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Mechanobiology of Cardiac Fibroblasts
Published in Jiro Nagatomi, Eno Essien Ebong, Mechanobiology Handbook, 2018
Peter A. Galie, Jan P. Stegemann
This chapter also highlights the importance of loading protocols and configurations on cellular response. It has been shown that cells respond differently depending on what type of surrounding ECM is present, whether the loading is in a 2D or 3D system, and whether the applied load is static or cyclic. Therefore, comparing results between studies is difficult, since even though the general loading scheme may be similar, inconsistency in other factors can lead to very different results between studies. Studying cell responses in 2D configurations has provided important information about how cardiac fibroblasts sense, transduce, and react to mechanical forces. However, it is becoming increasingly clear that the cell response may be significantly different in 3D systems that more closely mimic the cellular environment in tissues. For these reasons, despite the thorough and robust data generated from research on this topic, there is no unified theory explaining how cardiac fibroblasts generate biological responses when strained mechanically. In the future, further research on the response of these cells to mechanical stimuli in 3D environments can be expected to provide insight into how they behave in the in vivo microenvironment. Such research is important to understand a variety of disease states, including cardiac fibrosis, in which changes in mechanical environment have been implicated in causing undesirable changes in cell function.
Development of a three dimensional (3D) knitted scaffold for myocardial tissue engineering. Part II: biological performance of the knitted scaffolds
Published in The Journal of The Textile Institute, 2025
Derya Haroglu, Ahmet Eken, Zeynep Burçin Gönen, Dilek Bahar
Based on the results of ELISA assays, cell attachment to fibronectin was observed to be resulted in higher levels of pro-inflammatory cytokines IL-1α, and IL-1β in cell-scaffold groups. However, further research is required to find out the underlying mechanisms leading to the regulation of IL-1α, and IL-1β. Absence of pro-inflammatory cytokine IL-12p40 is claimed to improve angiogenesis limiting the cardiac injury after MI (Kan et al., 2016; Rusinkevich et al., 2019). Thus, lower levels of IL-12p40 expressed by C2C12 cells seeded on 144 F and 144H when compared with the related control groups are in favor of cardiac regeneration. Currently, it is unclear whether IL-11, one of the IL-6 family cytokines, has beneficial roles after MI. It was reported that IL-11 had healing effects by keeping cells viable, diminishing adverse cardiac remodeling, and encourageing angiogenesis after MI (Kimura et al., 2007; Obana et al., 2010; Tamura et al., 2018). On the other hand, IL-11 was shown to be critical in fibrotic process causing cardiac fibrosis and ultimately heart failure (Corden et al., 2020; Nicholls, 2018; Schafer et al., 2017). In this study, higher expression levels of IL-11 were observed in cells seeded on 144H coated with fibronectin on Day 1 (p < 0.05) bearing in mind the fact that it remains unexplained if IL-11 performs as an anti-inflammatory cytokine.
Potential adverse cardiac remodelling in highly trained athletes: still unknown clinical significance
Published in European Journal of Sport Science, 2018
Luigi Gabrielli, Marta Sitges, Mario Chiong, Jorge Jalil, María Ocaranza, Silvana Llevaneras, Sebastian Herrera, Rodrigo Fernandez, Rodrigo Saavedra, Fernando Yañez, Luis Vergara, Alexis Diaz, Sergio Lavandero, Pablo Castro
The repetitive cycle of oxidative stress increase and heart muscle mechanical deformation during extreme exercise (Krip, Gledhill, Jamnik, & Warburton, 1997) might induce cardiomyocyte cell membrane damage that correlates with an elevation of multiple cardiac injury biomarkers such as myoglobin, cardiac troponin-I, creatine kinase MB and B-type natriuretic peptide (Fortescue et al., 2007). These biomarkers could stimulate immune cells recruitment – including lymphocytes, macrophages and mast cells – toward the damage area (Scherr et al., 2011). Then, immune cells would secrete pro-inflammatory cytokines, such as interleukin-6, which work as extracellular signals to induce fibroblast to myofibroblast differentiation with the subsequent secretion of procollagen (Benito et al., 2011). This phenomenon could be responsible for fibrosis deposited in patches in the myocardium and larges arteries (Figure 1(D)) (La Gerche et al., 2012). In fact, in rat models, prolonged strenuous exercise increased expression of transforming growth factor β-1 (TGF β-1) – the main mediator of fibroblast activation and cardiac fibrosis – in the right and left atria and right ventricle resulting in increased cardiac stiffness (Benito et al., 2011). Interestingly, this mechanism could be correlated with the elevation of galectin-3 plasma level and cardiac fibrosis in human (Hattasch et al., 2014).