Association Between Heat Stress Protein 70 Induction and Decreased Pulmonary Fibrosis in an Animal Model of Acute Lung Injury

Hagiwara, Satoshi; Iwasaka, Hideo; Matsumoto, Shigekiyo; Noguchi, Takayuki; Yoshioka, Hidekatsu

doi:10.1007/s00408-007-9018-x

Cited by 34 publications

(29 citation statements)

References 32 publications

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“…In support of this notion, Weiss and colleagues demonstrated that overexpression of Hsp70 in pulmonary epithelium reduces mortality and lung injury in a model of cecal ligation and puncture (55). Hsp70 induction was also associated with decreased pulmonary fibrosis (56), whereas ablation of the heat shock factor-1, which regulates HSP family members expression, increases susceptibility to hyperoxia in experimental models of ALI in mice (57). DnaJ (Hsp40) family proteins, Dnaja1 and Dnajb1, which are down-regulated by MV in the absence of Nrf2, by acting as co-chaperones modulate Hsp70 activity (58).…”

Section: Discussionmentioning

confidence: 90%

Genetic and Pharmacologic Evidence Links Oxidative Stress to Ventilator-induced Lung Injury in Mice

Papaiahgari

Yerrapureddy

Reddy

et al. 2007

Am J Respir Crit Care Med

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Rationale: Mechanical ventilation (MV) is an indispensable therapy for critically ill patients with acute lung injury and the adult respiratory distress syndrome. However, the mechanisms by which conventional MV induces lung injury remain unclear. Objectives: We hypothesized that disruption of the gene encoding Nrf2, a transcription factor that regulates the induction of several antioxidant enzymes, enhances susceptibility to ventilator-induced lung injury (VILI) and that antioxidant supplementation attenuates this effect. Methods: To test our hypothesis and to examine the relevance of oxidative stress in VILI, we assessed lung injury and inflammatory responses in Nrf2-deficient (Nrf2 2/2 ) mice and wild-type (Nrf2 1/1 ) mice after an acute (2-h) injurious model of MV with or without administration of antioxidant. Measurements and Main Results: Nrf2 2/2 mice displayed greater levels of lung alveolar and vascular permeability and inflammatory responses to MV as compared with Nrf2 1/1 mice. Nrf2 deficiency enhances the levels of several proinflammatory cytokines implicated in the pathogenesis of VILI. We found diminished levels of critical antioxidant enzymes and redox imbalance by MV in the lungs of Nrf2 2/2 mice; however, antioxidant supplementation to Nrf2 2/2 mice remarkably attenuated VILI. When subjected to a clinically relevant prolong period of MV, Nrf2 2/2 mice displayed greater levels of VILI than Nrf2 1/1 mice. Expression profiling revealed lack of induction of several VILI genes, stress response and solute carrier proteins, and phosphatases in Nrf2 2/2 mice. Conclusions: Our data demonstrate for the first time a critical role for Nrf2 in VILI, which confers protection against cellular responses induced by MV by modulating oxidative stress.

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Section: Discussionmentioning

confidence: 90%

Genetic and Pharmacologic Evidence Links Oxidative Stress to Ventilator-induced Lung Injury in Mice

Papaiahgari

Yerrapureddy

Reddy

et al. 2007

Am J Respir Crit Care Med

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“…These Hsps are believed to exert a protective effect for some tissues against stresses such as exposure to high temperature, ischemia/reperfusion, and cytotoxic substances (Kawana et al 2000;Eichler et al 2005;Hagiwara et al 2007). Hsps help to maintain the metabolic and structural Fig.…”

Section: Discussionmentioning

confidence: 98%

Expression and localization of Hsps in the heart and blood vessel of heat-stressed broilers

Bao

Yan

et al. 2008

Cell Stress and Chaperones

123

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The objective of this study was to investigate the kinetics of Hsp60, Hsp70, Hsp90 protein, and messenger RNA (mRNA) expression levels and to correlate these heat shock protein (Hsp) levels with tissue damage resulting from exposure to high temperatures for varying amounts of time. One hundred broilers were heat-stressed for 0, 2, 3, 5, and 10 h, respectively, by rapidly increasing the ambient temperature from 22 +/- 1 degrees C to 37 +/- 1 degrees C. Obvious elevations of plasma creatine kinase indicate damage to myocardial cells after heat stress. Hsp70 and Hsp90, and their corresponding mRNAs in the heart tissue of heat-stressed broilers, elevated significantly after 2 h of heat exposure and decreased quickly with continued heat stress. However, the levels of hsp60 mRNA in the heart of heat-stressed broilers increased sharply (P < 0.01) at 2 h of heat stress but then decreased quickly after 3 h, while the level of Hsp60 protein in the heart increased (P < 0.01) at 2 h of heat stress and maintained a high level throughout heat exposure. The results indicate that the elevation of the three Hsps, especially Hsp60 in heart, may be important markers at the beginning of heat stress and act as protective proteins in adverse environments. The reduction of Hsp signals in the cytoplasm of myocardial cells implies that myocardial cell lesions may have an adverse impact on the function of Hsps during heat stress. Meanwhile, the localization of Hsp70 in blood vessels of broiler hearts suggests another possible mechanism for protection of the heart after heat exposure.

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“…These Hsps help to maintain the metabolic and structural integrity of the cells and exert protective function for some tissues against some stressors such as heat stress, ischaemia and cytotoxicity (Eichler et al 2005;Hagiwara et al 2007). The heat shock proteins (Hsp-90 alpha, 90 beta and 60) mRNA expression revealed significant variation in heart, liver and spleens of N and HE groups in PB-2 chicken which were lower in HE birds indicating the possible impact of thermal adaptation except in liver (Table 2).…”

Section: Discussionmentioning

confidence: 99%

Effect of increased incubation temperature onHsp90 and 60 gene expressions in coloured broiler chickens

Rajkumar

Vinoth

Shanmugam

et al. 2016

Journal of Applied Animal Research

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The mRNA expression profiles of Hsp-90 alpha, Hsp-90 beta and Hsp-60 were evaluated in coloured broiler chickens, that is, Punjab broiler-2 (PB-2) and naked neck (NN), exposed to 2°C increased incubation temperature for 3 h each on 16th, 17th and 18th days of incubation. Another set of eggs were incubated at normal conditions that were utilized as control. A total of 432 chicks, 216 in each breed (PB-2; NN) and treatment (heat exposed; normal), randomly distributed were reared at high ambient temperatures (32-45°C) during summer in battery brooders. Birds were sacrificed on 0 and 28th days post-hatch and different tissues (heart, liver, muscle, spleen and bursa) were collected to assess the mRNA expression. Heat exposure during incubation significantly (P ≤ .05) influenced the expression of Hsp-90 alpha in spleen of day old; in heart, liver and spleen at 28 days in PB-2 chicken. Hsp-90 alpha mRNA expression was not significant among the tissues at different ages in NN chicken. Hsp-90 beta did not show any significant variations in gene expression across the tissues at both the age groups either in NN or in PB-2 chicken. Heat exposure had significant effect in the expression patterns of Hsp-60 at 28 days in heart, liver and spleen in PB-2 chicken. The mRNA expression of all the three genes significantly (P ≤ .05) varied in different tissues across the age groups in both PB-2 and NN chickens. The study concluded that thermal adaptation during the embryonic stage to higher incubation temperature reduced Hsp gene expression in different tissues in postnatal life during high ambient temperature which might result in increased heat tolerance capacity of the broiler chickens. ARTICLE HISTORY

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Association Between Heat Stress Protein 70 Induction and Decreased Pulmonary Fibrosis in an Animal Model of Acute Lung Injury

Cited by 34 publications

References 32 publications

Genetic and Pharmacologic Evidence Links Oxidative Stress to Ventilator-induced Lung Injury in Mice

Genetic and Pharmacologic Evidence Links Oxidative Stress to Ventilator-induced Lung Injury in Mice

Expression and localization of Hsps in the heart and blood vessel of heat-stressed broilers

Effect of increased incubation temperature onHsp90 and 60 gene expressions in coloured broiler chickens

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