Lp(a) promotes arterial smooth muscle cell proliferation via two distinct pathways: apo(a)-mediated inhibition of TGF-beta and LDL-particle-mediated stimulation.
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Lp(a) effects on SMC proliferation in animal models support mechanistic hypotheses; leaves open relevance to human atherosclerosis and Lp(a) therapies.
We investigated the effect of lipoprotein(a) (Lp(a)) on proliferation of human arterial smooth muscle cells (SMCs) and its mechanisms of action. Low density lipoprotein (LDL), Lp(a) and apolipoprotein(a) (apo(a)) significantly stimulated the proliferation of SMCs. Lp(a) and apo(a) reduced the amount of active transforming growth factor-beta (TGF-beta) with the mink lung epithelial cell bioassay, however LDL had no effect. Lp(a), but not apo(a), significantly stimulated the proliferation of SMCs even in the presence of a neutralizing antibody for TGF-beta. Our results suggest that Lp(a) stimulates the proliferation of SMCs via apo(a)-induced inhibition of TGF-beta activation and stimulation of SMCs by the LDL-particle of Lp(a).
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Miyata et al. (1995) studied this question.
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