Desmosomal cadherin tension loss in pemphigus vulgaris mediated by the inhibition of active RhoA at cell-cell adhesions.

ABSTRACT: Autoantibody binding to keratinocyte surface antigens, primarily desmoglein 3 (Dsg3) in the desmosome, leads to dissociation of cell-cell adhesions in pemphigus vulgaris. Much of the biophysical transformations after antibody binding remain underexplored. It is unclear how tensions in desmosomes and cell-cell adhesion structures change in response to antibodies, and how the altered tensional states translate to cellular responses. Here, using fluorescence resonance energy transfer-based tension sensors and traction force microscopy, we observed tension loss at Dsg3 and the entire cell-cell adhesion after antibody binding, along with potentially compensatory increase in junctional traction force at cell-extracellular matrix adhesions. Our data also indicate that this tension loss is mediate

SUBMITTER: Jin X 

PROVIDER: S-EPMC12307676 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature