular pathogen resistance 1 (Ipr1) gene with the role of resistance of MTB infection in mice model. However, until now, its binding proteins have been little known even for its human homology, SP110. In this study, the homology for mouse Ipr1 in canines was found to have an extra domain structure, h.1.5.1. And 30 potential candidate proteins were predicted to bind canine Ipr1, which were characterized of the interacting structure with the h.1.5.1. Among them, MYBBP1A was verified to bind with both Ipr1 and eGFP-Ipr1 in mouse macrophage J774A.1 clone 21 cells using co-immunoprecipitation method. And with the constructed high-confidence Ipr1-involved network, we suggested that Ipr1 might be involved in apoptosis pathway via MYBBP1A.

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Section: Resultsmentioning

confidence: 99%

MYBBP1A: a new Ipr1’s binding protein in mice

et al. 2010

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“…The increased levels of HSPA8 following P2 infection presented in this report may seem to contradict our earlier report and that of Djavani et al (22) which show decreases in both transcript and protein levels. However, as this study was performed on nuclear extracts, the increase in nuclear HSPA8 is indicative of activation (20,36,38), which is regulated by phosphorylation, resulting in nuclear translocation of the protein (14). Nuclear translocation of HSP70 has also been shown to be induced early following cytomegalovirus infection (50).…”

Section: Discussionmentioning

confidence: 99%

Analysis of the Differential Host Cell Nuclear Proteome Induced by Attenuated and Virulent Hemorrhagic Arenavirus Infection

Bowick

Spratt

Hogg³

et al. 2009

J Virol

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Arenaviruses are important emerging pathogens and include a number of hemorrhagic fever viruses classified as NIAID category A priority pathogens and CDC potential biothreat agents. Infection of guinea pigs with the New World arenavirus Pichindé virus (PICV) has been used as a biosafety level 2 model for the Lassa virus. Despite continuing research, little is known about the molecular basis of pathogenesis, and this has hindered the design of novel antiviral therapeutics. Modulation of the host response is a potential strategy for the treatment of infectious diseases. We have previously investigated the global host response to attenuated and lethal arenavirus infections by using high-throughput immunoblotting and kinomics approaches. In this report, we describe the differential nuclear proteomes of a murine cell line induced by mock infection and infection with attenuated and lethal variants of PICV, investigated by using two-dimensional gel electrophoresis. Spot identification using tandem mass spectrometry revealed the involvement of a number of proteins that regulate inflammation via potential modulation of NF-B activity and of several heterogeneous nuclear ribonuclear proteins. Pathway analysis revealed a potential role for transcription factor XBP-1, a transcription factor involved in major histocompatibility complex II (MHC-II) expression; differential DNA-binding activity was revealed by electrophoretic mobility shift assay, and differences in surface MHC-II expression were seen following PICV infection. These data are consistent with the results of several previous studies and highlight potential differences between transcriptional and translational regulation. This study provides a number of differentially expressed targets for further research and suggests that key events in pathogenesis may be established early in infection.

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“…Due to the lack of knowledge of prostanoid signaling pathways activated during ovulation, and lack of information on prostanoid receptor subtype expression patterns in different follicular cell compartments (TC and GC) during the preovulatory period, we cannot determine from the present studies whether both TC and GC of bovine preovulatory follicles can respond to prostanoids directly, or whether the differential regulation observed is attributable to direct versus indirect effects of prostanoids and/or differential sensitivity of various PG-responsive genes to the signal transduction pathways involved. Furthermore, although the best-established function of INDO is to inhibit COX activity, other roles independent of prostanoid inhibition, including induction of Hsc70 nuclear Intrafollicular regulation of TIMP-4 and tPA 541 translocation (Lagunas et al 2004) and activation of PPARg (Tegeder et al 2001), have been demonstrated.…”

Section: Discussionmentioning

confidence: 99%

Effect of intrafollicular indomethacin injection on gonadotropin surge-induced expression of select extracellular matrix degrading enzymes and their inhibitors in bovine preovulatory follicles

Li¹,

Jimenez-Krassel²,

Kobayashi³

et al. 2006

Reproduction

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A growing body of evidence supports an obligatory role for intrafollicular prostanoids in the mechanism of ovulation. However, the prostanoid-dependent mediators of the follicular extracellular matrix degradation required for ovulation are unknown. The objectives of this study were to determine the cellular compartment(s) in which the gonadotropin surgeinduced regulation of select extracellular matrix degrading enzymes and their cognate inhibitors occurs in bovine preovulatory follicles, and to test whether such regulation is blocked by intrafollicular administration of the prostanoid synthesis and ovulation inhibitor, indomethacin (INDO). Follicular fluid prostaglandin E 2 concentrations were elevated in diluenttreated follicles before ovulation (24 h after GnRH injection), but the increase was blocked in INDO-treated follicles. Realtime PCR analysis revealed the specific follicular cell types where gonadotropin surge-induced increases in mRNA abundance for members of the matrix metalloproteinase/tissue inhibitor of metalloproteinase and plasminogen activator families occurred. INDO treatment increased thecal cell mRNA for tissue inhibitor of metalloproteinase-4 and its protein abundance in the apex of preovulatory follicles before ovulation, but suppressed granulosal cell mRNA and activity for tissue plasminogen activator in follicular fluid and the follicle apex. Plasmin activity was also suppressed in the follicular fluid of INDO-treated follicles. Effects of INDO injection on select matrix metalloproteinases were not observed. The results suggest that gonadotropin surge-induced regulation of tissue inhibitor of metalloproteinase-4 and tissue plasminogen activator may be prostanoid dependent, and support a potential role for increased tissue plasminogen activator expression and decreased tissue inhibitor of metalloproteinase-4 expression in the mechanism of ovulation.

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Indomethacin and ibuprofen induce Hsc70 nuclear localization and activation of the heat shock response in HeLa cells

Cited by 19 publications

References 32 publications

MYBBP1A: a new Ipr1’s binding protein in mice

MYBBP1A: a new Ipr1’s binding protein in mice

Analysis of the Differential Host Cell Nuclear Proteome Induced by Attenuated and Virulent Hemorrhagic Arenavirus Infection

Effect of intrafollicular indomethacin injection on gonadotropin surge-induced expression of select extracellular matrix degrading enzymes and their inhibitors in bovine preovulatory follicles

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