Cigarette smoking induces heat shock protein 70 kDa expression and apoptosis in rat brain: Modulation by bacoside A

Kothandapani, Anbarasi; Kathirvel, G.; Vani, G.; Jayaraman, G.; Devi, C. S. Shyamala

doi:10.1016/j.neuroscience.2005.11.029

Cited by 66 publications

(30 citation statements)

References 55 publications

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“…Reactive oxidant species from inhaled cigarette smoke cause cell necrosis or apoptosis of both parenchyma and alveolar septae (31). Dying cells produce danger signals such as hsp (11), or high mobility group box 1 protein (13), which may activate TLR2 and TLR4 and/or the receptor for advanced glycation end products (9,14) and cause apoptosis (32,33). We show a marked expression of hsp70 in the BAL fluid after cigarette smoke exposure, which is independent of TLR4 and MyD88 signaling.…”

Section: Discussionmentioning

confidence: 79%

Cigarette Smoke-Induced Pulmonary Inflammation Is TLR4/MyD88 and IL-1R1/MyD88 Signaling Dependent

Doz

Noulin

Boichot

et al. 2008

The Journal of Immunology

302

240

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Acute cigarette smoke exposure of the airways (two cigarettes twice daily for three days) induces acute inflammation in mice. In this study, we show that airway inflammation is dependent on Toll-like receptor 4 and IL-1R1 signaling. Cigarette smoke induced a significant recruitment of neutrophils in the bronchoalveolar space and pulmonary parenchyma, which was reduced in TLR4-, MyD88-, and IL-1R1-deficient mice. Diminished neutrophil influx was associated with reduced IL-1, IL-6, and keratinocyte-derived chemokine levels and matrix metalloproteinase-9 activity in the bronchoalveolar space. Further, cigarette smoke condensate (CSC) induced a macrophage proinflammatory response in vitro, which was dependent on MyD88, IL-1R1, and TLR4 signaling, but not attributable to LPS. Heat shock protein 70, a known TLR4 agonist, was induced in the airways upon smoke exposure, which probably activates the innate immune system via TLR4/MyD88, resulting in airway inflammation. CSC-activated macrophages released mature IL-1β only in presence of ATP, whereas CSC alone promoted the TLR4/MyD88 signaling dependent production of IL-1α and pro-IL-1β implicating cooperation between TLRs and the inflammasome. In conclusion, acute cigarette exposure results in LPS-independent TLR4 activation, leading to IL-1 production and IL-1R1 signaling, which is crucial for cigarette smoke induced inflammation leading to chronic obstructive pulmonary disease with emphysema.

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Section: Discussionmentioning

confidence: 79%

Cigarette Smoke-Induced Pulmonary Inflammation Is TLR4/MyD88 and IL-1R1/MyD88 Signaling Dependent

Doz

Noulin

Boichot

et al. 2008

The Journal of Immunology

302

240

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“…The confounding variables of smoking (Anbarasi et al 2006), caffeine (Lu et al 2008), glutamine (Singleton et al 2004), generic supplementation (Hillman et al 2011), thermal exposures (Selkirk et al 2009), hypoxic exposures (Taylor et al 2010a), hyperbaric exposures (Taylor et al 2012) and alcohol (Taylor et al 2010b) were all controlled in line with previous work in the field . Each volunteer was given instructions for dietary requirements in accordance with published guidelines and requested to maintain identical diets in the immediate 48 h prior to each experimental session (Canada 2009).…”

Section: Volunteersmentioning

confidence: 99%

Extracellular Hsp72 concentration relates to a minimum endogenous criteria during acute exercise-heat exposure

Gibson

Alex

Parfitt

et al. 2014

Cell Stress and Chaperones

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Extracellular heat shock protein 72 (eHsp72) concentration increases during exercise-heat stress when conditions elicit physiological strain. Differences in severity of environmental and exercise stimuli have elicited varied response to stress. The present study aimed to quantify the extent of increased eHsp72 with increased exogenous heat stress, and determine related endogenous markers of strain in an exercise-heat model. Ten males cycled for 90 min at 50 % V : O 2peak in three conditions (TEMP, 20°C/63 % RH; HOT, 30.2°C/51%RH; VHOT, 40.0°C/37%RH). Plasma was analysed for eHsp72 pre, immediately post and 24-h post each trial utilising a commercially available ELISA. Increased eHsp72 concentration was observed post VHOT trial (+172.4 %) (p <0.05), but not TEMP (−1.9 %) or HOT (+25.7 %) conditions. eHsp72 returned to baseline values within 24 h in all conditions. Changes were observed in rectal temperature (T rec ), rate of T rec increase, area under the curve for T rec of 38.5 and 39.0°C, duration T rec ≥38.5 and ≥39.0°C, and change in muscle temperature, between VHOT, and TEMP and HOT, but not between TEMP and HOT. Each condition also elicited significantly increasing physiological strain, described by sweat rate, heart rate, physiological strain index, rating of perceived exertion and thermal sensation.Stepwise multiple regression reported rate of T rec increase and change in T rec to be predictors of increased eHsp72 concentration. Data suggests eHsp72 concentration increases once systemic temperature and sympathetic activity exceeds a minimum endogenous criteria elicited during VHOT conditions and is likely to be modulated by large, rapid changes in core temperature.

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“…), vigorous physical activity and alcohol for 7 days prior to study commencement and compliance was monitored via a pre-study questionnaire. Smokers were excluded from the study as it has been shown that smoking may illicit HSP72 expression as a consequence of oxidative stress (Anbarasi et al 2006). Alterations in core temperature have been shown to impact upon monocyte-expressed HSP72 (Sandstrom et al 2009); however, pilot work utilising the same hypoxic exposure under almost identical environmental conditions (temperature-controlled laboratory) demonstrated no signiWcant changes in subject core temperature throughout the 12 h protocol (unpublished).…”

Section: Subjectsmentioning

confidence: 99%

The effect of acute hypoxia on heat shock protein 72 expression and oxidative stress in vivo

et al. 2010

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The inducible human stress protein HSP72 performs vital roles within the body at rest and during periods of stress. Recently, a previously disclosed quadratic trend in basal HSP72 expression was shown to be reliable and repeatable. The notion of a physiological stressor such as hypoxia disrupting this basal quadratic trend is an interesting one. Monocyte-expressed HSP72 and TBARS were determined every 3 h, over a 12-h period in 12 healthy male subjects on two separate days, with trial day one ascertaining control values. A hypoxic intervention consisting of 75 min at a simulated altitude of 2,980 m, commencing and ceasing at 0930 and 1045, respectively, was incorporated on trail day 2. The hypoxic condition induced significantly (elevated) HSP72 values at 1100 (P = 0.002), 1400 (P < 0.001), 1700 (P = 0.034) and 2000 (P = 0.041) compared to control. Significant increases in plasma TBARS were seen in the hypoxic condition compared to control at 1100 (P = 0.006) and 1400 (P = 0.032). The results demonstrate that a 75-min bout of normobaric hypoxia is sufficient to induce significant increases in HSP72 expression, which disrupts the basal quadratic trend shown by others and here in the control condition. This increase may be linked to the observed changes in oxidative stress. These results may provide a tool for manipulating basal monocyte HSP72 expression within human heat acclimation exercise protocols.

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Cigarette smoking induces heat shock protein 70 kDa expression and apoptosis in rat brain: Modulation by bacoside A

Cited by 66 publications

References 55 publications

Cigarette Smoke-Induced Pulmonary Inflammation Is TLR4/MyD88 and IL-1R1/MyD88 Signaling Dependent

Cigarette Smoke-Induced Pulmonary Inflammation Is TLR4/MyD88 and IL-1R1/MyD88 Signaling Dependent

Extracellular Hsp72 concentration relates to a minimum endogenous criteria during acute exercise-heat exposure

The effect of acute hypoxia on heat shock protein 72 expression and oxidative stress in vivo

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