Abstract
Atherosclerosis is a chronic inflammatory disease in which both innate and adaptive immunity are involved. Although there have been major advances in the involvement of toll-like receptor 4 (TLR4) and CD36 in the initiation and development of this disease, detailed mechanisms remain unknown. Here, we show that tenascin-C (TN-C) can stimulate foam cell formation and this can be inhibited by a TLR4-blocking antibody or CD36 gene silencing. Our results identify TN-C-TLR4 activation as a common molecular mechanism in oxLDL-stimulated foam cell formation and atherosclerosis. In addition, CD36 is the major scavenger receptor responsible for the TN-C-mediated foam cell formation. Taken together, we have identified that TNC produced by oxLDL-stimulated macrophages increases foam cell formation through TLR4 and scavenger receptor CD36.
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Liu, R., He, Y., Li, B. et al. Tenascin-C produced by oxidized LDL-stimulated macrophages increases foam cell formation through toll-like receptor-4. Mol Cells 34, 35–41 (2012). https://doi.org/10.1007/s10059-012-0054-x
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DOI: https://doi.org/10.1007/s10059-012-0054-x