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Contact-dependent signaling, as the name suggests, requires that communicating cells be in direct contact with each other. This is achieved either through receptor-ligand interactions or by specialized cytoplasmic channels that allow the flow of small molecules between cells. In animal cells, channels called gap junctions facilitate contact-dependent signaling in certain tissues, whereas, plasmodesmata perform a similar function in plants.
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Related Experiment Video

Updated: Jul 25, 2026

Gap Junctional Intercellular Communication: A Functional Biomarker to Assess Adverse Effects of Toxicants and Toxins, and Health Benefits of Natural Products

Gap Junctional Intercellular Communication: A Functional Biomarker to Assess Adverse Effects of Toxicants and Toxins, and Health Benefits of Natural Products

Published on: December 25, 2016

Does transmembrane communication through gap junctions enable stem cells to overcome stromal inhibition?

M Rosendaal¹, A Mayen, A de Koning

¹Department of Anatomy and Developmental Biology, University College London, UK.

|August 1, 1997

Summary

Amphotericin B halts hematopoietic stem cell (HSC) growth by disrupting communication with bone marrow stroma, not through toxicity. Restoring this intercellular communication allows HSC to resume normal proliferation.

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Gap Junctional Intercellular Communication: A Functional Biomarker to Assess Adverse Effects of Toxicants and Toxins, and Health Benefits of Natural Products

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Isolation and Functional Assessment of Human Breast Cancer Stem Cells from Cell and Tissue Samples

Isolation and Functional Assessment of Human Breast Cancer Stem Cells from Cell and Tissue Samples

Published on: October 2, 2020

Area of Science:

Hematology
Stem Cell Biology
Cellular Communication

Background:

Long-term bone marrow cultures (LTC) are crucial for studying hematopoietic stem cells (HSCs).
Amphotericin B (AB) is known to inhibit HSC growth in LTC.
The mechanism of AB-induced HSC growth inhibition requires clarification.

Purpose of the Study:

To elucidate the mechanism by which Amphotericin B inhibits hematopoietic stem cell proliferation in long-term bone marrow cultures.
To investigate the role of cell-to-cell communication between HSCs and bone marrow stromal cells in this process.

Main Methods:

Utilized long-term bone marrow cultures (LTC) with and without Amphotericin B (AB).
Employed Transwell inserts to separate HSCs from stromal cells.
Assessed colony-forming unit-culture (CFU-c) and cobblestone-area forming cell (CAFC) formation.
Investigated gap junction intercellular communication (GJIC) using micro-injection of lucifer yellow.
Analyzed cytokine and chemokine transcript levels in stromal cells.

Main Results:

AB-induced inhibition of HSC growth was reversible upon drug removal, indicating a non-toxic effect.
HSC growth inhibition by AB occurred only when HSCs were in direct contact with stromal cells, not when separated by Transwell inserts.
Blocking gap junction intercellular communication (GJIC) mimicked the inhibitory effect of AB on HSC growth.
Extensive GJIC in stromal cell lines correlated with their ability to support primitive HSC clones (CAFCs).

Conclusions:

Amphotericin B likely inhibits HSC proliferation by interfering with transmembrane communication between HSCs and stromal cells, rather than direct toxicity.
Gap junctions are implicated as a key mechanism in this stromal-dependent regulation of HSC proliferation.
These findings highlight the importance of cell-cell communication in maintaining hematopoietic stem cell function.