The present experiments were aimed to characterize in immortalized human HaCat keratinocytes the gene expression induced by paraquat and capsaicin, two agents known to induce cell death or to affect inflammatory and pain pathways, respectively. In particular, the following set of genes were analysed by qRealtime PCR: CXCL10, CXCL11, IL-10 (inflammatory and immune responses), TP73, BCL2, (apoptotic and anti-apoptotic genes), MMP9 (proteolysis), SOD-1, BAK-1 and CAT (peroxysomal and microsomal oxidation pathways). In this way, we were able to differentiate the two toxins since they had a different profile of gene expression. In fact, paraquata was found to activate set of genes involved in inflammatory (CXL10, CXL11 and IL-10), and cell death (BCL2, BAK-1, MMP9) pathways. Another specific site of action of paraquat was represented by an activation of the gene involved in SOD-I transcription. On the contrary, capsaicin was found to produce only an up-regulation of BCL2, an anti-apoptotic gene and MMP9, whereas no significant changes were reported in genes involved in inflammatory and immune responses. Finally, in comparison to previous experiments carried out with TNF-alpha and IL-1 beta, we have shown that paraquat produced a similar pattern of activation of set of genes involved both in inflammation and apoptosis

Effects of paraquat and capsaicin on the expression of genes related to inflammatory, immune responses and cell death in immortalized human HaCat keratinocytes / N., Paolillo; S., Piccirilli; E., Giardina; V., Rispoli; C., Colica; Nistico', S. - In: INTERNATIONAL JOURNAL OF IMMUNOPATHOLOGY AND PHARMACOLOGY. - ISSN 0394-6320. - 24:4(2011), pp. 861-868. [10.1177/039463201102400405]

Effects of paraquat and capsaicin on the expression of genes related to inflammatory, immune responses and cell death in immortalized human HaCat keratinocytes

Nistico' S
2011

Abstract

The present experiments were aimed to characterize in immortalized human HaCat keratinocytes the gene expression induced by paraquat and capsaicin, two agents known to induce cell death or to affect inflammatory and pain pathways, respectively. In particular, the following set of genes were analysed by qRealtime PCR: CXCL10, CXCL11, IL-10 (inflammatory and immune responses), TP73, BCL2, (apoptotic and anti-apoptotic genes), MMP9 (proteolysis), SOD-1, BAK-1 and CAT (peroxysomal and microsomal oxidation pathways). In this way, we were able to differentiate the two toxins since they had a different profile of gene expression. In fact, paraquata was found to activate set of genes involved in inflammatory (CXL10, CXL11 and IL-10), and cell death (BCL2, BAK-1, MMP9) pathways. Another specific site of action of paraquat was represented by an activation of the gene involved in SOD-I transcription. On the contrary, capsaicin was found to produce only an up-regulation of BCL2, an anti-apoptotic gene and MMP9, whereas no significant changes were reported in genes involved in inflammatory and immune responses. Finally, in comparison to previous experiments carried out with TNF-alpha and IL-1 beta, we have shown that paraquat produced a similar pattern of activation of set of genes involved both in inflammation and apoptosis
2011
paraquat; capsaicin; keratinocytes; inflammation; apoptosis: transcriptional response: gene expression
01 Pubblicazione su rivista::01a Articolo in rivista
Effects of paraquat and capsaicin on the expression of genes related to inflammatory, immune responses and cell death in immortalized human HaCat keratinocytes / N., Paolillo; S., Piccirilli; E., Giardina; V., Rispoli; C., Colica; Nistico', S. - In: INTERNATIONAL JOURNAL OF IMMUNOPATHOLOGY AND PHARMACOLOGY. - ISSN 0394-6320. - 24:4(2011), pp. 861-868. [10.1177/039463201102400405]
File allegati a questo prodotto
File Dimensione Formato  
Paolillo_Effects_2011.pdf

solo gestori archivio

Tipologia: Versione editoriale (versione pubblicata con il layout dell'editore)
Licenza: Tutti i diritti riservati (All rights reserved)
Dimensione 789.17 kB
Formato Adobe PDF
789.17 kB Adobe PDF   Contatta l'autore

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1687272
 Attenzione

Attenzione! I dati visualizzati non sono stati sottoposti a validazione da parte dell'ateneo

Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 18
  • ???jsp.display-item.citation.isi??? 17
social impact