October 15, 1992Proceedings of the National Academy of SciencesOpen Access

Roles of mechano-sensitive ion channels, cytoskeleton, and contractile activity in stretch-induced immediate-early gene expression and hypertrophy of cardiac myocytes.

Q: What is the clinical evidence from this study?

Population: Cardiac hypertrophy (in vitro model). Intervention: Gadolinium, colchicine, cytochalasin D, and tetrodotoxin vs. Control (no drug). Primary outcome: Stretch-induced immediate-early gene expression and protein synthesis.

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Key result

Inhibition of stretch-activated channels, disruption of the cytoskeleton, and arrest of contractile activity did not prevent stretch-induced immediate-early gene expression and hypertrophy in cardiac myocytes.

Structured PICO

Population

Primary cultures of cardiac ventricular myocytes from 1-day-old Wistar rats grown on a deformable silicone sheet

Intervention

Mechanical stretch (20% linear static stretch) with pharmacological inhibition of putative mechanotransducers (Gd3+, colchicine, cytochalasin D, TTX, high K+, Ba2+)

Comparator

Stretched myocytes without inhibitors, and unstretched myocytes

Outcome

Immediate-early (IE) gene expression (c-fos, c-jun, zif268, c-myc, JE) and protein synthesis ([3H]phenylalanine incorporation)surrogate

Mechanotransduction of stretch into hypertrophic gene expression in cardiac myocytes does not require Gd3+-sensitive stretch-activated channels, intact microtubules/microfilaments, or contractile activity.

Limitations

Patch-clamp recordings could not be performed on myocytes while they were undergoing static stretch on the silicone sheet.
Cannot formally deny the possibility that a mechano-sensitive channel which is Gd3+ insensitive and cannot be detected by the patch-clamp technique may work as a mechanotransducer.
Cannot exclude a role for other components of cytoskeleton, such as intermediate filaments, or non-RGD-binding integrins.
Patch-clamp recording cannot be performed during static stretch on the silicone sheet
Cannot rule out Gd3+-insensitive mechanosensitive channels
Cannot exclude role for intermediate filaments or non-RGD-binding integrins

Discussion

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Implication

Questions necessity of stretch-activated channels and cytoskeleton for myocyte hypertrophy; leaves open identification of alternative mechanotransduction mechanisms.

Cite This Study

Sadoshima et al. (1992) studied Cardiac hypertrophy (in vitro model). Gadolinium, colchicine, cytochalasin D, and tetrodotoxin vs. Control (no drug) was evaluated on Stretch-induced immediate-early gene expression and protein synthesis. Inhibition of stretch-activated channels, disruption of the cytoskeleton, and arrest of contractile activity did not prevent stretch-induced immediate-early gene expression and hypertrophy in cardiac myocytes.

synapsesocial.com/papers/6a0f82158090e499da5fdaa4 https://doi.org/10.1073/pnas.89.20.9905

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Implication

Questions necessity of stretch-activated channels and cytoskeleton for myocyte hypertrophy; leaves open identification of alternative mechanotransduction mechanisms.

Roles of mechano-sensitive ion channels, cytoskeleton, and contractile activity in stretch-induced immediate-early gene expression and hypertrophy of cardiac myocytes.

Structured PICO

Limitations

Discussion

Implication

Cite This Study

Roles of mechano-sensitive ion channels, cytoskeleton, and contractile activity in stretch-induced immediate-early gene expression and hypertrophy of cardiac myocytes.

Structured PICO

Limitations

Discussion

Implication

Cite This Study

Also Consider

Also Consider