Heat Shock Protein Gene Expression Research Articles

Glycine betaine‐mediated potentiation of HSP gene expression involves calcium signaling pathways in tobacco exposed to NaCl stress

Glycine betaine (GB) can enhance heat tolerance and the accumulation of heat-shock protein (HSP) in plants, but the effects of GB on HSP accumulation during salt stress were not previously known. To investigate the mechanism of how GB influences the expression of HSP, wild-type tobacco (Nicotiana tabacum) seedlings pretreated with exogenous GB and BADH-transgenic tobacco plants that accumulated GB in vivo were studied during NaCl stress. A transient Ca(2+) efflux was observed in the epidermal cells of the elongation zone of tobacco roots after NaCl treatment for 1-2 min. After 24 h of NaCl treatment, an influx of Ca(2+) was observed; a low concentration of GB significantly increased NaCl-induced Ca(2+) influx. GB increased the intracellular free calcium ion concentration and enhanced the expression of the calmodulin (CaM) and heat-shock transcription factor (HSF) genes resulting in potentiated levels of HSPs. Pharmacological experiments confirmed that Ca(2+) and CaM increased HSFs and HSPs gene expression, which coincided with increased the levels of HSP70 accumulation. These results suggest a mechanism by which GB acted as a cofactor in the NaCl induction of a Ca(2+) -permeable current. A possible regulatory model of Ca(2+) -CaM in the signal transduction pathway for induction of transcription and translation of the active HSPs is described.

Effect of elevated temperatures on bovine corpus luteum function: expression of heat-shock protein 70, cell viability and production of progesterone and prostaglandins by cultured luteal cells

Summer heat stress lowers fertility in cattle in hot environments by influencing oocyte quality, follicular activity and progesterone (P4) level in blood plasma. However, the mechanisms by which elevated temperature influences corpus luteum function remain unclear. Elevated temperature has generally been known to upregulate the gene expression of heat-shock protein (HSP) 70 in a variety of cell types. To clarify the direct effects of elevated temperature on bovine corpus luteum function, we examined the expressions of HSP70, cell viability and the production of P4 and prostaglandins (PGs) in luteal cells cultured at 37.5°C (normal temperature in our culture system), 39.0°C (moderately elevated temperature) or 41.0°C (severely elevated temperature) for 12 or 24 h. HSP70 mRNA expression was increased by incubation at 39.0°C for 12 h and at 41.0°C for 12 and 24 h, whereas HSP70 protein expression was not significantly affected. The viability of luteal cells cultured for 24 h, measured by flow cytometry with propidium iodide staining, was not significantly affected by temperature. Interestingly, the production of P4 by cultured luteal cells was higher at 39.0°C than at 37.5°C after 12 and 24 h of incubation. The production of PGF2α was higher at 39.0°C and 41.0°C than at 37.5°C after 12 and 24 h of incubation. The production of PGE2 was higher at 41.0°C than at 37.5°C after 24 h of incubation. The overall results suggested that elevated temperature does not negatively affect luteal function, and that the low fertility observed during summer is not due to a direct effect of elevated temperature on luteal cells.

Mediator Affects Pol II Recruitment and Nucleosome Displacement at Heat Shock Protein (HSP) Genes in Saccharomyces cerevisiae

Mediator, an evolutionarily conserved transcriptional coactivator, plays a critical role in governing both constitutive and induced levels of heat shock protein (HSP) gene expression in budding yeast. Yet how Mediator, and in particular each of its four structural modules – Head, Middle, Tail and Kinase – participates in HSP gene regulation and crosstalk with other transcriptional coactivators remains unclear. Using the conditional depletion technique termed Anchor Away, we have studied the role of two essential Middle Module subunits, Med14 and Med7, in the transcription and chromatin remodeling of HSP genes. Depletion of either subunit disrupts integrity of Mediator, as assessed by a failure of Med20 (Head) to be recruited to induced HSP genes. Pol II recruitment is also affected, and its loss parallels that of Med7. Strikingly, quantitative depletion of Med14 has a relatively modest effect on Pol II recruitment at HSP genes. Nucleosome disassembly triggered by heat shock is likewise differentially affected by loss of Med14 and Med7. These findings suggest that Mediator integrity is important, but not essential, for Pol II recruitment and chromatin remodeling upon heat shock. The interplay between Mediator and other transcriptional coactivators (SAGA, TFIID, RSC, Swi/Snf) in regulating stress‐induced transcription is under investigation. This work is supported by NSF grant MCB‐1025025 awarded to D.S.G.

Efficacy of Geranylgeranylacetone for heat stroke recovery in Fischer 344 rats

Heat Shock Protein 70 (HSP70) functions as a molecular chaperone to prevent the misfolding and aggregation of proteins under stressful conditions. Geranylgeranylacetone (GGA) is a pharmacologic inducer of HSP70 in the absence of heat stress, making GGA a potential candidate for post‐heat injury/stroke (HI/S) therapy. We hypothesized that GGA administered 24h post‐HI/S would augment liver HSP70 gene expression and accelerate HI/S recovery in rats. Male F344 rats (277.5 ± 5.3 g) were orally administered GGA (200 mg/kg bw; n=9) or vehicle (Veh; 1mL; n=9) 24h post‐HI/S (Tc,Max, 41.8°C; radiotelemetry). GGA had no effect on thermal load accrued during heat exposure. Liver HSP70 gene expression (qPCR) and biomarkers of liver function (VetScan; ALT, albumin, bile acids, BUN) were examined at 2 and 10d of recovery. Liver HSP70 gene expression was increased ~2000‐fold through 10d of recovery; GGA had no effect on this response. Bile acids, ALT and BUN were similar between HI/S and non‐heated controls on 2 and 10d regardless of treatment. Conversely, HI/S rats treated with GGA showed significantly lower albumin levels compared to non‐heated controls at 2d (4.24±0.07 v 4.78±0.03 U/L, respectively; ANOVA, p<0.01). Our results suggest that GGA administration 24h post‐HI/S is not an efficacious treatment in rats and may delay recovery of liver function. Research supported by MRMC. Author views not official US Army or DoD policy.

Effects of mannan oligosaccharide on the physiological responses, HSP70 gene expression and disease resistance of Allogynogenetic crucian carp (Carassius auratus gibelio) under Aeromonas hydrophila infection

We evaluated the effect of dietary supplementation with mannan oligosaccharide (MOS) on the resistance to Aeromonas hydrophi1a infection in Allogynogenetic crucian carp. The fish were randomly divided into five groups: a control group was fed with basal diet, and four treatment groups fed with basal diet supplemented with 60, 120, 240, 480 mg/kg MOS for 10 weeks, respectively. We then challenged the fish with A. hydrophi1a and recorded the mortality and the changes in serum cortisol, T3, T4, lysozyme, alkaline phosphatase (ALP), globin and hepatic total anti-oxidative capacity, superoxide dismutase (SOD), malondialdehyde (MDA) and the relative expression of heat shock protein 70 (HSP70) mRNA for a period of 7 d. Supplementation with 240 mg/kg MOS significantly increased serum ALP activity before infection, 1d and 2d after infection, serum globin concentration prior to infection, 1d and 7d after infection, serum lysozyme activity at 2d after infection, T3 concentration at 2d after infection, hepatic total anti-oxidative capacity prior to infection, hepatic SOD activity at 7d after infection and reduced serum cortisol concentration at 2d after infection, hepatic malondialdehyde content at 1d and 2d after infection. Supplementation with 480 mg/kg MOS significantly increased serum ALP activity before infection, 1d and 2d after infection, T3 content 1d after infection, T4 content prior infection and 7d after infection, serum globin concentration prior to infection, 1d and 7d after infection, serum lysozyme activity prior infection and 1d after infection, serum total anti-oxidative capacity prior to infection and 7d after infection, hepatic SOD activity at 7d after infection and the relative level of hepatic HSP70 mRNA at 2d and 7d after infection, had decreased levels of serum cortisol concentration before the infection, at 2d after infection, T4 concentration at 1d and 2d after infection, hepatic malondialdehyde content at 1d and 2d after infection. Mortality was significantly lower in the group of 240 and 480 mg/kg MOS than the control. Our results suggest that ingestion of a basal diet supplemented with 240–480 mg/kg MOS can enhance resistance against pathogenic infections in Allogynogenetic crucian carp.

Spaceflight engages heat shock protein and other molecular chaperone genes in tissue culture cells of Arabidopsis thaliana

Gravity has been a major force throughout the evolution of terrestrial organisms, and plants have developed exquisitely sensitive, regulated tropisms and growth patterns that are based on the gravity vector. The nullified gravity during spaceflight allows direct assessment of gravity roles. The microgravity environments provided by the Space Shuttle and International Space Station have made it possible to seek novel insights into gravity perception at the organismal, tissue, and cellular levels. Cell cultures of Arabidopsis thaliana perceive and respond to spaceflight, even though they lack the specialized cell structures normally associated with gravity perception in intact plants; in particular, genes for a specific subset of heat shock proteins (HSPs) and factors (HSFs) are induced. Here we ask if similar changes in HSP gene expression occur during nonspaceflight changes in gravity stimulation. Quantitative RT-qPCR was used to evaluate mRNA levels for Hsp17.6A and Hsp101 in cell cultures exposed to four conditions: spaceflight (mission STS-131), hypergravity (centrifugation at 3 g or 16 g), sustained two-dimensional clinorotation, and transient milligravity achieved on parabolic flights. We showed that HSP genes were induced in cells only in response to sustained clinorotation. Transient microgravity intervals in parabolic flight and various hypergravity conditions failed to induce HSP genes. We conclude that nondifferentiated cells do indeed sense their gravity environment and HSP genes are induced only in response to prolonged microgravity or simulated microgravity conditions. We hypothesize that HSP induction upon microgravity indicates a role for HSP-related proteins in maintaining cytoskeletal architecture and cell shape signaling.

OP10.09: Heat shock protein gene expression in placental insufficiency related pregnancy complications—correlation with severity of the disease and Doppler‐determined umbilical artery PI

OP10.09: Heat shock protein gene expression in placental insufficiency related pregnancy complications—correlation with severity of the disease and Doppler‐determined umbilical artery PI

Bisphenol-A affects the developmental progression and expression of heat-shock protein genes in the moth Sesamia nonagrioides

The effects of bisphenol A (BPA) on the endocrine system of vertebrates have been demonstrated in several studies. Here, we report the impact of BPA on the developmental progression and expression of heat shock protein genes on the terrestrial insect Sesamia nonagrioides (Lepidoptera: Noctuidae). S. nonagrioides 1st instar larvae were exposed until the end of 6th (last) instar to selected concentrations of BPA (1 μg/L, 10 μg/L, 100 μg/L, 1 mg/L and 10 mg/L) applied in their artificial diets. The lower doses of BPA (1-10 μg/L) were found to decrease larvae's weight while the 100 μg/L dose increased it. The higher doses of BPA were found to induce various abnormal phenotypes during 5th instar larval molting, larval-pupal transformation and metamorphosis. The developmental and metamorphosis endpoints presented here may indicate the possible impact of BPA on terrestrial insects. Additionally, 6th instar larvae were injected with several concentrations of BPA. Semi-quantitative and Real-Time PCR assays were used to identify the effects of BPA in the transcriptional regulation of five heat shock protein genes (SnoHsp19.5, SnoHsp20.8, SnoHsp70, SnoHsc70 and SnoHsp83). Application of BPA by feeding or by injection induced the synthesis of the SnoHsp19.5 and SnoHsp20.8 mRNAs. The expression levels of SnoHsp70 were not affected. In contrast, SnoHsc70 and SnoHsp83, which play a pivotal role in vertebrate sex steroid signal transduction, were elevated by BPA. Our results suggest that SnoHsp19.5, SnoHsp20.8, SnoHsp83 and SnoHsc70 genes can be modulated by BPA.

Transcriptional profiling of microdissected areas of active multiple sclerosis lesions reveals activation of heat shock protein genes

Heat shock proteins (HSPs) are stress-responsive proteins that serve as important molecules contributing to cellular "protein triage." We and others have reported an increase of selected HSPs in multiple sclerosis (MS) lesions. However, the exact expression pattern of HSP family genes in MS is not known. The aim of our research was to assess global transcriptional changes of all gene members of the HSP families within MS lesions and associated normal-appearing white matter (NAWM). To this end, we used laser capture microdissection (LCM) to isolate defined regions of chronic-active MS lesions (n = 5), one of the most common types of MS lesions. To identify changes in HSP genes in relation to different areas of the plaque, we used genome-wide microarray analysis. We detected a significant change in the transcriptional profile of the demyelinated region compared with NAWM. In particular, overall expression of different HSP genes was upregulated in different areas of chronic-active lesion. These changes were linked to an upregulation of heat shock factor 4 (HSF4). This is the first global analysis of transcriptional changes in HSPs in the central nervous system during MS. The results support a relationship between HSP activation and lesion activity.

A heat‐activated calcium‐permeable channel – Arabidopsis cyclic nucleotide‐gated ion channel 6 – is involved in heat shock responses

An increased concentration of cytosolic calcium ions (Ca²⁺) is an early response by plant cells to heat shock. However, the molecular mechanism underlying the heat-induced initial Ca²⁺ response in plants is unclear. In this study, we identified and characterized a heat-activated Ca²⁺-permeable channel in the plasma membrane of Arabidopsis thaliana root protoplasts using reverse genetic analysis and the whole-cell patch-clamp technique. The results indicated that A. thaliana cyclic nucleotide-gated ion channel 6 (CNGC6) mediates heat-induced Ca²⁺ influx and facilitates expression of heat shock protein (HSP) genes and the acquisition of thermotolerance. GUS and GFP reporter assays showed that CNGC6 expression is ubiquitous in A. thaliana, and the protein is localized to the plasma membrane of cells. Furthermore, it was found that the level of cytosolic cAMP was increased by a mild heat shock, that CNGC6 was activated by cytosolic cAMP, and that exogenous cAMP promoted the expression of HSP genes. The results reveal the role of cAMP in transduction of heat shock signals in plants. The correlation of an increased level of cytosolic cAMP in a heat-shocked plant with activation of the Ca²⁺ channels and downstream expression of HSP genes sheds some light on how plants transduce a heat stimulus into a signal cascade that leads to a heat shock response.

Glutamine activates heat shock transcription factor‐1 (HSF1) gene transcription

We have demonstrated that glutamine (GLN) enhances cytoprotective heat shock protein (HSP) expression. Heat shock transcription factor‐1 (HSF1) is the master regulator for HSP gene expression. We are aimed to explore GLN's effects on HSF1's activity and expression. Non‐stressed or heat‐stressed YAMC colonic epithelial cells were exposed to GLN at 0, 0.5 or 2mM. HSF1 expression, nuclear localization, trimerization and DNA binding were determined. HSF1 promoter‐driven reporter assay and deletion analysis of HSF1 gene promoter were conducted. GLN upregulated HSF1's transactivation activity by increasing its trimerization, nuclear localization and DNA binding. Further, GLN increased HSF1 protein and mRNA expression in both non‐stressed and stressed cells. Deletion analysis of HSF1 promoter shows that the key cis‐ element responsible for GLN response is present between bp −331 to −200. Within this region, deletion of the putative CCAAT enhancer binding protein (C/EBP) binding site resulted in decreased GLN response. In absence of glutamine, HSF1 expression was de‐repressed in C/EBPβ‐silenced cells. Over‐expression of the inhibitory dominant‐negative isoform of C/EBPβ repressed HSF1 expression in presence of adequate glutamine. We for the first time show that GLN not only activates HSF1's transactivation activity, but also activates HSF‐1 gene transcription per se in a C/EBPβ‐dependent manner.

Telomeric DNA quantity, DNA damage, and heat shock protein gene expression as physiological stress markers in chickens

In this longitudinal study with Single Comb White Leghorn chickens, we investigated the effects of stress conditions in birds that were subjected to a high stocking density with feed restrictions on the quantity of telomeric DNA, the rate of DNA damage, and the expression levels of heat shock proteins (HSP) and hydroxyl-3-methyl-glutaryl coenzyme A reductase (HMGCR) genes. The telomere length and telomere-shortening rates were analyzed by quantitative fluorescence in situ hybridization on the nuclei of lymphocytes. The DNA damage rate of lymphocytes was quantified by the comet assay. The expression levels of HSP70, HSP90, and HMGCR genes were measured by quantitative real-time PCR in lymphocytes. The telomere-shortening rate of the lymphocytes was significantly higher in the stress group than in the control. The DNA damage also increased in birds raised under stress conditions, as compared with the control group. The stress conditions had a significant effect on the expressions of HMGCR and HSP90α in lymphocytes but had no significance on HSP70 and HSP90β in blood. We conclude that the telomere length, especially the telomere-shortening rates, the quantification of total DNA damage, and the expression levels of the HMGCR and HSP90α genes can be used as sensitive physiological stress markers in chickens.

Stress levels over time in the introduced ascidian Styela plicata: the effects of temperature and salinity variations on hsp70 gene expression

Species distribution, abundance, and long-term survival are determined by biotic and abiotic regimes. However, little is known about the importance of these factors in species range expansion. Styela plicata is a solitary ascidian introduced all over the world by ship fouling, including salt marsh habitats, where introduced populations must tolerate high seasonal variations in temperature and salinity. To determine the seasonal stress levels in a salt marsh population of S. plicata, we quantified heat shock protein (hsp70) gene expression using quantitative real-time PCR throughout a 2-year cycle. Results showed that hsp70 expression varied over time, with higher stress levels recorded in summer and winter. Periodic conditions of high temperatures, particularly when coupled with low salinities, increased hsp70 gene expression. Mortality events observed every year around June were concurrent with sharp increases in temperature (>6°C), indicating that drastic changes in abiotic factors may overwhelm the observed stress response mechanisms. Determining the ability of introduced species to cope with stress, and the thresholds above which these mechanisms fail, is fundamental to predict the potential expansion range of introduced species and design efficient containment plans.

Effects of heat stress on non-specific immune parameters and HSP70 gene expression in Taisho Sanke koi(Cyprinus carpio)

In order to explore the mechanism of koi's anti-stress,the study was performed to examine the effect of continuous heat stress on non-specific immune parameters and HSP70 gene expression in Taisho Sanke koi under the laboratory conditions.Samples for detections of respiratory burst,complement protein 3(C3),superoxide dismutase(SOD),malondialdehyde(MDA)and relative expression content of heat shock protein 70(HSP70)were taken before stress,2,6,10,14,18,22 and 26 h after stress,respectively.The results were as follows.Respiratory burst activity decreased after stress,and it decreased significantly after stress 2,10,18-26 h(P0.05).The content of serum C3 was increased slightly 2 h after stress.Compared to before stress,the level of serum C3 decreased 6-26 h after stress,and it decreased significantly 14-22 h after stress(P0.05).The level of serum SOD had the trend of augment,but not significantly(P0.05).The concentration of serum MDA increased after stress,and it increased significantly after stress 10-18 h(P0.05).Compared to before stress,the relative expression content of HSP70 gene significantly increased by 5.93 times 2 h after stress and 2 times 26 h after stress(P0.05).6-22 h after stress,the relative expression content of HSP70 gene had no significant difference from that before stress(P0.05).These results indicated that heat stress affected non-specific immune parameters,and lowered non-specific immunity of Taisho Sanke koi.The expression of HSP70 gene was regulated by heat stress.HSP70 induced by heat stress played a role of stress protection to koi.

Response of preosteoblasts to thermal stress conditioning and osteoinductive growth factors

Conditioning protocols involving mechanical stress independently or with chemical cues such as growth factors (GFs) possess significant potential to enhance bone regeneration. However, utilization of thermal stress conditioning alone or with GFs for bone therapy has been under-investigated. In this study, a preosteoblast cell line (MC3T3-E1) was exposed to treatment with water bath heating (44°C, 4 and 8 min) and osteoinductive GFs (bone morphogenetic protein-2 and transforming growth factor-β1) individually or in combination to investigate whether these stimuli could promote induction of bone-related markers, an angiogenic factor, and heat shock proteins (HSPs). Cells remained viable when heating durations were less than 20 min at 40ºC, 16 min at 42ºC, and 10 min at 44ºC. Increasing heating duration at 44°C, promoted gene expression of HSPs, osteocalcin (OCN), and osteopontin (OPN) at 8 h post-heating (PH). Heating in combination with GFs caused the greatest gene induction of osteoprotegerin (OPG; 6.9- and 1.6-fold induction compared to sham-treated and GF only treated groups, respectively) and vascular endothelial growth factor (VEGF; 16.0- and 1.6-fold compared to sham and GF-only treated groups, respectively) at 8 h PH. Both heating and GFs independently suppressed the matrix metalloproteinase-9 (MMP-9) gene. GF treatment caused a more significant decrease in MMP-9 protein secretion to non-detectable levels compared to heating alone at 72 h PH. Secretion of OCN, OPN, and OPG increased with the addition of GFs but diminished with heating as measured by ELISA at 72 h PH. These results suggest that conditioning protocols utilizing heating and GFs individually or in combination can induce HSPs, bone-related proteins, and VEGF while also causing downregulation of osteoclastic activity, potentially providing a promising bone therapeutic strategy.

Expression of CAMKIIγ, HSP70 and HSP90 Genes Are Differentially Associated with the Mutational Status of Tirosine Kinase Domain in Chronic Myeloid Leukemia Resistant Patients

Abstract 4877Chronic Myeloid Leukemia (CML) is a clonal myeloproliferative disorder characterized by the reciprocal chromosomal translocation between chromosome 9 and 22, t(9;22)(q34;q11), known as Philadelphia chromosome. At molecular level, this cytogenetic aberration associates with a chimeric BCR-ABL fusion gene responsible for the pathogenesis of the disease. Targeting BCR-ABL with tyrosine kinase inhibitors (TKIs) has led to a rapid clinical response in most CML cases; however, harboring of point mutations within the kinase domain (KD) of BCR-ABL is the most common mechanism responsible for acquired resistance to therapy.The objective of this work was to evaluate the expression profiles of 4 different genes involved in proliferation, differentiation or cell survival, in order to study their association with acquired missense mutations within the KD of BCR-ABL.Due to its clear involvement in cell proliferation and apotosis the following genes were analyzed. CAMKIIγ (Ca2+ /calmodulin dependent protein kinase IIγ) is a critical regulator of multiple signalling networks regulating the proliferation in myeloid leukaemia. HSP70 (Heat Shock protein 70) is a chaperone protein that protects cells from apoptotic and necrotic stimuli. HSP90 (Heat Shock protein 90) is a chaperone that facilitates folding of client proteins such as BCR-ABL. Ki-67 is a nuclear antigen associated with cellular proliferation and ribosomal RNA transcription.Total RNA was extracted from 50 TKI-resistant CML-patient’s PBMC samples; by quantitative real time-PCR (QRT-PCR) (SybrGreen method, melting analysis and β2-microglobulin as an endogenous control reference gene) we measured the gene expression of CaMKIIγ, Ki67, HSP70, HSP90 and BCR-ABL. All patients were treated with TKIs (26 imatinib, 13 nilotinib, 11 dasatinib) and showed primary lack or loss of haematological and/or cytogenetic response according to the ELN (European Leukaemia Net) criteria.To characterize TKI-resistant mutations within the KD of the chimeric BCR-ABL gene, ABL exons 4, 5, 6 and 7 were subjected to automated DNA sequencing following a nested- BCR-ABL-specific PCR. Mutations were observed in 27/50 cases at 15 different residues: 1 L248V, 1 G250E, 1 Y253H, 5 E255K/V, 1 E279K, 1 V289F, 4 T315I, 2 F317L, 1 L348M, 3 M351T, 1 E355G, 1 N358S, 2 F359V/C, 2 L387M and 1 L389V. Remaining 23 CML cases did not show mutations (detection limit 10–20%).Our results showed a significant increase in the expression of CaMKIIγ and HSP70 and decrease of HSP90 in mutated patients (MT) with respect to cases without mutations (WT) (p<0.01). On the contrary, transcript levels of Ki67 and BCR-ABL did not show significant differences between MT and WT, likely due to the resistant status of both groups.Taking into account these results we design a score (TKI-MT) to estimate the likelihoods for a patient to harbor TKI-resistance mutations using the transcript normalised expression of CaMKIIγ, HSP70 and HSP90 as follows: [Log10(CaMKIIγ) + Log10(HSP70) – Log10(HSP90)]. TKI-MT scores from 27 and 23 patients from the MT and WT groups respectively were analysed by use of ROC curves in order to find an optimal cut-off value to classify new unstudied cases. We found that patients with TKI-MT scores over a cut-off value of −0.79 showed 4.8 times more probabilities to present TKI-resistance mutations than those below −0.79 (OR 4.8, CI95% 1.3–17.6, P<0.02).We concluded that the expression of CaMKIIγ, HSP70 and HSP90 allowed prediction of mutations in the ABL tyrosine kinase domain with 82% of specificity in CML patients treated with TKIs and associated with lack or loss of response. Disclosures:No relevant conflicts of interest to declare.

Gene expression analysis of heat shock proteins in the nucleus accumbens of rats with different morphine seeking behaviours

Heat-shock proteins play functional roles on brain regulatory processes which are deeply involved in drug addiction, such as synaptic plasticity. However, few studies have been focused on gene expression of heat-shock proteins (Hsp) as potential diagnostic tools for addiction risk. This work tries to provide new knowledge on this field by using two rat models of differential vulnerability to morphine addiction in order to study differential gene expression of a selected group of Hsp genes in the nucleus accumbens (NAc). Hsp70-1A, 84, 86 and 105 genes were similarly regulated by an acute injection of morphine in two subpopulations of Sprague Dawley (SD) rats showing different rates of extinction of morphine conditioned preference. However, Lewis and Fischer rats, two strains that differ in many aspects of drug seeking behaviours, exhibited marked differences in their expression patterns of Hsp84, 86 and 105. These results suggest that differential Hsp gene expression could be related to addiction vulnerability and recommend further work to validate these proteins as potential markers for drug addiction risk.

Importance of heat shock proteins in maize

Abiotic and biotic stress conditions cause extensive losses to maize production, mainly due to protein dysfunction in these conditions. In higher plants, the occurrence of heat-shock proteins (HSPs) in response to different environmental stresses is a universal phenomenon and has been well documented. Many studies have demonstrated that most HSPs are involved in many regulatory pathways, act as molecular chaperones for other cell proteins, and have strong cytoprotective effects. Although many functional roles for HSPs are known, the mechanisms for these multiple functions are not entirely understood. Here we reviewed the correlation among HSP genes/proteins and plant tolerance, especially maize, in different environmental stresses. Due to the low availability of information regarding the expression of HSP genes in response to different stresses in maize, we decided to mine databases in order to generate new insights related to this topic.

Cellular stress response pathways and ageing: intricate molecular relationships.

Ageing is driven by the inexorable and stochastic accumulation of damage in biomolecules vital for proper cellular function. Although this process is fundamentally haphazard and uncontrollable, senescent decline and ageing is broadly influenced by genetic and extrinsic factors. Numerous gene mutations and treatments have been shown to extend the lifespan of diverse organisms ranging from the unicellular Saccharomyces cerevisiae to primates. It is becoming increasingly apparent that most such interventions ultimately interface with cellular stress response mechanisms, suggesting that longevity is intimately related to the ability of the organism to effectively cope with both intrinsic and extrinsic stress. Here, we survey the molecular mechanisms that link ageing to main stress response pathways, and mediate age-related changes in the effectiveness of the response to stress. We also discuss how each pathway contributes to modulate the ageing process. A better understanding of the dynamics and reciprocal interplay between stress responses and ageing is critical for the development of novel therapeutic strategies that exploit endogenous stress combat pathways against age-associated pathologies.

Erratum: Effects of mercury on reproduction, avoidance, and heat shock protein gene expression of the soil springtail Folsomia candida

Liu YR, Zheng YM, Zhang LM, Luan YX, He JZ. 2010. Effects of mercury on reproduction, avoidance, and heat shock protein gene expression of the soil springtail Folsomia candida. Environ Toxicol Chem 29: 654-659. Table 2 on page 656 should be replaced with the following table: