Synchronized beating of myocardial cells mediated by FL cells in monolayer culture and its inhibition by trypsin-treated FL cells

doi:10.1016/S0014-4827(71)80062-9

Experimental Cell Research

Volume 65, Issue 1, March 1971, Pages 161-169

https://doi.org/10.1016/S0014-4827(71)80062-9 Get rights and content

Summary

When two myocardial cells were connected through FL cells in a monolayer culture, synchronized beating of the myocardial cells was observed. When two myocardial cells were connected through FL cells treated with trypsin, the beat of the myocardial cells was almost asynchronous in the presence of puromycin in the culture medium. The inhibition of the mediation of synchronized beating by FL cells on trypsin treatment was gradually reversed on culture in normal medium for one day.

When two myocardial cells were connected through L cells, no synchronized beating was observed. When two myocardial cells were connected through hybrid cells between L and Ehrlich ascites tumor cells, synchronized beating was occasionally observed.

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A tumour promoter, 12-O-tetradecanoyl phorbol-13-acetate (TPA), reversibly inhibits the onset and maintenance of cell-cell communication measured by electrophysiological method. We have now studied the mechanism by which TPA inhibits communication of human cells (FL) in culture. Using [³H]phorbol-12,13-dibutyrate ([³H]PDBu), we found a class of specific, high-affinity, saturable binding sites in intact FL cells; they have a dissociation constant of 15.4 nM, and at saturation about 3 × 10⁵ PDBu molecules were bound to each cell. The binding of [³H]PDBu to FL cells was inhibited by TPA, phorbol-12-13-didecanoate and mezerein, whereas phorbol and 4α-phorbol-12-13-didecanoate had no effect. There is a close correlation between the ability of the former compounds to inhibit [³H]PDBu binding and their capacity to inhibit cell-cell communication. When FL cells are dispersed with EDTA and plated onto a culture dish, they start to couple electrically within 2 h; such cell coupling was not affected by the presence of cycloheximide or actinomycin D. TPA inhibits the formation of electrical cell coupling as well as its maintenance, even in the presence of cycloheximide; the recovery of cell-cell communication after the removal of TPA was not significantly affected by the addition of cycloheximide or actinomycin D. Taken together, these results suggest that TPA-mediated reversible inhibition of intercellular communication is mediated by specific binding of TPA to cellular receptors and that macromolecular synthesis is not necessary.
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Metabolic cooperation is the exchange of molecules among cells through permeable junctions formed at sites of cell contact. The phenomenon is alternatively termed “contact feeding” and is different from cross feeding, where material is transferred from one cell to another via the extracellular medium. This chapter reviews the various techniques used to demonstrate metabolic cooperation and the evidence that these techniques share a common mechanistic basis. It focuses on the techniques based on the phenotypic modification of cells consequent upon cell contact. The chapter also discusses the properties of permeable junctions, the factors controlling their formation, and the possible functions of metabolic cooperation in vivo. Metabolic cooperation has features that make it an attractive candidate for the transmission of many kinds of intercellular signals.
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^*: This work was supported by grants to Professor Y. Tonomura from the Muscular Dystrophy Associations of America and the Ministry of Education of Japan.

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Synchronized beating of myocardial cells mediated by FL cells in monolayer culture and its inhibition by trypsin-treated FL cells*

Summary

Develop biol

Exptl cell res

Exptl cell res

Exptl cell res

Explt cell res

Exptl cell res

Exptl cell res

Exptl cell res

Physiol behavior

J gen physiol

J gen physiol