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Cell‐Type Specific Patterns of Gene Expression Predict the Existence of VEGF and PLGF Homo‐ and Heterodimer Gradients in the Vascular Wall
Author(s) -
Xiang Lingjin,
Yin Wei,
Lloyd Pamela G.
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.1031.11
Subject(s) - placental growth factor , vascular endothelial growth factor , in vivo , cell type , vegf receptors , gene expression , cell , microbiology and biotechnology , biology , gene , cancer research , biochemistry , genetics
Vascular endothelial growth factor (VEGF‐A) and placenta growth factor (PLGF) are related angiogenic factors which exist as dimers in vivo . Interestingly, VEGF‐A and PLGF can form heterodimers with unique signaling properties. Thus, the PLGF:VEGF‐A ratio in vascular cells may be physiologically significant. We hypothesized that PLGF and VEGF‐A would show cell‐type specific patterns of expression in smooth muscle cells (SMC) vs endothelial cells (EC). Ten cell lines were studied (4 SMC and 6 EC), including both established and primary cell lines derived from both conduit and microvascular sources. PLGF gene expression varied over a ~4000‐fold range in the cell lines tested, with expression in EC⋙SMC (p<0.05). In contrast, VEGF‐A expression varied over a smaller range (~20‐fold), with expression in SMC>EC (p<0.05). These data suggest that gradients of PLGF and VEGF‐A homodimers and PLGF:VEGF heterodimers may exist across the vascular wall. Based on our data from cultured cells, PLGF homodimers are predicted to be the major species found in and around the EC layer, whereas VEGF homodimers and PLGF:VEGF heterodimers are expected to predominate in the media. Additional studies are needed to assess whether PLGF and VEGF‐A gradients do in fact exist in the vascular wall, and to identify the functional role of such gradients in vivo , e.g. in regulating monocyte infiltration. Support: NIH R01 HL084494 (PL).