
Platelet gel supernatant as a potential tool to repopulate acellular heart valves
Author(s) -
Somers P.,
Robyns L.,
Nollet E.,
Somer F.,
Cornelissen M.,
Thierens H.,
Nooten G.
Publication year - 2012
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/j.1365-2184.2012.00830.x
Subject(s) - platelet , chemistry , heart valve , biomedical engineering , microbiology and biotechnology , cardiology , medicine , biology
Objective The aim of this study was to repopulate decellularized heart valve matrices with ovine mesenchymal stem cells (o MSC s) by the use of platelet gel ( PG ) supernatant, a storage vehicle for growth factors. Methods o MSC s were exposed to different concentrations of PG ‐released supernatant and cell proliferation was evaluated using the MTS assay. o MSC motility and invasiveness were assayed using a Boyden chamber. A quantitative sandwich enzyme immunoassay was used to examine amounts of b FGF and TGF ‐β1 in the PG supernatant. Repopulation of acellular heart valve matrices was stimulated by seeding matrices with o MSC s supplemented with the PG supernatant. Results The most significant increase in proliferation induced by PG supernatant appeared at 1 × 10 5 plts/ml concentration. Higher concentrations evoked reduction of the stimulatory process. o MSC motility was most significantly stimulated at 1 × 10 6 plts/ml. Stimulating invasiveness of o MSC s needed the much higher concentration of 2 × 10 6 plts/ml. Immunoassays revealed that sheep PG supernatant contains 184.8 pg/ml b FGF and 60.5 ng/ml TGF ‐β1. Moreover, repopulation of acellular heart valve matrices was significantly enhanced by PG supernatant addition and resulted in upregulation of the myofibroblast marker alpha‐smooth muscle actin. Conclusions Growth factors released from platelets had the potential to induce cell repopulation in a heart valve tissue engineering procedure, through stimulation of mesenchymal stem‐cell migration and invasion.