Evidence of apoptotic smooth muscle cells in proliferative intima of injured arteries

来源 :Chinese Medical Journal | 被引量 : 0次 | 上传用户:money51
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Objective To investigate the occurrence and extent of apoptosis in the course of restenosis Methods The experimental models of vessel narrowness and intima thickness were established in minipigs’ iliac arteries by balloon injury and specimens were retrieved on the 1st, 3rd, 6th,12th and 30th days for dynamic observation Apoptotic smooth muscle cells (SMCs) were detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) Results Apoptotic SMCs occurred only in the thickened intima 12 days after injury accompanied with the proliferative SMCs, the percentage of apoptosis was 1 94%±0 42% on the 12th day and 1 36%±0 31% on the 30th day respectively The low frequency of apoptosis compared with the proliferative SMCs was a feature in the restenotic pathology Conclusions Apoptosis participates in the pathogenetic process of intimal thickening and its level was low compared with proliferation The findings suggest that attempts to modulate apoptosis after vessel injury constitute a theoretical approach to the prevention of restenosis Objective To investigate the occurrence and extent of apoptosis in the course of restenosis Methods The experimental models of vessel narrowness and intima thickness were established in minipigs’ iliac arteries by balloon injury and specimens were retrieved on the 1st, 3rd, 6th, 12th and 30th days for dynamic observation Apoptotic smooth muscle cells (SMCs) were detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) Results Apoptotic SMCs occurred only in the thickened intima 12 days after injury accompanied with the proliferative SMCs, the percentage of apoptosis was 1 94 % ± 0 42% on the 12th day and 1 36% ± 0 31% on the 30th day respectively The low frequency of apoptosis compared with the proliferative SMCs was a feature in the restenotic pathology Conclusions Apoptosis participates in the pathogenetic process of intimal thickening and its level was low compared with proliferation The findings suggest that attempts to modulate ap optosis after vessel injury constitutes a theoretical approach to the prevention of restenosis
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