| Atherosclerosis is one of the common diseases that damage human health. Although multiple epidemiological, experimental, and genetic studies have supported that the elevated level of HDL-C is very important for protection against atherogenesis, the effective therapeutic methods aimed at selectively elevated HDL-C level in patients are not currently available. In 1996, the scavenger receptor class B, type I (SR-B I) was reported as the first molecularly well-defined and functionally active cell-surface HDL receptor (HDL-R). Human HDL-R is also known as CLA-1 (CD36 and LIMPII analogous-1). Experiments using transgenic and knockout mice have directly indicated that SR-B I is a physiologically relevant HDL receptor for protection against atherosclerosis. Hepatic overexpression of the murine gene encoding SR-B I through short-term adenovirus-mediated gene transfer in LDL-receptor-knockout mice resulted in marked decreases in atherosclerosis. Furthermore, apoE-deficient mice with attenuated SR-B I expression on a western-type diet showed a significant increase in atherosclerotic lesion size relative to apoE-deficient controls. Taken together, these studies demonstrated the anti-atherogenic effect of SR-B I expression. As a result, SR-B I may represent a new appealing therapeutic target for coronary heart disease in human, either by developing conventional pharmacological drugs to modulate SR-B I activity and /or expression or by SR-B I gene-based therapy.In this paper, with the RNA of human hepatoma BEL-7402 as template, the complementary DNA (cDNA) fragment encoding CLA-1 was amplified by RT-PCR. The resulted sequence cloned CLA-1 cDNA was the same as the known sequence. The recombinant expression plasmid pFastBacl-CLA-1 was constructed by cloning CLA-1 cDNA downstream of the polyhedrin promoter of baculovirus transfer vector pFastBac1. By transposing a mini-Tn7 element from the pFastBac1-CLA-1 to the... |
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