July 1, 2004Human Gene Therapy
Gene Transfer of Connexin43 into Skeletal Muscle
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Key result
Expression of connexin43 driven by the muscle creatine kinase (MCK) promoter delayed until after differentiation allowed skeletal myotubes to remain viable and express gap junction proteins after grafting into the heart.
Why the study?
Does gene transfer of Connexin43 using the MCK promoter improve viability and gap junction formation in skeletal myoblasts grafted into nude mouse hearts?
Population
Preclinical models including mouse myoblast lines, primary Fischer neonatal rat myoblasts, and adult male…
Comparison
Gene transfer of Connexin43 into skeletal… vs Control vectors or wild-type non-transfected…
Design
Preclinical
Follow-up
up to 4 weeks
Authors
Discussion
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Implication
May improve myoblast viability in preclinical cardiac grafts; leaves open translation of MCK-driven connexin43 to cellular cardiomyoplasty.
Structured PICO
Does gene transfer of Connexin43 using the MCK promoter improve viability and gap junction formation in skeletal myoblasts grafted into nude mouse hearts?
P
Population
Preclinical study evaluating the gene transfer of connexin43 into skeletal myoblasts and myotubes in vitro and in adult male nude mice to assess viability and gap junction formation for cellular cardiomyoplasty.
I
Intervention
Gene transfer of Connexin43 (Cx43) into skeletal myoblasts using retroviral, adenoviral, and plasmid-mediated (muscle creatine kinase [MCK] promoter) vectors.
C
Comparator
Control vectors (empty retrovirus, GFP-adenovirus) or wild-type non-transfected myoblasts.
O
Outcome
Expression of Cx43 in differentiated skeletal myotubes, cell viability during differentiation, and formation of gap junctions with host cardiomyocytes in vivo.surrogate
Using a differentiation-specific promoter (MCK) to overexpress Connexin43 in skeletal myoblasts prevents cell death and enables gap junction formation with host cardiomyocytes, advancing cellular cardiomyoplasty strategies.
Limitations
- Physiological studies are required to definitively test whether electrical coupling between host and graft actually occurred and whether it promotes contractile function or exerts arrhythmic potential.
Cite This Study
Reinecke et al. (2004) studied Myocardial ischemia / Cellular cardiomyoplasty. Gene transfer of Connexin43 (Cx43) using MCK promoter vs. Empty vector / GFP-adenovirus / Constitutive viral promoters (LTR, CMV) was evaluated on Cell survival and Cx43 expression/gap junction formation after differentiation and grafting. Expression of connexin43 driven by the muscle creatine kinase (MCK) promoter delayed until after differentiation allowed skeletal myotubes to remain viable and express gap junction proteins after grafting into the heart.
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