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Sirtinol treatment reduces inflammation in human dermal microvascular endothelial cells.

Histone deacetylases (HDAC) are key enzymes in the epigenetic control of gene expression. Recently, inhibitors of class I and class II HDAC have been successfully employed for the treatment of different inflammatory diseases such as rheumatoid arthritis, colitis, airway inflammation and asthma. So f... Full description

Journal Title: PloS one 2011, Vol.6(9), p.e24307
Main Author: Orecchia, Angela
Other Authors: Scarponi, Claudia , Di Felice, Francesca , Cesarini, Elisa , Avitabile, Simona , Mai, Antonello , Mauro, Maria Luisa , Sirri, Valentina , Zambruno, Giovanna , Albanesi, Cristina , Camilloni, Giorgio , Failla, Cristina M
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0024307
Link: http://search.proquest.com/docview/893292047/?pq-origsite=primo
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title: Sirtinol treatment reduces inflammation in human dermal microvascular endothelial cells.
format: Article
creator:
  • Orecchia, Angela
  • Scarponi, Claudia
  • Di Felice, Francesca
  • Cesarini, Elisa
  • Avitabile, Simona
  • Mai, Antonello
  • Mauro, Maria Luisa
  • Sirri, Valentina
  • Zambruno, Giovanna
  • Albanesi, Cristina
  • Camilloni, Giorgio
  • Failla, Cristina M
subjects:
  • Acetylation–Drug Effects
  • Benzamides–Pharmacology
  • Carbazoles–Therapeutic Use
  • Cell Adhesion–Pharmacology
  • Cell Adhesion Molecules–Drug Effects
  • Cell Proliferation–Metabolism
  • Chemokines–Drug Effects
  • Dermis–Metabolism
  • Endothelial Cells–Blood Supply
  • Furans–Drug Effects
  • Gene Expression Regulation–Metabolism
  • Histones–Pathology
  • Humans–Pharmacology
  • Inflammation–Drug Effects
  • Microvessels–Metabolism
  • Monocytes–Drug Therapy
  • Naphthols–Pathology
  • Quinolines–Pathology
  • Sirtuins–Drug Effects
  • Time Factors–Pathology
  • Time Factors–Pharmacology
  • Time Factors–Therapeutic Use
  • Time Factors–Pharmacology
  • Time Factors–Genetics
  • Time Factors–Metabolism
  • 6-Chloro-2,3,4,9-Tetrahydro-1h-Carbazole-1-Carboxamide
  • Agk2 Compound
  • Benzamides
  • Carbazoles
  • Cell Adhesion Molecules
  • Chemokines
  • Furans
  • Histones
  • Naphthols
  • Quinolines
  • Sirtinol
  • Sirtuins
ispartof: PloS one, 2011, Vol.6(9), p.e24307
description: Histone deacetylases (HDAC) are key enzymes in the epigenetic control of gene expression. Recently, inhibitors of class I and class II HDAC have been successfully employed for the treatment of different inflammatory diseases such as rheumatoid arthritis, colitis, airway inflammation and asthma. So far, little is known so far about a similar therapeutic effect of inhibitors specifically directed against sirtuins, the class III HDAC. In this study, we investigated the expression and localization of endogenous sirtuins in primary human dermal microvascular endothelial cells (HDMEC), a cell type playing a key role in the development and maintenance of skin inflammation. We then examined the biological activity of sirtinol, a specific sirtuin inhibitor, in HDMEC response to pro-inflammatory cytokines. We found that, even though sirtinol treatment alone affected only long-term cell proliferation, it diminishes HDMEC inflammatory responses to tumor necrosis factor (TNF)[alpha] and interleukin (IL)-1[beta]. In fact, sirtinol significantly reduced membrane expression of adhesion molecules in TNF#227;- or IL-1[beta]-stimulated cells, as well as the amount of CXCL10 and CCL2 released by HDMEC following TNF[alpha] treatment. Notably, sirtinol drastically decreased monocyte adhesion on activated HDMEC. Using selective inhibitors for Sirt1 and Sirt2, we showed a predominant involvement of Sirt1 inhibition in the modulation of adhesion molecule expression and monocyte adhesion on activated HDMEC. Finally, we demonstrated the in vivo expression of Sirt1 in the dermal vessels of normal and psoriatic skin. Altogether, these findings indicated that sirtuins may represent a promising therapeutic target for the treatment of inflammatory skin diseases characterized by a prominent microvessel involvement.
language: eng
source:
identifier: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0024307
fulltext: fulltext
issn:
  • 19326203
  • 1932-6203
url: Link


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titleSirtinol treatment reduces inflammation in human dermal microvascular endothelial cells.
creatorOrecchia, Angela ; Scarponi, Claudia ; Di Felice, Francesca ; Cesarini, Elisa ; Avitabile, Simona ; Mai, Antonello ; Mauro, Maria Luisa ; Sirri, Valentina ; Zambruno, Giovanna ; Albanesi, Cristina ; Camilloni, Giorgio ; Failla, Cristina M
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identifierE-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0024307
subjectAcetylation–Drug Effects ; Benzamides–Pharmacology ; Carbazoles–Therapeutic Use ; Cell Adhesion–Pharmacology ; Cell Adhesion Molecules–Drug Effects ; Cell Proliferation–Metabolism ; Chemokines–Drug Effects ; Dermis–Metabolism ; Endothelial Cells–Blood Supply ; Furans–Drug Effects ; Gene Expression Regulation–Metabolism ; Histones–Pathology ; Humans–Pharmacology ; Inflammation–Drug Effects ; Microvessels–Metabolism ; Monocytes–Drug Therapy ; Naphthols–Pathology ; Quinolines–Pathology ; Sirtuins–Drug Effects ; Time Factors–Pathology ; Time Factors–Pharmacology ; Time Factors–Therapeutic Use ; Time Factors–Pharmacology ; Time Factors–Genetics ; Time Factors–Metabolism ; 6-Chloro-2,3,4,9-Tetrahydro-1h-Carbazole-1-Carboxamide ; Agk2 Compound ; Benzamides ; Carbazoles ; Cell Adhesion Molecules ; Chemokines ; Furans ; Histones ; Naphthols ; Quinolines ; Sirtinol ; Sirtuins
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descriptionHistone deacetylases (HDAC) are key enzymes in the epigenetic control of gene expression. Recently, inhibitors of class I and class II HDAC have been successfully employed for the treatment of different inflammatory diseases such as rheumatoid arthritis, colitis, airway inflammation and asthma. So far, little is known so far about a similar therapeutic effect of inhibitors specifically directed against sirtuins, the class III HDAC. In this study, we investigated the expression and localization of endogenous sirtuins in primary human dermal microvascular endothelial cells (HDMEC), a cell type playing a key role in the development and maintenance of skin inflammation. We then examined the biological activity of sirtinol, a specific sirtuin inhibitor, in HDMEC response to pro-inflammatory cytokines. We found that, even though sirtinol treatment alone affected only long-term cell proliferation, it diminishes HDMEC inflammatory responses to tumor necrosis factor (TNF)[alpha] and interleukin (IL)-1[beta]. In fact, sirtinol significantly reduced membrane expression of adhesion molecules in TNF#227;- or IL-1[beta]-stimulated cells, as well as the amount of CXCL10 and CCL2 released by HDMEC following TNF[alpha] treatment. Notably, sirtinol drastically decreased monocyte adhesion on activated HDMEC. Using selective inhibitors for Sirt1 and Sirt2, we showed a predominant involvement of Sirt1 inhibition in the modulation of adhesion molecule expression and monocyte adhesion on activated HDMEC. Finally, we demonstrated the in vivo expression of Sirt1 in the dermal vessels of normal and psoriatic skin. Altogether, these findings indicated that sirtuins may represent a promising therapeutic target for the treatment of inflammatory skin diseases characterized by a prominent microvessel involvement.
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titleSirtinol treatment reduces inflammation in human dermal microvascular endothelial cells.
authorOrecchia, Angela ; Scarponi, Claudia ; Di Felice, Francesca ; Cesarini, Elisa ; Avitabile, Simona ; Mai, Antonello ; Mauro, Maria Luisa ; Sirri, Valentina ; Zambruno, Giovanna ; Albanesi, Cristina ; Camilloni, Giorgio ; Failla, Cristina M
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