Aim: The overexpression of the human tissue kallikrein (HK) gene can reduce blood pressure and ameliorate the secondary syndromes associated with hypertension in animal models. The current study was designed to investigate hy-potensive effect of intramuscular delivery of HK gene.
 Methods: We generated an recombinant adeno-associated virus (rAAV) vector expressing human tissue kallikrein under the control of a cytomegalovirus promoter and administered the rAAV-HK vector to a spontaneously hypertensive rat model at a dose of 1×10 10 virons/rat through intramuscular injection.
 Results: A persistent, high-level expression of HK post-gene delivery was confirmed by ELISA. The systolic blood pressure in the rats receiving rAAV-LacZ and saline increased from 171.3 mmHg to 182.3 mmHg 28 weeks' post injection. In contrast, the delivery of the HK gene by AAV vectors attenuated the increase of the systolic blood pressure in the treated group. The systolic blood pressure was only slightly lowered (from a level of 174 mmHg to 170.5 mmHg) post-vector administration. The difference in blood pressure between the treated group and the control groups is statistically significant at 12.6 mmHg. The hypotensive effect of rAAV-HK persisted until the end of the testing period. In addition, a significant amelioration of cardiovascular hypertrophy, renal injury, and collagen depositions in the rAAV-HK-treated animals were also observed.
 Conclusion: All the effects are comparable with those of intravenous delivery. Therefore, the intramuscular administration of rAAV-HK may be used in gene therapy for hypertension.

/pdf/intramuscular-delivery-of-raav-mediated-kallikrein-gene-1i4h0xevok.pdf

Intramuscular delivery of rAAV-mediated kallikrein gene reduces hypertension and prevents cardiovascular injuries in model rats

SKELETAL MUSCLE AGING By Angela M. Thornton A Dissertation submitted to the Graduate School-New Brunswick Rutgers, The State University of New Jersey and the UMDNJ Graduate School of Biomedical Sciences in partial fulfillment of the requirements for the degree of Doctor of Philosophy Graduate Programs in Biomedical Engineering and in Physiology and Integrative Biology written under the direction of Dr. Jianjie Ma and Dr. Marco A. DePaula Brotto and approved by ________________________________ ________________________________ ________________________________ ________________________________

/pdf/regulation-of-store-operated-calcium-channel-by-mitsugumin29-zsmpwir0wl.pdf

Regulation of store-operated calcium channel by Mitsugumin29 in skeletal muscle aging

Muscle-specific overexpression of the coxsackie-adenovirus receptor in transgenic mice Enhanced efficiency of gene transfer to mature skeletal muscle of hemizygous mice

Dystrophin, the protein product of the Duchenne muscular dystrophy (DMD) gene, is a major component of the subsarcolemmal cytoskeleton and exists in a large oligomeric complex tightly associated with several sarcolemmal glycoproteins which provide a linkage to the extracellular matrix protein, laminin. In the present study, we investigated the status of the dystrophin-associated proteins in the skeletal muscle from 17 DMD patients of various ages. The results revealed a dramatic reduction in all of the dystrophin-associated proteins in the sarcolemma of DMD muscle compared with normal muscle and muscle from a variety of other neuromuscular diseases. This abnormality was common in all 17 DMD patients, irrespective of age. Our results indicate that the absence of dystrophin leads to the loss in all of the dystrophin-associated proteins, which renders DMD muscle fibers susceptible to necrosis. The analysis of dystrophin-associated proteins is important in the assessment of experimental therapies that attempt to replace dystrophin in DMD muscle.

Duchenne muscular dystrophy

Morency MJ, Larochelle N, Guay JM, Sanschagrin F, Levesque RC. Primary structure of flanking DNA sequence from the genomic dhfr-ts locus of Toxoplasma gondii. 1994: American Society for Microbiology, Las Vegas, Nevada, USA. Larochelle N., Lochmuller H., Nalbantoglu J., Jani A., Massie B., Karpati G. Muscle-specific gene expression after adenovirus-mediated gene transfer. Neurology 1996, 46: A389. Larochelle N., Lochmuller H., Prescott S., Allen C., Oualikene W., Massie B., Karpati G, Nalbantoglu J. Sustained muscle-specific dystrophin expression after adenovirus-mediated gene transfer to skeletal muscle of newborn mdx mice. 1998: Third Canadian Gene Therapy Symposium, Montreal, Canada. Nalbantoglu J, Larochelle N, Lochmuller H, Petrof BJ, Wolf E, Karpati G, Holland PC. Transgenic mice expressing the adenovirus (AdV) primary receptor CAR: increased tropism of AdV and gene transfer to mature skeletal muscle. 2000: Third Annual Meeting of American Society of Gene Therapy, Denver, Colorado, USA. Lochmuller H, Orlopp K, Dunant P, Larochelle N, Stucka R. New deletion constructs of dystrophin for gene therapy of Duchenne muscular dystrophy (DMD). 2000: American Society for Neurology, San Diego, California, USA.

Gene transfer to skeletal muscle using adenoviral recombinants

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Gene transfer to skeletal muscle using adenoviral recombinants