title: Caspase 3 blocking avoids the expression of autoantigens triggered by apoptosis in neonatal Balb/c mice skin.
abstract: OBJECTIVE
  To assess the effect of caspase 3 inhibition, in the expression of intracellular antigens induced by apoptosis.
  
  
  METHODS
  Skin explants of neonatal Balb/c mice were used to assess the autoantigen expression. Skin was obtained by punch biopsies, tissues were cultured in DMEM; cell death was induced by chemicals and assessed by TUNEL. The expression of La, Ro, Sm, RNP, Cajal Bodies and NuMa antigens were monitored by immunohistochemistry using autoantibodies or monoclonal antibodies against these antigens.
  
  
  RESULTS
  Chemicals used to induce cell death, successfully produced apoptosis or necrosis in more than 60% of keratinocytes, and viability was significantly decreased when it was compared with those in controls. An increased expression of all skin intracellular antigens in skin biopsies treated with chemicals, major antigenic expression was detected with anti-La and anti-Ro antibodies. The caspase 3 inhibitor DEVD-CMK significantly decreased the expression of antigens induced by chemicals.
  
  
  CONCLUSIONS
  By this result we can infer that caspase inhibitors modify apoptosis and decrease the autoantigens associated to cell death.
authors.affiliation: Departamento de Immunología UBE y Area de Ciencias de la Salud, Universidad Autónoma de Zacatecas, 98600, Guadalupe, Zacatecas, México.
authors.forename: R
authors.initials: R
authors.lastname: Ramírez-Sandoval
authors.forename: M
authors.initials: M
authors.lastname: Vazquez-del-Mercado
authors.forename: A
authors.initials: A
authors.lastname: Daneri-Navarro
authors.forename: J J
authors.initials: JJ
authors.lastname: Bollain-y-Goytia
authors.forename: E
authors.initials: E
authors.lastname: Avalos-Diaz
authors.forename: R
authors.initials: R
authors.lastname: Herrera-Esparza
mesh_terms: D000590:Amino Acid Chloromethyl Ketones / Q000494:pharmacology*; D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis / Q000276:immunology*; D001324:Autoantigens / Q000096:biosynthesis*; D001327:Autoimmune Diseases / Q000209:etiology / Q000517:prevention & control*; D001706:Biopsy; D002166:Camptothecin / Q000494:pharmacology; D061945:Caspase Inhibitors; D002478:Cells, Cultured / Q000187:drug effects / Q000201:enzymology / Q000276:immunology; D003513:Cycloheximide / Q000494:pharmacology; D015853:Cysteine Proteinase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D004353:Drug Evaluation, Preclinical; D006861:Hydrogen Peroxide / Q000494:pharmacology; D020287:In Situ Nick-End Labeling; D008627:Mercuric Chloride / Q000494:pharmacology; D051379:Mice; D008807:Mice, Inbred BALB C; D009924:Organ Culture Techniques; D012867:Skin / Q000201:enzymology / Q000276:immunology*
chemical_list: D000590:Amino Acid Chloromethyl Ketones; D001324:Autoantigens; D061945:Caspase Inhibitors; D015853:Cysteine Proteinase Inhibitors; C096713:benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; D008627:Mercuric Chloride; D003513:Cycloheximide; D006861:Hydrogen Peroxide; D002166:Camptothecin