Right heart failure chronically stimulates heat shock protein 72 in heart and liver but not in other tissues

Comini, Laura; Gaia, Giuseppina; Curello, Salvatore; Ceconi, Claudio; Pasini, Evasio; Benigno, Massimo; Bachetti, Tiziana; Ferrari, Roberto

doi:10.1016/s0008-6363(96)00039-9

Cited by 19 publications

(12 citation statements)

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“…5B). The present results are in agreement with those of Comini et al (14), which showed that congestive heart failure, but not compensatory hypertrophy, was a specific stimulus for the induction of HSP72 in the heart. Nevertheless, we cannot exclude the possibility that significant changes could have been detected soon after the beginning of hypoxic exposure but was no longer present after 20 days of hypoxia.…”

Section: Changes In Whole Cell Potassium Current Densitysupporting

confidence: 94%

“…With the higher levels of NE in the RV than in the LV in the adult and the decrease of ϳ70% in the RV and LV NE contents with advancing age, our data agree with previous results (14,23). In RV hypertrophy induced with monocrotaline, no modification in ventricular content of NE was reported compared with control (14). In contrast, in RV hypertrophy induced by chronic high-altitude hypoxia, our results show a significant specific decrease in the RV content of NE, whatever the age.…”

Section: Changes In Whole Cell Potassium Current Densitysupporting

confidence: 93%

“…These responses play a major role in the cardiovascular adaptations to offset the decrease in tissue oxygen supply. With the higher levels of NE in the RV than in the LV in the adult and the decrease of ϳ70% in the RV and LV NE contents with advancing age, our data agree with previous results (14,23). In RV hypertrophy induced with monocrotaline, no modification in ventricular content of NE was reported compared with control (14).…”

Section: Changes In Whole Cell Potassium Current Densitysupporting

confidence: 92%

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Effects of aging on the cardiac remodeling induced by chronic high-altitude hypoxia in rat

Chouabe¹,

Ricci²,

Amsellem³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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Effects of chronic high-altitude hypoxia on the remodeling of right ventricle were examined in three age groups of rats: 2, 6, and 18 mo. The extent of right ventricular (RV) hypertrophy (RVH) showed an age-associated diminution. RV cell size and pericellular fibrosis showed a significant increase in the 2- and 6-mo-old exposed rats but not in the 18-mo-old exposed rats compared with control. A hyperplasic response was underscored in the three exposed age groups but appeared less pronounced in the 18-mo-old rats. A significant decrease in the transient outward potassium current (Ito) density was observed in RV cell only in the 2-mo-old exposed group compared with the control group. In the control group, there was a clear tendency for Ito density to decrease as a function of age. The sustained outward current density was modified neither by the hypoxia condition nor by the age. Neither the cytochrome c oxidase activity nor the heat shock protein 72 content in the RV was altered after hypoxic exposure regardless of age. The norepinephrine content in the RV was significantly decreased in each age group exposed to hypoxia when compared with their age-matched control group. Our findings indicate that the remodeling (at morphological and electrophysiological levels) induced by chronic hypoxia in the RV can be decreased by the natural aging process.

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Section: Changes In Whole Cell Potassium Current Densitysupporting

confidence: 94%

Section: Changes In Whole Cell Potassium Current Densitysupporting

confidence: 93%

Section: Changes In Whole Cell Potassium Current Densitysupporting

confidence: 92%

See 1 more Smart Citation

Effects of aging on the cardiac remodeling induced by chronic high-altitude hypoxia in rat

Chouabe¹,

Ricci²,

Amsellem³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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“…The increased amounts of the mitochondrial stress 70 related protein, a member of the heat shock protein HSP70 family, in the paced heart could counteract the decreased levels of HSP70 inducible, detected in the IPG4±7 study [3]. Induction of HSP72 has been observed in congestive heart failure [25] and other HSPs have recently been demonstrated to be involved in heart failure [26]. The role of the HSPs is protective suggesting that increased expression mediates stress tolerance in the cardiomyocyte.…”

Section: Significance Of Protein Changesmentioning

confidence: 99%

Changes in myocardial protein expression in pacing-induced canine heart failure

Heinke

Wheeler²,

Yan³

et al. 1999

Electrophoresis

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Canine rapid ventricular pacing produces a low output cardiomyopathic state which is similar to dilated cardiomyopathy. In this study dogs were paced at 245 beats per minute (bpm) for 3—4 weeks until signs of heart failure were apparent. Unpaced dogs were used as controls. A previous study identified myocardial protein changes in the pH region 4—7 following ventricular pacing by using two‐dimensional electrophoresis (2‐DE) (Heinke et al., Electrophoresis 1998 19, 2021—2030). Many of these proteins were associated with mitochondria, energy metabolism within the cardiomyocyte, the cytoskeleton and calcium cycling. The present study aimed to examine the proteins migrating in the more basic region of the 2‐DE pattern using immobilised pH gradient 3—10 strips to separate myocardial proteins. The expression of 31 proteins was altered in the paced myocardium: 21 were decreased and 10 increased. Following the identification of 23 of these spots by either amino acid compositional analysis or peptide mass fingerprinting or a combination of both, we confirm that many of the proteins whose expression is altered following ventricular pacing are associated with the mitochondria and energy production within the cardiomyocyte, including creatine kinase M, triosephosphate isomerase, phosphoglycerate mutase, cytochrome c oxidase, cytochrome b5, hydroxymethyl glutaryl CoA synthase, myoglobin, and 3,2‐trans‐enoyl‐CoA transferase. Additionally, the cytoskeletal protein actin was increased in the paced hearts. These results strongly support the notion that energy production is impaired and mitochondrial dysfunction is involved in the development of heart failure in the paced dog.

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“…Induction of HSP72 confers resistance to these stress conditions and plays a pivotal role in protection of cells from subsequent myocardial injury. Comini et al (1996) have also demonstrated the induction of HSP72 upon congestive heart failure. HSP72 is referred as a 'chaperokine' to describe its unique function as a chaperone as well as a cytokine.…”

Section: Hsp70 Classmentioning

confidence: 92%

Heat Shock Proteins in Cardiovascular Stress

Geraldine

Mala

Takeuchi

2008

Clinical medicine. Cardiology

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Heat shock proteins (HSPs) are primarily induced in response to stress stimuli. In cardiovascular diseases, HSPs are expressed pronouncedly and act to protect the cardiac tissue by inhibition of cellular apoptopic mechanisms. An ischemic condition preceded by angina prevents degeneration of tissue by 'ischemic preconditioning' in which HSPs produced in an earlier response have a protective effect towards subsequent cardiac injuries. This review highlights the manifestations of HSPs upon stress conditions of the cardiovascular system. The distinctive features of different HSP families in view of their unique behavior in maintenance of stressed cardiac tissues are briefl y described. A correlation of the fundamental roles of HSPs in certain cardiac pathological conditions is also discussed. A proteomic approach to study the interactions of HSPs is also documented. Hence, an understanding of the physiological mechanisms of HSPs in cardiac stress offers potential solutions for management of cardiac pathologies and to undertake suitable prophylactic measures.

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Right heart failure chronically stimulates heat shock protein 72 in heart and liver but not in other tissues

Cited by 19 publications

References 0 publications

Effects of aging on the cardiac remodeling induced by chronic high-altitude hypoxia in rat

Effects of aging on the cardiac remodeling induced by chronic high-altitude hypoxia in rat

Changes in myocardial protein expression in pacing-induced canine heart failure

Heat Shock Proteins in Cardiovascular Stress

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