Therapeutic angiomyogenesis using human non-viral transduced VEGF₁₆₅-myoblasts

This article reviews the scientific development of angiomyogenesis using VEGF165-myoblasts, a patented biotechnology platform in regenerative medicine associated with Human Myoblast Genome Therapy (HMGT), also known as Myoblast Transfer Therapy (MTT). VEGF165-myoblasts are the leading biologics for angiomyogenesis. This review also compares the safety and efficacy of VEGF165-myoblasts transduced using adenoviral vectors, nanoparticles or liposomes, in anticipation of their application in clinical trials in the near future. VEGF165-myoblasts are differentiated myogenic cells capable of extensive division, natural cell fusion, nucleus transfer, cell therapy and genome therapy. Following transplantation they survive, develop and function to revitalize degenerative myocardium in heart failure and ischemic cardiomyopathy animal studies. VEGF165-myoblasts are second generation products of HMGT/MTT which replenishes live cells and genetically repairs degenerating myofibers in Type II diabetes, muscular dystrophies, aging dysfunction and disfigurement. Myoblasts have also been used to enhance skin and muscle appearance in cosmetology. We envision that VEGF165-myoblasts will provide better outcome than their non-tranduced counterparts. Myoblasts are not stem cells. Their competitive advantages over stem cells are presented.

Manipulation of collagen synthesis influences progenitor cell engraftment and angiomyogenesis

Myocardial infarction(MI)results in loss of cardiomyocytes(CM) in the ischemic area of the heart followed by an inflammatory response and replacement of contractile CM with fibrosis.Myocardial fibrosis,a key contributor to cardiac dysfunction after MI,presents as a secondary response to the pathophysiological remodeling of long-standing disease including ischemia,obstruction,and microvascular abnormalities.Cardiac fibroblasts and myofibroblasts are responsible for post-MI remodeling which occurs via regulation of extracellular matrix (ECM),presenting as increased collagenⅠandⅢinto the interstitial and perivascular space.In addition to the pluripotency of stem cells following stem/ progenitor cell transplantation,decreased apoptosis, hypertrophy,and fibrosis in the infarcted heart have been demonstrated.This has made transplantation of progenitor/stem cells a primary research focus in the field of tissue regeneration.Unfortunately,the accumulation of ECM and myofibroblasts in areas of tissue injury presents a barrier that can impair penetration of reparative stem/progenitor cells mobilized from peripheral reservoirs.Therefore,cardiac fibroblast production and degradation of ECM are critical in regulating cardiac remodeling and stem/progenitor cell mobilization.This study used transgenic mice overexpressing adenylyl cyclaseⅥ(AC6) in which collagen synthesis was decreased to determine the role of collagen deposition on the engraftment of iPSC from a tri-cell patch applied to infarcted area after MI.