Abstract
Cardiac functions can be altered by changes in the microstructure of the heart, i.e., remodeling of the cardiac tissue, which may activate pathologies such as hypertrophy, dilation, or cardiac fibrosis. Cardiac fibrosis can develop due to an excessive deposition of extracellular matrix proteins, which are products of the activation of fibroblasts. In this context, the anatomical–histological change may interfere with the functioning of the cardiac tissue, which requires specialized cells for its operation. The purpose of the present study was to determine the cellular interactions and morphological changes in cocultures of 3T3 fibroblasts and RL-14 cardiomyocytes via the generation of a platform an in vitro model. For this purpose, a platform emulating the biological characteristics of endomyocardial fibrosis was generated using a cell patterning technique to study morphological cellular changes in compact and irregular patterns of fibrosis. It was found that cellular patterns emulating the geometrical distributions of endomyocardial fibrosis generated morphological changes after interaction of the RL-14 cardiomyocytes with the 3T3 fibroblasts. Through this study, it was possible to evaluate biological characteristics such as cell proliferation, adhesion, and spatial distribution, which are directly related to the type of emulated endomyocardial fibrosis. This research concluded that fibroblasts inhibited the proliferation of cardiomyocytes via their interaction with specific microarchitectures. This behavior is consistent with the histopathological distribution of cardiac fibrosis; therefore, the platform developed in this research could be useful for the in vitro assessment of cellular microdomains. This would allow for the experimental determination of interactions with drugs, substrates, or biomaterials within the engineering of cardiac tissues.
Highlights
The mechanisms responsible for cardiac arrhythmias are grouped into two categories: impulse generation disorders and electrical conduction [1,2]
A pathology that produces alterations in the electrical conduction pathways is the endomyocardial fibrosis (EMF), from which microstructural and functional changes are derived. These changes lead to inadequate electrical conduction, which can result in slight alterations, or complete chaos in impulse transmission, which occurs in some arrhythmias, such as atrial fibrillations, ventricular fibrillations, and cardiac blocks [2,3,4,5,6]
Our results allowed to replicate EMF behaviors imitating the disruption of tissue, in which changes in the morphology of cardiomyocytes in interaction with fibroblasts were evidenced, mientras que, only a minority of the fibroblast population is usually affected due to its rapid proliferation
Summary
The mechanisms responsible for cardiac arrhythmias are grouped into two categories: impulse generation disorders and electrical conduction [1,2]. A pathology that produces alterations in the electrical conduction pathways is the endomyocardial fibrosis (EMF), from which microstructural and functional changes are derived. These changes lead to inadequate electrical conduction, which can result in slight alterations, or complete chaos in impulse transmission, which occurs in some arrhythmias, such as atrial fibrillations, ventricular fibrillations, and cardiac blocks [2,3,4,5,6]. Multifactorial processes are involved in EMF as a result of complex cellular interactions [7]. Among these processes, the proliferation of fibroblasts plays an important role in the production of extracellular matrix (ECM) proteins. Contrary to what happens in pathological conditions or tissue damage, these fibroblasts sustain the interstitial medium of the cardiomyocytes and regulate the supporting structure of the heart, actively participating in the healing process [8,9,10,11]
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