In-stent restenosis is still a clinic trouble for percutaneous coronary intervention in drug-stent era. The molecular basis of restenosis is intensively associated with inflammation. TLR3 and TLR4 as innate immune factors have been proven to play a key role in atherosclerosis disease. The aim of this study is to study the TLR3 and TLR4 expressions and their downstream signaling proteins in the inflammatory process of restenosis after drug-stent therapy. mRNA and protein expression of TLR3 and TLR4 were detected in peripheral blood monocytes of primary group (n = 38), N-ISR group (n = 36) and ISR group (n = 33). Some inflammatory factors (including TLR3 and TLR4) were evaluated in serum of three groups. mRNA and protein expression of TLR3 and TLR4 and their downstream signaling proteins have shown a higher level in restenosis patients than non-restenosis patients and even primary patients who accepted first stent therapy. In serum, different from some nonspecific and downstream inflammatory factors, TLR3 and TLR4 also show a significantly higher level in ISR group compared with N-ISR group and primary group. This study provides a potential clinical biomarker for in-stent restenosis in drug-stent patients and some interesting data about the role of TLRs and their downstream signaling factors in the inflammatory process of in-stent restenosis. Compared with first stent therapy and non-restenosis patients, it is hopeful that TLR3 and TLR4 are potential noninvasive biomarkers in prognosis restenosis.
Keywords: In-stent restenosis; Inflammation; TLR.