For its critical location, the skin represents the major interface between the body and the environment, therefore is one of the major biological barriers against the outdoor environmental stressors. Among the several oxidative environmental stressors, cigarette smoke (CS) has been associated with the development and worsening of many skin pathologies such as acne, dermatitis, delayed wound healing, aging and skin cancer. In our previous work we have demonstrated that CS is able to affect genes involved in skin cholesterol trafficking, among which SRB1, a receptor involved in the uptake of cholesterol from HDL, seems to be very susceptible to the oxidative stress induced by CS. In the present work we wanted to investigate the presence of SRB1 in human sebocytes and whether CS can affect cholesterol cellular uptake via the redox modulation of SRB1. By using a co-culture system of keratinocytes/sebocytes, we found that CS exposure induced a SRB1 protein loss without affecting sebocytes viability. The decrease of SRB1 levels was a consequence of SRB1/HNE adducts formation that leads to SRB1 ubiquitination and degradation. Moreover, the CS-induced loss of SRB1 induced an alteration of sebocytes lipid content, also demonstrated by cholesterol quantification in SRB1 siRNA experiments. In conclusion, exposure to CS, induced SRB1 post-translational modifications in sebocytes and this might affect sebocytes/skin functionality.

SRB1 as a new redox target of cigarette smoke in human sebocytes

CRIVELLARI, Ilaria
Primo
;
STICOZZI, Claudia;MURESAN, Ximena Maria;CERVELLATI, Franco;PECORELLI, Alessandra;BENEDUSI, Mascia;CERVELLATI, Carlo
Penultimo
;
VALACCHI, Giuseppe
Ultimo
2017

Abstract

For its critical location, the skin represents the major interface between the body and the environment, therefore is one of the major biological barriers against the outdoor environmental stressors. Among the several oxidative environmental stressors, cigarette smoke (CS) has been associated with the development and worsening of many skin pathologies such as acne, dermatitis, delayed wound healing, aging and skin cancer. In our previous work we have demonstrated that CS is able to affect genes involved in skin cholesterol trafficking, among which SRB1, a receptor involved in the uptake of cholesterol from HDL, seems to be very susceptible to the oxidative stress induced by CS. In the present work we wanted to investigate the presence of SRB1 in human sebocytes and whether CS can affect cholesterol cellular uptake via the redox modulation of SRB1. By using a co-culture system of keratinocytes/sebocytes, we found that CS exposure induced a SRB1 protein loss without affecting sebocytes viability. The decrease of SRB1 levels was a consequence of SRB1/HNE adducts formation that leads to SRB1 ubiquitination and degradation. Moreover, the CS-induced loss of SRB1 induced an alteration of sebocytes lipid content, also demonstrated by cholesterol quantification in SRB1 siRNA experiments. In conclusion, exposure to CS, induced SRB1 post-translational modifications in sebocytes and this might affect sebocytes/skin functionality.
2017
Crivellari, Ilaria; Sticozzi, Claudia; Belmonte, G; Muresan, Ximena Maria; Cervellati, Franco; Pecorelli, Alessandra; Cavicchio, C; Maioli, E; Zouboulis, Cc; Benedusi, Mascia; Cervellati, Carlo; Valacchi, Giuseppe
File in questo prodotto:
File Dimensione Formato  
1-s2.0-S0891584916310449-main SRB1 Crivellari 2016.pdf

solo gestori archivio

Descrizione: Full text editoriale
Tipologia: Full text (versione editoriale)
Licenza: NON PUBBLICO - Accesso privato/ristretto
Dimensione 1.45 MB
Formato Adobe PDF
1.45 MB Adobe PDF   Visualizza/Apri   Richiedi una copia
11392-2356500 SRB1 as a new redox target of cigarette smoke in human sebocytes.doc.pdf

accesso aperto

Descrizione: Pre print
Tipologia: Pre-print
Licenza: PUBBLICO - Pubblico con Copyright
Dimensione 3.18 MB
Formato Adobe PDF
3.18 MB Adobe PDF Visualizza/Apri

I documenti in SFERA 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/11392/2356500
Citazioni
  • ???jsp.display-item.citation.pmc??? 5
  • Scopus 13
  • ???jsp.display-item.citation.isi??? 13
social impact