Bioprosthetic mesh used for ventral hernia repair becomes incorporated into the musculofascial edge by cellular infiltration and vascularization. Adipose tissue–derived stem cells promote tissue repair and vascularization and may increase the rate or degree of tissue incorporation. The authors hypothesized that introducing these cells into bioprosthetic mesh would result in adipose tissue–derived stem cell engraftment and proliferation and enhance incorporation of the bioprosthetic mesh.
Adipose tissue–derived stem cells were isolated from the subcutaneous adipose tissue of syngeneic Brown Norway rats, expanded in vitro, and labeled with green fluorescent protein. Thirty-six additional rats underwent inlay ventral hernia repair with porcine acellular dermal matrix. Two 12-rat groups had the cells (1.0 × 106) injected directly into the musculofascial/porcine acellular dermal matrix interface after repair or received porcine acellular dermal matrix on which the cells had been preseeded; the 12-rat control group received no stem cells.
At 2 weeks, adipose tissue–derived stem cells in both stem cell groups engrafted, survived, migrated, and proliferated. Mean cellular infiltration into porcine acellular dermal matrix at the musculofascial/graft interface was significantly greater in the preseeded and injected stem cell groups than in the control group. Mean vascular infiltration of the porcine acellular dermal matrix was significantly greater in both stem cell groups than in the control group.
Preseeded and injected adipose tissue–derived stem cells engraft, migrate, proliferate, and enhance the vascularity of porcine acellular dermal matrix grafts at the musculofascial/graft interface. These cells can thus enhance incorporation of porcine acellular dermal matrix into the abdominal wall after repair of ventral hernias.
From the Departments of Plastic Surgery and Molecular Pathology, University of Texas M. D. Anderson Cancer Center.
Received for publication December 23, 2009; accepted February 25, 2010.
This first two authors contributed equally to this article.
Presented in part at the 54th Annual Meeting of the Plastic Surgery Research Council, in Pittsburgh, Pennsylvania, May 27 through 30, 2009.
Disclosures: Dr. Alt is a board member of InGeneron, Inc., and Dr. Butler serves on the speakers' bureau of LifeCell Corp. Neither of the other authors has any financial interests to disclose.
Charles E. Butler, M.D., Department of Plastic Surgery, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Unit 443, Houston, Texas 77030, email@example.com