Cell transplantation atherosclerosis

The potential use of gene therapy has since expanded as conditions such as cancer, atherosclerosis, transplant operations, and infectious disease are now viewed as suitable targets for intervention. For example, HTV and parasitic infection (2-5). Furthermore, the ability to transfer genes into cell in vitro is also an important tool in the research of gene expression. 

Caplice NM, Bunch TJ, Stalboerger PG, et al. Smooth muscle cells in human coronary atherosclerosis can originate from cells administered at marrow transplantation. Proc Natl Acad Sci USA 2003 100 4754-4759. 

Similarly, L-arginine may provide some protection against graft atherosclerosis in heart transplant recipients via -NO-mediated inhibition of intimal cell proliferation (Drexler et al., 1994) and may attenuate the adhesion of monocytes to the EC surface in a dietary model of experimental atherosclerosis (Tsao et al., 1994). In contrast, other data suggest that NO production is actually enhanced in hypercholesterolemic vessels (Minor et al., 1990). Using chemiluminescent techniques. Minor et al. (1990) showed that the basal release of -NO and its metabolites was increased in the aortas of hypercholesterolemic rabbits. This implies that impaired relaxation responses are due to the rapid reaction of NO with other target molecules. 

Based on their broad range of fimctions, the chemokines are easily deduced to be important players in diseases characterized by inflammation and cell infiltration, such as asthma, atherosclerosis, rheumatoid arthritis, multiple sclerosis, colitis, Crohn s disease, experimental autoimmune encephalomyelitis (EAE), and psoriasis, among others (8). Finally, CXCR4 and CCR5 are the two main coreceptors for HIV-1 infection (9)., some chemokine receptors also participate in tumor metastasis (7) and transplant rejection (10). 

A more frequent complication is restenosis of the angioplasty site which occurs in 25-30% of patients over 6-9 months " . Pathological studies in patients with recurrence of symptoms are infrequent but demonstrate proliferation of fibroblasts and vascular smooth muscle cells overlying and distinct from the traumatized atherosclerotic plaque . Similar lesions have been described in early atherosclerosis and there is evidence to suggest a role for platelets in the development of such lesions , possibly through release of platelet-derived growth factors which stimulate fibroblast and vascular smooth muscle proliferation . Thus, depletion or inhibition of platelets prevents the development of atherosclerosis in animal models and aspirin inhibits the accelerated coronary atherosclerosis which occurs in cardiac transplant recipients. Furthermore, restenosis is more frequent when there is evidence of a thrombus at the angioplasty site consistent with previous... 

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