Specific attachment of collagen to cardiac myocytes: In vivo and in vitro

Borg, Thomas K.; Johnson, Lewis D.; Lill, Patsy H.

doi:10.1016/0012-1606(83)90098-2

Cited by 54 publications

(9 citation statements)

References 26 publications

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“…3a), and the “fine” endomysial collagen fiber network that surrounds individual myofibers as well as interconnects extensively with the large collagen fibers (Figs. 3a,b) (Borg and Caulfield 1981; Borg et al 1983). Also, the non-fibrous phase, referred to as the matrix phase, includes remaining mechanically insignificant substances such as vasculature, neural tissues, myofibroblasts, etc.…”

Section: Methodsmentioning

confidence: 99%

A novel constitutive model for passive right ventricular myocardium: evidence for myofiber–collagen fiber mechanical coupling

Avazmohammadi

Hill

Simon

et al. 2016

Biomech Model Mechanobiol

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The function of right ventricle (RV) is recognized to play a key role in the development of many cardiopulmonary disorders, such as pulmonary arterial hypertension (PAH). Given the strong link between tissue structure and mechanical behavior, there remains a need for a myocardial constitutive model that accurately accounts for right ventricular myocardium architecture. Moreover, most available myocardial constitutive models approach myocardium at the length scale of mean fiber orientation, and do not explicitly account for different fibrous constituents and possible interactions among them. In the present work, we developed a fiber-level constitutive model for the passive mechanical behavior of the right ventricular free wall (RVFW) that explicitly distinguished between the mechanical contributions of myofiber and collagen fiber ensembles, and accounted for the fiber mechanical interactions. To obtain model parameters for the healthy passive RVFW, the model was informed by transmural orientation distribution measurements of myo- and collagen fibers, and was fit to the mechanical testing data, where both sets of data were obtained from recent experimental studies on non-contractile, but viable, murine RVFW specimens. Results supported the hypothesis that in the low strain regime the behavior of the RVFW is governed by myofiber response alone, which does not demonstrate any coupling between different myofiber ensembles. At higher strains, the collagen fibers and their interactions with myofibers begin to gradually contribute and dominate the behavior as recruitment proceeds. Due to the use of viable myocardial tissue, the contribution of myofibers was significant at all strains with the predicted tensile modulus of ~ 35 kPa. This was in contrast to earlier reports (Horowitz et al. 1988) where the contribution of myofibers was found to be insignificant. Also, we found that the interaction between myo- and collagen fibers was greatest under equibiaxial strain, with its contribution to the total stress not exceeding 20%. The present model can be applied to organlevel computational models of right ventricular dysfunction for efficient diagnosis and evaluation of pulmonary hypertension disorder.

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Section: Methodsmentioning

confidence: 99%

A novel constitutive model for passive right ventricular myocardium: evidence for myofiber–collagen fiber mechanical coupling

Avazmohammadi

Hill

Simon

et al. 2016

Biomech Model Mechanobiol

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“…Fibroblasts were isolated at 3, 7, 14, and 28 days following aortic constriction or sham surgery as described previously (Borg et al 1983; Burgess et al 2002). Following sacrifice of the animals, hearts were removed and rinsed in sterile saline.…”

Section: Methodsmentioning

confidence: 99%

Temporal alterations in cardiac fibroblast function following induction of pressure overload

et al. 2010

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Increases in cardiovascular load (pressure overload) are known to elicit ventricular remodeling including cardiomyocyte hypertrophy and interstitial fibrosis. While numerous studies have focused on the mechanisms of myocyte hypertrophy, comparatively little is known regarding the response of the interstitial fibroblasts to increased cardiovascular load. Fibroblasts are the most numerous cell type in the mammalian myocardium and have long been recognized as producing the majority of the myocardial extracellular matrix. It is only now becoming appreciated that other aspects of fibroblast behavior are important to overall cardiac function. The present studies were performed to examine the temporal alterations in fibroblast activity in response to increased cardiovascular load. Rat myocardial fibroblasts were isolated at specific time-points (3, 7, 14, and 28 days) after induction of pressure overload by abdominal aortic constriction. Bioassays were performed to measure specific parameters of fibroblast function including remodeling and contraction of 3-dimensional collagen gels, migration, and proliferation. In addition, the expression of extracellular matrix receptors of the integrin family was examined. Myocardial hypertrophy and fibrosis were evident within 7 days after constriction of the abdominal aorta. Collagen gel contraction, migration, and proliferation were enhanced in fibroblasts from pressure-overloaded animals compared to fibroblasts from sham animals. Differences in fibroblast function and protein expression were evident within 7 days of aortic constriction, concurrent with the onset of hypertrophy and fibrosis of the intact myocardium. These data provide further support for the idea that rapid and dynamic changes in fibroblast phenotype accompany and contribute to the progression of cardiovascular disease.

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“…1) are the exclusive source of new collagen production (such as type I, II, III, V, and VI collagens). However, this concept needs further mechanistic evaluation in vivo because other cell types can make and secrete particular types of collagens, including epithelial and endothelial cells 23 − 25 , skeletal muscle myotubes and fibers 26 − 28 , and cardiac myocytes 29,30 . Therefore, to characterize all the roles of fibroblasts and activated fibroblasts in the heart, one would need to delete these cells or inactivate them at specific times.…”

Section: Resident Cardiac Fibroblastsmentioning

confidence: 99%

“…Therefore, whether fibroblasts are the only relevant source of collagen and ECM production in the heart, either at baseline or with acute and chronic injury, remains to be tested. Indeed, mammalian cardiac myocytes can express and secrete collagens that could easily contribute to healing in the border areas of an MI 29,30 .…”

Section: Unanswered Questionsmentioning

confidence: 99%

Redefining the identity of cardiac fibroblasts

Tallquist¹,

Molkentin²

2017

Nat Rev Cardiol

437

366

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Cardiac fibroblasts deposit and maintain extracellular matrix during organogenesis and under physiological conditions. In the adult heart, activated cardiac fibroblasts also participate in the healing response after acute myocardial infarction and during chronic disease states characterized by augmented interstitial fibrosis and ventricular remodelling. However, delineation of the characteristics, plasticity, and origins of cardiac fibroblasts is an area of ongoing investigation and controversy. A set of genetic mouse models has been developed that specifically addresses the nature of these cells, in terms of both their origins and their response during cardiac disease and ventricular remodelling. As our understanding of cardiac fibroblasts becomes more defined and refined, so does the potential to develop new therapeutic strategies to control fibrosis and adverse ventricular remodelling.

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Specific attachment of collagen to cardiac myocytes: In vivo and in vitro

Cited by 54 publications

References 26 publications

A novel constitutive model for passive right ventricular myocardium: evidence for myofiber–collagen fiber mechanical coupling

A novel constitutive model for passive right ventricular myocardium: evidence for myofiber–collagen fiber mechanical coupling

Temporal alterations in cardiac fibroblast function following induction of pressure overload

Redefining the identity of cardiac fibroblasts

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