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In Vivo Application of Dynamic Hyaluronic Acid Material for Myocardial Infarction Therapy
Author(s) -
Young Jennifer L,
Schaefer Jacquelyn,
Tuler Jeremy,
Schup-Magoffin Pamela,
Braden Rebecca,
Christman Karen L,
Engler Adam J
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.1060.8
Subject(s) - hyaluronic acid , in vivo , extracellular matrix , myocardial infarction , in vitro , embryonic stem cell , microbiology and biotechnology , mesenchymal stem cell , chemistry , tissue engineering , capsule , cell , matrix (chemical analysis) , biomedical engineering , andrology , medicine , anatomy , biology , biochemistry , botany , chromatography , gene
Tissue‐specific elasticity arises from developmental changes, e.g. ~10‐fold myocardial stiffening from E3 to E10 in the chick embryo. We have shown that pre‐cardiac mesodermal cells plated on top of a thiolated hyaluronic acid (HA) hydrogel engineered to mimic this time‐dependent stiffening improves cardiomyocyte maturation compared to cells on static matrices. Here we determined cell‐matrix interactions using in vivo injections and in vitro encapsulation assays. Prior to assembly, HA was injected subcutaneously or intramyocardially into rats. Histological analysis showed minimal infiltration of host cells and capsule formation around the matrix. Hematological analysis showed no significant systemic immune response was elicited in pre‐ vs. post‐injection animals for all time points. Atomic force microscopy of subcutaneously injected gels showed increasing hydrogel stiffness over time similar to that previously found in vitro . Improved pre‐cardiac and embryonic stem cell distribution and viability was observed when cells were encapsulated with HA and immobilized thiolated protein. These data indicate the presentation of developmentally appropriate matrix stiffness may improve cell differentiation for use in future studies for treating heart failure post‐myocardial infarction. Funding: AHA (0865150F to A.J.E.), NIH (1DP02OD006460 to A.J.E.), ARCS (to J.L.Y.), AHA (10PRE4160143 to J.L.Y.)