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Updated: Jul 19, 2026
10:54
A Cell Culture Model of Resistance Arteries
Published on: September 8, 2017
ROCK controls matrix synthesis in vascular smooth muscle cells: coupling vasoconstriction to vascular remodeling
Rene Chapados1, Khotaro Abe, Kaori Ihida-Stansbury
1Children's Hospital of Philadelphia, PA, USA.
Circulation Research
|September 23, 2006
Summary
Rho kinase (ROCK) regulates tenascin-C (TN-C) production in vascular smooth muscle cells (SMCs) by controlling cell shape and cytoskeletal architecture, impacting arterial remodeling and hypertension.
Area of Science:
- Vascular Biology
- Extracellular Matrix Biology
- Cell Signaling
Background:
- Tenascin-C (TN-C) is an extracellular matrix (ECM) protein crucial for vascular smooth muscle cell (SMC) proliferation in remodeling arteries.
- Previous work indicated TN-C expression correlates with SMC morphology and F-actin cytoskeleton organization.
Purpose of the Study:
- To investigate the role of cytoskeletal architecture in regulating TN-C expression in SMCs.
- To determine if Rho kinase (ROCK) signaling mediates TN-C production through modulation of cell shape and actin cytoskeleton.
Main Methods:
- Culturing SMCs on native and denatured collagen to alter morphology.
- Pharmacological inhibition of cytoskeletal regulators (cytochalasin D) and RhoA/ROCK pathway.
- Assessing SMC spreading, ERK1/2 activation, and TN-C transcription.
- Evaluating ROCK inhibition effects in a rat model of hypertension.
Main Results:
- SMCs on denatured collagen exhibited increased spreading, F-actin stress fibers, and TN-C expression, linked to ERK1/2 activation.
- Cytochalasin D treatment reduced SMC spreading, ERK1/2 activity, and TN-C transcription.
- Engineered SMC geometries showed that rounded cells had decreased ERK1/2 activity and TN-C transcription.
- RhoA/ROCK pathway activation was higher in spread SMCs, and its inhibition attenuated spreading, ERK1/2 activity, and TN-C expression.
- ROCK inhibition reduced TN-C expression and disease progression in hypertensive rat pulmonary arteries.
Conclusions:
- ROCK signaling controls SMC shape and F-actin cytoskeleton, which is permissive for ERK1/2-dependent TN-C production.
- ROCK plays a significant role in regulating ECM production, beyond its known function in vasoconstriction.
- ROCK inhibition represents a potential therapeutic strategy for vascular remodeling and hypertension by modulating matrix production.
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