Cell stretching systems in cardiovascular research

Cardiovascular diseases and pulmonary hypertension place significant mechanical stress on cardiac muscle and vascular tissue. These pathological forces can alter cell signaling, gene expression, stiffness, and tissue remodeling over time. Understanding how cardiomyocytes and endothelial cells respond to mechanical strain is essential for advancing cardiovascular research and developing new therapeutic strategies.

Cell stretching systems help researchers recreate these mechanical conditions in vitro through controlled cyclic or static stimulation. By simulating physiological and pathological strain in a controlled environment, investigators can study mechanotransduction, cellular remodeling, and disease progression with greater precision and reproducibility.

Modeling in vivo cardiovascular pathology with in vitro cell stretching systems

Pulmonary hypertension can induce structural and functional changes in cardiomyocyte and endothelial cells, leading to adverse outcomes such as cardiac muscle and vessel stiffening or thickening (Liu et al. 2022). Insights into these changes are vital for unraveling the complexities of hypertensive heart disease. Tools like the Strex manual and automated cell stretching systems are capable of replicating the endogenous mechanical forces exerted on cardiomyocytes in vitro, allowing researchers to recreate the pathological conditions involved in hypertension. By subjecting cells to controlled stretching with set cyclic or static parameters, Strex systems provide realistic, reliable, and replicable simulations of the mechanical stress exerted by hypertension on cardiac muscles and vessels (Naruse 2018), much like other cell types that experience similar mechanical stress (Constantinou and Bastounis 2023).

Manual Cell Stretching System (left), Automated Cell Stretching System (right)

Visualizing and Imaging Cardiac Muscle Cell Response to Stretching in Real Time

With the Strex Microscope Mountable Uniaxial or Biaxial Cell Stretching Systems, cellular responses to stretching can also be monitored in real-time. Changes in cell morphology, drug response, and mechanotransduction mechanisms involving signaling pathways, gene expression, and protein interactions (Evans et al 2021; Wang et al 2021; Zhao et al 2022) can be observed as cardiomyocytes and endothelial cells undergo mechanical stress. This dynamic approach offers a comprehensive understanding of the immediate and long-term effects of pulmonary hypertension on cardiomyocytes and endothelial cells, and the resulting outcomes of the disease on cardiac muscle and vessel characteristics. Coupled with their intuitive and easy to install microscope mountable modules, Strex Cell Stretching Systems simplify the setup for cell stretch experiments, and offer the reliability necessary for rigor and reproducibility in cardiovascular research.

Microscope Mountable Uniaxial Cell Stretching System (left), Microscope Mountable Biaxial Cell Stretching System (right)

Strex’s Automated Cell Stretching Systems are Customizable, Easy to Use, and Offer Peace of Mind

Strex is focused on providing investigators, including cardiovascular disease researchers, with experimental setups tailored for their specific needs. Strex Cell Stretching Systems offer a high degree of customization to accommodate a range of applications, from custom mounting brackets to recommendations for cell embedding media. Using Automated Cell Stretching Systems, researchers can set cell stretching protocols with adjustable parameters including stretch amplitude, frequency, and duration to closely model the variable mechanotransduction experienced by cardiomyocytes in pulmonary hypertension. This versatility contributes to a more nuanced understanding of the underpinnings of cardiovascular disease.

Revolutionizing Pulmonary Hypertension Research

Strex Cell Stretching Systems have revolutionized cardiovascular disease research by providing a platform for studying cardiomyocytes and changes in cardiac muscle characteristics, including stiffness and thickness, in pathological conditions like pulmonary hypertension. From realistic simulation of mechanotransduction to real-time monitoring of cellular and molecular changes, Strex systems help provide insight into the mechanisms of hypertensive heart disease, supporting groundbreaking discoveries in cardiovascular research and advancements in medicine.

References

Constantinou I, Bastounis EE. Cell-stretching devices: advances and challenges in biomedical research and live-cell imaging. Trends Biotechnol. 2023;41(7):939-950. doi:10.1016/j.tibtech.2022.12.009

Evans CE, Cober ND, Dai Z, Stewart DJ, Zhao YY. Endothelial cells in the pathogenesis of pulmonary arterial hypertension. Eur Respir J. 2021;58(3):2003957. Published 2021 Sep 2. doi:10.1183/13993003.03957-2020

Liu SF, Nambiar Veetil N, Li Q, Kucherenko MM, Knosalla C, Kuebler WM. Pulmonary hypertension: Linking inflammation and pulmonary arterial stiffening. Front Immunol. 2022;13:959209. Published 2022 Oct 5. doi:10.3389/fimmu.2022.959209

Naruse K. Mechanomedicine. Biophys Rev. 2018;10(5):1257-1262. doi:10.1007/s12551-018-0459-7
Wang Z, Chen J, Babicheva A, et al. Endothelial upregulation of mechanosensitive channel Piezo1 in pulmonary hypertension. Am J Physiol Cell Physiol. 2021;321(6):C1010-C1027. doi:10.1152/ajpcell.00147.2021

Zhao T, Parmisano S, Soroureddin Z, et al. Mechanosensitive cation currents through TRPC6 and Piezo1 channels in human pulmonary arterial endothelial cells. Am J Physiol Cell Physiol. 2022;323(4):C959-C973. doi:10.1152/ajpcell.00313.2022