Mechanically Induced Potentials in Fibroblasts from Human Right Atrium

Kamkin, Andre; Kiseleva, Irina; Wagner, Kay-Dietrich; Lammerich, Andreas; Böhm, J.; Persson, Pontus B.; Günther, J

doi:10.1111/j.1469-445x.1999.01794.x

Cited by 51 publications

(25 citation statements)

References 24 publications

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“…In order to convert the fluorescence readings into membrane potentials, the resting potential of human fibroblasts and embryonic kidney cells (HEK) was determined in another preliminary experiment. They were found to be À17 mV for human fibroblasts and À30 for HEK cells, respectively, in agreement with previous measurements [Voets et al, 1996;Kamkin et al, 1999].…”

Section: Membrane Potential Of Human Fibroblastssupporting

confidence: 90%

Depolarization of the membrane potential by hyaluronan

Hagenfeld

Schulz

Ehling³

et al. 2010

J of Cellular Biochemistry

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The membrane potential is mainly maintained by the K(+) concentration gradient across the cell membrane between the cytosol and the extracellular matrix. Here, we show that extracellular addition of high-molecular weight hyaluronan depolarized the membrane potential of human fibroblasts, human embryonic kidney cells (HEK), and central nervous system neurons in a concentration-dependent manner, whereas digestion of cell surface hyaluronan by hyaluronidase caused hyperpolarization. This effect could not be achieved by other glycosaminoglycans or hyaluronan oligosaccharides, chondroitin sulfate, and heparin which did not affect the membrane potential. Mixtures of high-molecular weight hyaluronan and bovine serum albumin had a larger depolarization effect than expected as the sum of both individual components. The different behavior of high-molecular weight hyaluronan versus hyaluronan oligosaccharides and other glycosaminoglycans can be explained by a Donnan effect combined with a steric exclusion of other molecules from the water solvated chains of high-molecular weight hyaluronan. Depolarization of the plasma membrane by hyaluronan represents an additional pathway of signal transduction to the classical CD44 signal transduction pathway, which links the extracellular matrix to intracellular metabolism.

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Section: Membrane Potential Of Human Fibroblastssupporting

confidence: 90%

Depolarization of the membrane potential by hyaluronan

Hagenfeld

Schulz

Ehling³

et al. 2010

J of Cellular Biochemistry

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show abstract

“…It is known that cardiac fibroblasts of human heart are not electrically excitable but mechanosensitive. The resting membrane potential of these cells is around -16 mV [81]. It is unlikely that the potentials we recorded are from supportive fibroblasts as when the heart is not contracting, during blebbistatin treatment, the pacing potentials are still detected.…”

Section: Discussionmentioning

confidence: 88%

Roles of the Sarcoplasmic/Endoplasmic Reticulum Ca2+-ATPase, Plasma Membrane Ca2+-ATPase and Na+/Ca2+ Exchanger in Regulation of Heart Rate in Larval Drosophila~!2010-03-10~!2010-08-13~!2010-08-27~!

Desai-Shah¹,

Papoy²,

Ward³

et al. 2010

TOPHYJ

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Abstract:We investigated the roles of three regulatory proteins that impact [Ca 2+ ] i within cardiac myocytes of Drosophila melanogaster. The NCX (Na + /Ca 2+ exchanger), PMCA (plasma membrane Ca 2+ -ATPase) and SERCA (sarcoplasmic/endoplasmic reticulum Ca 2+ -ATPase) were compromised by ionic, pharmacological, mutationalmanipulation, and with a combination of approaches, while heart rate (HR) was monitored. A decrease in SERCA function reduced HR more for intact larva in comparison to a dissected larva. Dissected preparations were used to expose the heart directly to agents. A compromised PMCA also reduced HR; however, attenuated NCX function by low [Na + ] o increased HR. KBR7943, a blocker of Ca 2+ entry via NCX, exposure increased HR. A combined loss of function in all three channels did not show a significant change in HR. The results indicate that NCX and PMCA are important in regulating HR, whereas SERCA does not have as pronounced role for dissected preparations. However, with intact preparations the loss of SERCA function by a mutation does have a significant impact on HR. Pharmacological approaches to alter PMCA and SERCA paralleled the results obtained by ionic and mutational approaches. To further understand the pacemaker activity, intracellular recordings were obtained. Mapping of action-potentials in myocytes revealed that the caudal region of the heart has large amplitude potentials and is likely to contain the pacemaker cells. The Drosophila heart can serve as a genetic model in understanding regulation of ionic currents for pacing cells of various types.

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“…The G f ranges from 0.1 to 4 nS (Kohl et al, 1994) and E f from −60 to 0 mV (Kamkin et al, 1999;Kohl, 2003;Camelliti et al, 2005). In this study, E f was set to −20 mV, and G f was chosen to be 0.2 and 2 nS, to investigate the effects of various parameters in the cellular fibroblast model on the output of the simulations.…”

Section: Model Frameworkmentioning

confidence: 99%

Fibroblast proliferation alters cardiac excitation conduction and contraction: a computational study

Zhan

Xia

Shou

et al. 2014

J. Zhejiang Univ. Sci. B

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Abstract:In this study, the effects of cardiac fibroblast proliferation on cardiac electric excitation conduction and mechanical contraction were investigated using a proposed integrated myocardial-fibroblastic electromechanical model. At the cellular level, models of the human ventricular myocyte and fibroblast were modified to incorporate a model of cardiac mechanical contraction and cooperativity mechanisms. Cellular electromechanical coupling was realized with a calcium buffer. At the tissue level, electrical excitation conduction was coupled to an elastic mechanics model in which the finite difference method (FDM) was used to solve electrical excitation equations, and the finite element method (FEM) was used to solve mechanics equations. The electromechanical properties of the proposed integrated model were investigated in one or two dimensions under normal and ischemic pathological conditions. Fibroblast proliferation slowed wave propagation, induced a conduction block, decreased strains in the fibroblast proliferous tissue, and increased dispersions in depolarization, repolarization, and action potential duration (APD). It also distorted the wave-front, leading to the initiation and maintenance of re-entry, and resulted in a sustained contraction in the proliferous areas. This study demonstrated the important role that fibroblast proliferation plays in modulating cardiac electromechanical behaviour and which should be considered in planning future heart-modeling studies.

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Mechanically Induced Potentials in Fibroblasts from Human Right Atrium

Cited by 51 publications

References 24 publications

Depolarization of the membrane potential by hyaluronan

Depolarization of the membrane potential by hyaluronan

Roles of the Sarcoplasmic/Endoplasmic Reticulum Ca2+-ATPase, Plasma Membrane Ca2+-ATPase and Na+/Ca2+ Exchanger in Regulation of Heart Rate in Larval Drosophila~!2010-03-10~!2010-08-13~!2010-08-27~!

Fibroblast proliferation alters cardiac excitation conduction and contraction: a computational study

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