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Proteomic profile of mouse fibroblasts with a targeted disruption of the peroxisome proliferator activated receptor‐ β/δ gene
Author(s) -
Adamkiewicz Jürgen,
Kaddatz Kerstin,
Rieck Markus,
Wilke Bernhard,
MüllerBrüsselbach Sabine,
Müller Rolf
Publication year - 2007
Publication title -
proteomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.26
H-Index - 167
eISSN - 1615-9861
pISSN - 1615-9853
DOI - 10.1002/pmic.200601003
Subject(s) - biology , carcinogenesis , null cell , peroxisome proliferator activated receptor , gene expression , microbiology and biotechnology , phenotype , receptor , proteomics , lipid metabolism , gene , cancer research , genetics , endocrinology
The peroxisome proliferator activated receptor‐β (PPARβ) plays an essential role in lipid metabolism, immune modulation, differentiation and cell proliferation. There is also strong evidence for a function in oncogenesis and tumor vascularization, but the underlying molecular mechanisms remain elusive. In the present study, we have used fibroblasts derived from Pparb wild‐type and null mice to determine by 2‐DE and PMF analysis the contribution of PPARβ to the protein profile of fibroblasts. Thirty‐one differentially expressed proteins of different functional categories were identified. For at least two proteins a role in tumorigenesis and/or tumor vascularization has previously been reported: while the calcium intracellular channel‐4 (CLIC4) was expressed at lower levels in Pparb null cells, expression of the cellular retinol binding protein 1 (CRBP1) was enhanced. Clic4 and Crbp1 gene expression patterns observed in different experimental settings in vitro and in vivo confirmed the proteomics data. Our findings indicate that the expression of a defined set of proteins is altered in fibroblasts and endothelial cells from Pparb null mice, that this is due to aberrant gene regulation, and that the altered expression of these proteins is consistent with the tumor vascularization phenotype of Pparb null mice.