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Mesenchymal stem cells isolated from bone marrow and compact bone express both VEGF and PLGF
Author(s) -
Varshney Rohan R.,
Lloyd Pamela G.
Publication year - 2012
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.26.1_supplement.856.4
Subject(s) - mesenchymal stem cell , vascular endothelial growth factor , placental growth factor , bone marrow , cd44 , medicine , flow cytometry , vascular endothelial growth factor a , cancer research , pathology , immunology , andrology , vegf receptors , biology , cell , genetics
Chronic obstructive pulmonary disease (COPD) is associated with dysregulation of vascular endothelial growth factor (VEGF) family protein levels (decreased VEGF and/or increased placental growth factor, PLGF). We hypothesized that mesenchymal stem cells (MSC) could enhance maintenance and repair of lung vasculature in COPD through VEGF family signaling. Toward this goal, we characterized VEGF and PLGF expression in MSC isolated from mouse bone marrow and compact bone. MSC were cultured in 5% O 2 , 10% CO 2 and 85% N 2 and characterized by flow cytometry. MSC from both sources highly expressed the MSC marker CD44 and moderately expressed MSC markers CD105 and CD73. MSC were cultured up to passage 2. Media was collected from primary MSC and p1–2 MSC for ELISA of VEGF and PLGF expression. Fresh media (DMEM + 15% FBS) contained neither PLGF nor VEGF. ELISA of conditioned media from MSC showed that MSC express both VEGF and PLGF, with VEGF>PLGF. VEGF expression increased with passage number, whereas PLGF expression decreased with passage number. Pericytes, cells found in association with the vascular wall, are very similar structurally and functionally to MSC. MSC have also been reported to share similarity with vascular smooth muscle cells (SMC). Our findings suggest that MSCs have a SMC‐like pattern of VEGF and PLGF expression, consistent with a role in vascular maintenance and repair. Funding: OCASCR, NIH R01 HL084494 (PL).