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- Title
shRNA-Targeting Caspase-3 Inhibits Cell Detachment Induced by Pemphigus Vulgaris Autoantibodies in HaCaT Cells.
- Authors
Pacheco-Tovar, Deyanira; Pacheco-Tovar, María-Guadalupe; Saavedra-Alonso, Santiago; Zapata-Benavides, Pablo; Torres-del-Muro, Felipe-de-Jesús; Bollain-y-Goytia, Juan-José; Herrera-Esparza, Rafael; Rodríguez-Padilla, Cristina; Avalos-Díaz, Esperanza
- Abstract
Pemphigus is an autoimmune disease that affects the skin and mucous membranes, induced by the deposition of pemphigus IgG, which mainly targets desmogleins 1 and 3 (Dsg1 and 3). This autoantibody causes steric interference between Dsg1 and 3 and the loss of cell adhesion, producing acantholysis. This molecule and its cellular effects are clinically reflected as intraepidermal blistering. Pemphigus vulgaris-IgG (PV-IgG) binding involves p38MAPK-signaling-dependent caspase-3 activation. The present work assessed the in vitro effect of PV-IgG on the adherence of HaCaT cells dependent on caspase-3. PV-IgG induced cell detachment and apoptotic changes, as demonstrated by annexin fluorescent assays. The effect of caspase-3 induced by PV-IgG was suppressed in cells pre-treated with caspase-3-shRNA, and normal IgG (N-IgG) as a control had no relevant effects on the aforementioned parameters. The results demonstrated that shRNA reduces caspase-3 expression, as measured via qRT-PCR and via Western blot and immunofluorescence, and increases cell adhesion. In conclusion, shRNA prevented in vitro cell detachment and the late effects of apoptosis induced by PV-IgG on HaCaT cells, furthering our understanding of the molecular role of caspase-3 cell adhesion dependence in pemphigus disease.
- Subjects
PEMPHIGUS vulgaris; CELL adhesion; MUCOUS membranes; AUTOIMMUNE diseases; CASPASES; DESMOGLEINS
- Publication
International Journal of Molecular Sciences, 2024, Vol 25, Issue 16, p8864
- ISSN
1661-6596
- Publication type
Article
- DOI
10.3390/ijms25168864