scholarly journals Stiffness of vascular smooth muscle cells from monkeys studied using atomic force microscopy

2020 ◽  
Author(s):  
Yi Zhu
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Mechanical Forces ◽  
Force Microscopy ◽  
Atomic Force ◽  
Significant Difference ◽  
Cellular Components

Vascular smooth muscle cells (VSMC) are the main cellular components of blood vessel walls and bear external mechanical forces caused by blood flow and pressure. In this report, we have verified the following hypothesis through experiments: The increase in VSMC stiffness may be mainly due to changes in vascular stiffness due to aging. Although aging enhances the stiffness and adhesion of VSMC, there is no significant difference in apparent elastic modulus and adhesion between the VSMC obtained by male and female. The effect of aging through the ECM-integrin-cytoskeleton axis is related to increased VSMC stiffness and matrix adhesion rather than gender.

Mechanical properties of the interaction between fibronectin and α5β1-integrin on vascular smooth muscle cells studied using atomic force microscopy

2005 ◽  
Vol 289 (6) ◽  
pp. H2526-H2535 ◽  
Author(s):  
Zhe Sun ◽  
Luis A. Martinez-Lemus ◽  
Andreea Trache ◽  
Jerome P. Trzeciakowski ◽  
George E. Davis ◽  
...  
Keyword(s):  
Mechanical Properties ◽  
Atomic Force Microscopy ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Focal Contact ◽  
Force Microscopy ◽  
Atomic Force

The mechanical properties of integrin-extracellular matrix (ECM) interactions are important for the mechanotransduction of vascular smooth muscle cells (VSMC), a process that is associated with focal adhesions, and can be of particular significance in cardiovascular disease. In this study, we characterized the unbinding force and binding activity of the initial fibronectin (FN)-α5β1 interaction on the surface of VSMC using atomic force microscopy (AFM). It is postulated that these initial binding events are important to the subsequent focal adhesion assembly. FN-VSMC adhesions were selectively blocked by antibodies against α5- and β1-integrins as well as RGD-containing peptides but not by antibodies against α4- and β3-integrins, indicating that FN primarily bound to α5β1. A characteristic unbinding force of 39 ± 8 pN was observed and interpreted to represent the FN-α5β1 single-bond strength. The ability of FN to adhere to VSMC (binding probability) was significantly reduced by integrin antagonists, serum starvation, and platelet-derived growth factor (PDGF)-BB, whereas lysophosphatidic acid (LPA) increased FN binding. However, no significant change in the resolved unbinding force was observed. After engagement, the force required to dislodge the FN-coated bead from VSMC increased with increasing of contact time, suggesting a time-dependent increase in number of adhesions and/or altered binding affinity. LPA enhanced this process, whereas PDGF reduced it, suggesting that these factors also affect the multimolecular process of focal contact assembly. Thus AFM is a powerful tool for the characterization of the mechanical properties of integrin-ECM interactions and their regulation. Our results indicate that the functional activity of α5β1 and focal contact assembly can be rapidly regulated.

Concentration-Dependent Effects of Insulin on Ca2+ Influx in Vascular Smooth Muscle Cells of Normotensive and Spontaneously Hypertensive Rats

1993 ◽  
Vol 85 (4) ◽  
pp. 425-429 ◽  
Author(s):  
Zhiming Zhu ◽  
Martin Tepel ◽  
Marcus Neusser ◽  
Norbert Mehring ◽  
Walter Zidek
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Spontaneously Hypertensive Rats ◽  
Muscle Cells ◽  
Hypertensive Rats ◽  
Maximum Increase ◽  
Spontaneously Hypertensive ◽  
Significant Difference

1. The effect of insulin on cytosolic free Ca2+ concentration was measured using fura-2 in vascular smooth muscle cells of normotensive and spontaneously hypertensive rats. 2. In both strains, insulin increased cytosolic free Ca2+ concentration in a concentration range between 10−6 and 10−3 units/ml. The maximum increase in cytosolic free Ca2+ concentration was observed with 10−5 units/ml insulin (107 +25 and 82+27 nmol/l in spontaneously hypertensive rats and normotensive rats, respectively). 3. The effect of insulin was dependent on extracellular Ca2+ and was enhanced by stimulation of protein kinase C. 4. Thus insulin appears to induce a Ca2+ influx in vascular smooth muscle cells only over a certain range of concentrations. No significant difference in the response to insulin of cells from normotensive and hypertensive rats was observed.

scholarly journals The Phenotypic Responses of Vascular Smooth Muscle Cells Exposed to Mechanical Cues

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2209
Author(s):  
Lise Filt Jensen ◽  
Jacob Fog Bentzon ◽  
Julian Albarrán-Juárez
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Vascular Diseases ◽  
Muscle Cells ◽  
Culture Conditions ◽  
Cell Phenotype ◽  
Signal Molecules ◽  
Mechanical Forces

During the development of atherosclerosis and other vascular diseases, vascular smooth muscle cells (SMCs) located in the intima and media of blood vessels shift from a contractile state towards other phenotypes that differ substantially from differentiated SMCs. In addition, these cells acquire new functions, such as the production of alternative extracellular matrix (ECM) proteins and signal molecules. A similar shift in cell phenotype is observed when SMCs are removed from their native environment and placed in a culture, presumably due to the absence of the physiological signals that maintain and regulate the SMC phenotype in the vasculature. The far majority of studies describing SMC functions have been performed under standard culture conditions in which cells adhere to a rigid and static plastic plate. While these studies have contributed to discovering key molecular pathways regulating SMCs, they have a significant limitation: the ECM microenvironment and the mechanical forces transmitted through the matrix to SMCs are generally not considered. Here, we review and discuss the recent literature on how the mechanical forces and derived biochemical signals have been shown to modulate the vascular SMC phenotype and provide new perspectives about their importance.

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