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shRNA targeting caspase-3 inhibits apoptosis and cell detachment induced by Pemphigus Vulgaris autoantibodies
Fecha
2022-12Autor
Pacheco-Tovar, Deyanira
Pacheco-Tovar, María-Guadalupe
Saavedra- Alonso, Santiago
Zapata-Benavides, Pablo
Bollain-y-Goytia, Juan-José
Herrera-Esparza, Rafael
Rodríguez-Padilla, Cristina
Avalos-Díaz, Esperanza
Institución
Resumen
Pemphigus is an organ-specific autoimmune disease that affects the skin and mucous
membranes. It is induced by the deposition of pemphigus IgG autoantibodies, which mainly
target Dsg1 and 3 and cause a loss of cell adhesion in a phenomenon known as
acantholysis, and clinically is reflected as intraepidermal blistering. The present work
assessed the effect of pemphigus vulgaris IgG (PV-IgG) on cell adhesion and caspase 3-
dependent apoptosis in HaCaT cells. The expression of caspase-3 induced by PV-IgG was
silenced in cells pre-treated with caspase 3-shRNA. PV-IgG induced cell detachment and
apoptotic changes as demonstrated by the annexin-FITC assays. Treatment of cell cultures
with normal IgG (control; N-IgG) did not have relevant effects on the aforementioned
parameters. Then, the effect of PV-IgG on cells previously treated with shRNA was tested.
The results demonstrated that shRNA reduced apoptotic features and the relative expression
of caspase-3 measured by qRT-PCR, which showed a decrease of 96%. In conclusion
shRNA prevented cell detachment and apoptosis of HaCaT cells induced by PV-IgG. The
presented results further our understanding of the molecular pathophysiologic mechanisms
involved in pemphigus diseases.