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Self-Assembly of Microtubule Tactoids

Self-Assembly of Microtubule Tactoids

Published on: June 23, 2022

Connexon-mediated cell adhesion drives microtissue self-assembly.

Brian Bao¹, Jean Jiang, Toshihiko Yanase

¹Department of Molecular Pharmacology, Physiology, and Biotechnology, Center for Biomedical Engineering, Brown University, Providence, RI 02912, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology

|September 30, 2010

Summary

Connexons, not just cadherins, influence microtissue self-assembly. Connexon 43 (Cx43) cell adhesion and communication play a significant role, comparable to cadherins, in how cells form microtissues.

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Area of Science:

Cell biology
Biophysics
Tissue engineering

Background:

Microtissue self-assembly is traditionally attributed to cadherin-mediated adhesion.
Connexons are primarily studied for their role in intercellular communication (gap junctions).
The role of connexons in cell adhesion and microtissue formation remains less understood.

Purpose of the Study:

To investigate the role of connexon 43 (Cx43)-mediated cell adhesion in the self-assembly of microtissues.
To compare the contribution of connexon-mediated adhesion with cadherin-mediated adhesion in microtissue formation.
To explore the influence of Cx43 docking and channel permeability on microtissue self-assembly kinetics.

Main Methods:

Utilized human KGN granulosa cells, normal human fibroblasts (NHFs), and MCF-7 breast cancer cells.
Employed nonadhesive agarose gels to facilitate microtissue formation.
Applied anti-Cx43 E2 antibody to inhibit Cx43 docking and carbenoxolone to inhibit gap junctions.
Used Gap26 peptide to inhibit connexon channel permeability.
Performed enzymatic digestion of cell adhesion molecules and used N-cadherin neutralizing antibodies.

Main Results:

Inhibition of Cx43 docking with anti-Cx43 E2 significantly reduced KGN and NHF self-assembly rates.
Gap junction inhibitor carbenoxolone dose-dependently inhibited self-assembly across all cell types tested.
Connexon mimetic peptide Gap26 accelerated self-assembly in KGN and NHF microtissues.
Disruption of connexin-mediated adhesion comparably affected self-assembly to the inhibition of cadherin-mediated adhesion.

Conclusions:

Connexon-mediated cell adhesion and intercellular communication differentially regulate microtissue self-assembly.
The contribution of connexons to microtissue self-assembly is comparable to that of cadherins.
Cx43 plays a crucial role in modulating the kinetics of microtissue formation.