What question did this study set out to answer?

To examine the expression and temporal profile of stress proteins in adult rat cardiac myocytes during the initial weeks following pressure or volume hemodynamic overload.

August 1, 1988Journal of Clinical InvestigationOpen Access

Synthesis of stress proteins in rat cardiac myocytes 2-4 days after imposition of hemodynamic overload.

Q: What is the clinical evidence from this study?

Study design: Other. Population: Hemodynamic overload (cardiac hypertrophy). Intervention: Hemodynamic overload (aortic stenosis or aortic insufficiency) vs. Sham-operated controls. Primary outcome: Expression of stress proteins (HSP 70, HSP 68, HSP 58) in cardiac myocytes.

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Key result

Hemodynamic overload induced by aortic stenosis or insufficiency in rats led to an early and transient expression of three major stress proteins (HSP 70, HSP 68, and HSP 58) in cardiac myocytes.

Population

Isolated adult myocytes from rat hearts

Comparison

Hemodynamic overload for up to 2 weeks vs Controls and sham-operated animals

Design

Preclinical

Follow-up

up to 2 weeks

Authors

CDClaude DelcayreInserm JSJane‐Lise SamuelUniversité Paris Cité FMF. MarotteInserm

Discussion

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Implication

Transient HSP induction may signal early cardiac stress adaptation; leaves open mechanistic and clinical roles pending in vivo validation.

Key Points

To examine the expression and temporal profile of stress proteins in adult rat cardiac myocytes during the initial weeks following pressure or volume hemodynamic overload.
Isolated adult rat cardiac myocytes were incubated with [35S]methionine during the first 2 weeks after imposing pressure or volume overload, alongside sham-operated and unoperated controls.
Proteins were characterized using two-dimensional gel electrophoresis, comigration with heat-induced (41°C) proteins, and immunoblotting as well as immunohistochemistry with anti-HSP 70 antisera.
Pressure and volume overload provoked an early (2–4 days) and transient expression of three major stress proteins (HSP 70, HSP 68, and HSP 58) and increased synthesis of putative ribosomal proteins, with only trace levels in controls.
Immunohistochemical staining and immunoblotting revealed HSP 70 was uniformly distributed among rod-shaped myocytes in both sham and overloaded hearts without isolating to a specific cell subpopulation.

Structured PICO

Population

Male Wistar rats subjected to aortic banding or aortic insufficiency to induce compensatory cardiac hypertrophy, evaluated 2 to 21 days post-surgery.

Intervention

Hemodynamic overload (pressure or volume overload) for up to 2 weeks

Comparator

Controls and sham-operated animals

Outcome

Expression of stress proteins (HSP 70, HSP 68, and HSP 58) and putative ribosomal proteinssurrogate

Hemodynamic overload induces early and transient expression of heat shock proteins in rat cardiac myocytes, suggesting a protective mechanism during early adaptation to overload.

Limitations

The measure of the degree of cardiac hypertrophy might be criticized since the whole heart was weighed after a rather rudimentary dissection.
The sensitivity of the immunoblot method does not allow a quantitative evaluation of the relative accumulation of the protein.

Cite This Study

Delcayre et al. (1988) studied Hemodynamic overload (cardiac hypertrophy). Hemodynamic overload (aortic stenosis or aortic insufficiency) vs. Sham-operated controls was evaluated on Expression of stress proteins (HSP 70, HSP 68, HSP 58) in cardiac myocytes. Hemodynamic overload induced by aortic stenosis or insufficiency in rats led to an early and transient expression of three major stress proteins (HSP 70, HSP 68, and HSP 58) in cardiac myocytes.

synapsesocial.com/papers/6a6542ef1b122b07e7b2e331 https://doi.org/10.1172/jci113619

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Implication

Transient HSP induction may signal early cardiac stress adaptation; leaves open mechanistic and clinical roles pending in vivo validation.

Synthesis of stress proteins in rat cardiac myocytes 2-4 days after imposition of hemodynamic overload.

Discussion

Member takes

Implication

Key Points

Structured PICO

Limitations

Cite This Study

Synthesis of stress proteins in rat cardiac myocytes 2-4 days after imposition of hemodynamic overload.

Discussion

Member takes

Implication

Key Points

Structured PICO

Limitations

Cite This Study

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