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정익모 대한심장학회 2004 Korean Circulation Journal Vol.34 No.11
Background:We have shown that extracellular matrix (ECM) rather than cell proliferation contributes to in-stent restenosis. Transforming growth factor-β (TGF-β), a positive regulator of ECM deposition by vascular cells, may be implicated in in-stent restenosis. We assessed if the blockade of TGF-β by catheter-based local delivery of an adenovirus expressing a soluble form of TGF-β type II receptor (AdTβ-ExR) can inhibit stent-induced neointima. Methods:AdTβ-ExR was applied onto a coronary arterial segment of a pig using an InfiltratorTM, and either of adenovirus expressing β-galactosidase (AdLacZ) or PBS was applied onto other remote segment of the same pig (n=10). Then, stents (n=20) were deployed in the treated arterial segment. Results:Computer-based morphometric analysis 4 weeks after stenting showed no significant difference in neointima area between the AdTβ-ExR-infected and control groups (AdLacZ and PBS). However cell density of neointima was significantly increased in the AdTβ-ExR group compared with control group (3121±331 vs 2812±183 cells/mm2, p<0.05). Notably, the AdTβ-ExR group had more extensive CD3 positive T cell infiltration. In addition matrix metalloproteinase (MMP)1 expression and accumulation of hyaluronan was greater in the AdTβ-ExR group. Cell proliferation rate was significantly increased in the media of the AdTβ-ExR group compared with control group (2.04±1.21% vs 1.18±1.06%, p<0.05). Conclusion:Blockade of TGF-β by use of catheter-based local in vivo gene delivery did not alter neointima formation significantly in our porcine coronary artery stent model, however it increased inflammation and pathological changes that could promote lesion formation.
정익모,최동훈,민필기,정구용 대한심장학회 2004 Korean Circulation Journal Vol.34 No.1
Background: Enhanced extracellular matrix (ECM) accumulation is an important finding in coronary stentrestenotic tissue, in which TGF-β, implicated in ECM formation, is expressed abundantly. We assessed thehypothesis that blockade of TGF-βby the local delivery of an adenovirus expressing a soluble form of the TGF-βtype II receptor (AdTβ-ExR), inhibits stent-induced neointima in porcine coronary arteries. Methods: Tworemote coronary arterial segments (n=20) per pig randomly received 1×109 pfu of either AdTβ-ExR or adenovirusexpressing β-galactosidase (AdLacZ)/PBS, using an InfiltratorTM. Stents (n=20) were deployed, aftergene transfer, in each segment of 10 pigs. Localized transgene expression was confirmed by both reverse transcription-PCR and immunohistochemistry. Computer-based morphometric assessment was performed in the stentedarteries 4 weeks after the gene transfer. Results: There was significantly less intimal area (1.57±0.49 vs. 2.13±0.34 mm2), area ratio of intima/media (0.84±0.44 vs. 1.32±0.48) and higher neointimal cell density (3121±330vs. 2812±183 cells/mm2) in the arteries treated with AdTβ-ExR compared to the controls (all, p<0.05). Neitherthe cell proliferation rate, assessed by PCNA immunohistochemistry, nor the injury score were significantlydifferent between the two groups. The distribution of hyaluronan in the intima was less in 4 of the 6 AdTβ-ExRtreated arteries compared to the controls. Conclusions: Blockade of TGF-β, by a local in vivo gene transfer of asoluble TGF-βreceptor, inhibits stent-induced neointima, probably by inhibiting the ECM accumulation in porcinecoronary arteries, which may have therapeutic potential in the inhibition of restenosis after stenting. (KoreanCirculation J 2004;34 (1):59-68)
Stress-Induced Atherosclerosis: Clinical Evidence and Possible Underlying Mechanism
정익모 대한심장학회 2005 Korean Circulation Journal Vol.35 No.2
There is increasing recognition in medical fields of the importance of behavioral and psychosocial factors in the development of cardiovascular disease. Although the pathogenesis underlying stress-induced atherosclerosis is not well known, inflammation may play a key role. Activation of stress-induced neuroendocrine pathways, such as the hypothalamo-pituitary-adrenal axis, and the sympathetic nervous and renin angiotensin systems, direct neurogenic inflammation may also contribute to the development of stress-induced atherosclerosis.
정익모 메디메디아코리아(주) 2004 심장과 혈관 Vol.6 No.3
HDL콜레스테롤은 혈장 지단백 중 크기가 가장 작고 밀도가 가장 높다. 내부는 주로 cholesteryl esters와 소량의 중성지방을 함유하는 hydrophobic core로 구성되어 있으며, 표면에는 한 층의 인지질, 유리(unesterified)콜레스테롤 등으로 둘러싸여져 있다. 주된 아포지단백은 apo A-Ⅰ과 apo A-Ⅱ이며, HDL콜레스테롤을 밀도에 따라 세분하면 HDL2와 밀도가 더 높은 HDL3로 크게 구분되는데, 이는 다시 질량의 크기에 따라서 HDL2b와 HDL2q, HDL3a, HDL3b, HDL3c로 나뉘다. apo A-Ⅰ과 apo A-Ⅱ를 함께 공유하는 HDL은 대부분 HDL3와 HDL2에서 중요한 비중을 차지한다.