The Role of PPAR Ligands in Controlling Growth-Related Gene Expression and their Interaction with Lipoperoxidation Products

被引：21

作者：

Barrera, Giuseppina ^{[1
]}

Toaldo, Cristina ^{[1
]}

Pizzimenti, Stefania ^{[1
]}

Cerbone, Angelo ^{[2
]}

Pettazzoni, Piergiorgio ^{[1
]}

Dianzani, Mario Umberto ^{[1
]}

Ferretti, Carlo ^{[3
]}

机构：

[1] Dipartimento Med & Oncol Sperimentale, Sez Patol Gen, I-10125 Turin, Italy

[2] Ist Ric Biomed A Marxer RBM Merck Serono, I-10010 Turin, Italy

[3] Dipartimento Anat Farmacol & Med Legale, Sez Farmacol, I-10125 Turin, Italy

来源：

PPAR RESEARCH | 2008年 / 2008卷

关键词：

D O I：

10.1155/2008/524671

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Peroxisome proliferators-activated receptors (PPARs) are ligand-activated transcription factors that belong to the nuclear hormone receptor superfamily. The three PPAR isoforms (alpha, gamma and beta/delta) have been found to play a pleiotropic role in cell fat metabolism. Furthermore, in recent years, evidence has been found regarding the antiproliferative, proapoptotic, and differentiation-promoting activities displayed by PPAR gamma ligands, particularly by PPAR. ligands. PPAR ligands affect the expression of different growth-related genes through both PPAR-dependent and PPAR-independent mechanisms. Moreover, an interaction between PPAR ligands and other molecules which strengthen the effects of PPAR ligands has been described. Here we review the action of PPAR on the control of gene expression with particular regard to the effect of PPAR ligands on the expression of genes involved in the regulation of cell-cycle, differentiation, and apoptosis. Moreover, the interaction between PPAR ligands and 4-hydroxynonenal (HNE), the major product of the lipid peroxidation, has been reviewed. Copyright (C) 2008 Giuseppina Barrera et al.

引用

页数：15

共 175 条

[1] Cloning and characterization of the 5′ flanking region of the human uncoupling protein 3 (UCP3) gene [J].

Acín, A ;

Rodriguez, M ;

Rique, H ;

Canet, E ;

Boutin, JA ;

Galizzi, JP .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1999, 258 (02) :278-283

[2] Diclofenac antagonizes peroxisome proliferator-activated receptor-γ signaling [J].

Adamson, DJA ;

Frew, D ;

Tatoud, R ;

Wolf, CR ;

Palmer, CNA .

MOLECULAR PHARMACOLOGY, 2002, 61 (01) :7-12

[3] PPARs and their metabolic modulation: new mechanisms for transcriptional regulation? [J].

Ahmed, W. ;

Ziouzenkova, O. ;

Brown, J. ;

Devchand, P. ;

Francis, S. ;

Kadakia, M. ;

Kanda, T. ;

Orasanu, G. ;

Sharlach, M. ;

Zandbergen, F. ;

Plutzky, J. .

JOURNAL OF INTERNAL MEDICINE, 2007, 262 (02) :184-198

[4] Role of prostacyclin versus peroxisome proliferator-activated receptor β receptors in prostacyclin sensing by lung fibroblasts [J].

Ali, FY ;

Egan, K ;

FitzGerald, GA ;

Desvergne, B ;

Wahli, W ;

Bishop-Bailey, D ;

Warner, TD ;

Mitchell, JA .

AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 2006, 34 (02) :242-246

[5] PPAR gamma induces cell cycle withdrawal: inhibition of E2F/DP DNA-binding activity via down-regulation of PP2A [J].

Altiok, S ;

Xu, M ;

Spiegelman, BM .

GENES & DEVELOPMENT, 1997, 11 (15) :1987-1998

[6]

Asou H, 1999, INT J ONCOL, V15, P1027

[7] Isoform specific changes in PPARα and β in colon and breast cancer with differentiation [J].

Aung, CS ;

Faddy, HM ;

Lister, EJ ;

Monteith, GR ;

Roberts-Thomson, SJ .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2006, 340 (02) :656-660

[8] Regulation of 4-hydroxynonenal mediated signaling by glutathione S-transferases [J].

Awasthi, YC ;

Ansari, GAS ;

Awasthi, S .

GLUTHIONE TRANSFERASES AND GAMMA-GLUTAMYL TRANSPEPTIDASES, 2005, 401 :379-407

[9]

Awasthi Yogesh C., 2003, Molecular Aspects of Medicine, V24, P219

[10] Critical role of c-Jun N-terminal protein kinase activation in troglitazone-induced apoptosis of human HepG2 hepatoma cells [J].

Bae, MA ;

Song, BJ .

MOLECULAR PHARMACOLOGY, 2003, 63 (02) :401-408

← 1 2 3 4 5 6 7 8 9 10 →