• BMB Reports
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• 제52권2호
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• pp.145-150
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• 2019

Endothelial dysfunction-induced lipid retention is an early feature of atherosclerotic lesion formation. Apoptosis of vascular smooth muscle cells (VSMCs) is one of the major modulating factors of atherogenesis, which accelerates atherosclerosis progression by causing plaque destabilization and rupture. However, the mechanism underlying VSMC apoptosis mediated by endothelial dysfunction in relation to atherosclerosis remains elusive. In this study, we reveal differential expression of several genes related to lipid retention and apoptosis, in conjunction with atherosclerosis, by utilizing a genetic mouse model of endothelial nitric oxide synthase (eNOS) deficiency manifesting endothelial dysfunction. Moreover, eNOS deficiency led to the enhanced susceptibility against pro-apoptotic insult in VSMCs. In particular, the expression of aggrecan, a major proteoglycan, was elevated in aortic tissue of eNOS deficient mice compared to wild type mice, and administration of aggrecan induced apoptosis in VSMCs. This suggests that eNOS deficiency may elevate aggrecan expression, which promotes apoptosis in VSMC, thereby contributing to atherosclerosis progression. These results may facilitate the development of novel approaches for improving the diagnosis or treatment of atherosclerosis.

• 순환기질환의공학회:학술대회논문집
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• 순환기질환의공학회 2002년도 제2회 학술대회 초록집
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• pp.29-30
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• 2002

• 동의생리병리학회지
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• 제16권5호
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• pp.1060-1065
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• 2002

LC20 phosphorylation and PKC α play an important role in modulation of contractile activity of smooth muscle. Besides, myosin phosphatase is also related with smooth muscle contraction in signaling pathways. We previously demonstrated that Crataegi Fructus inhibited phenylephrine-induced contraction and which might be implicated in nitrite formation(Son et al., 2002). In this study, we investigated the effects of butanol fraction of Crataegi Fructus(BFFC) on the localization of α-protein kinease C(PKC α) and myosin phosphatase subnits(MPs) in freshly isolated single ferret potal vein cells, and phosphorylation of LC20 during phenylephrine stimulation. In PKC α and MPs localization, BFFC blocked its translocation from the cytosol to the cell membrane by treatment of phenylephrine. BFFC have also dephosphorylated LC20 phosphorylation by phenylephrine stimulation under basal level, but no significant. These results indicate that the relaxation effect of BFFC is associated with inhibition of PKC α activation and MPs dissociation, and thus myosin phosphatase activity may be increased.

• Maxillofacial Plastic and Reconstructive Surgery
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• 제30권5호
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• pp.500-504
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• 2008

Angiomyoma is the vascular type of leiomyoma that the tumor cells are originated from vascular smooth muscle cells. It's frequently found in the subcutaneous tissues of the lower extremities. Such case of an angiomyoma within the oral cavity is rarely found. From a series of 7748 smooth muscle tumors of all types, only 0.06% were found in the oral cavity. This is a rare case of a young woman appeared with oral angiomyoma located in the left mandibular posterior region with plain radiograph, CT and histologic review.

• 동의생리병리학회지
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• 제19권3호
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• pp.797-801
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• 2005

While conducting an in vitro screening of various medicinal plant extracts, an aqueous extract of Rosa rugosa Radix (ARR) was found to exhibit a distinct vasorelaxant activity. ARR induced a concentration-dependent relaxation of the phenylephrine-precontracted aorta. This effect disappeared with the removal of functional endothelium. Pretreatment of the aortic tissues with NG-nitro-L-arginine methyl ester (L-NAME) or 1H-[1,2,4]-oxadiazole-[4,3-]-quinoxalin-1-one (ODQ) completely inhibited the relaxation induced by ARR. ARR-induced vascular relaxations were also markedly attenuated by addition of diltiazem or verapamil. However, the relaxant effect of ARR was not blocked by pretreatment with indomethacine, tetraethylammonium (TEA), glibenclamide, atropine, or propranolol. Taken together, the present study suggests that ARR dilates vascular smooth muscle via endothelium-dependent NO/cGMP signaling.

• 생명과학회지
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• 제21권1호
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• pp.36-43
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• 2011

Glycate화된 단백질이 혈관질환의 발생에 관여하는지 알아보기 위하여 glycated albumin (GA)이 혈관평활근 세포에서 인터루킨-6 발현에 영향을 주는지 조사하고 또한 그 기전을 구명하였다. GA에 노출된 혈관평활근세포에서 인터루킨-6 transcript가 증가하고, 인터루킨-6 단백질의 분비가 증가하고, 또한 인터루킨-6 유전자의 promoter가 활성화되었다. GA에 의한 인터루킨-6 유전자의 promoter 활성화는 dominant negative 형태의 Toll-like receptor (TLR)-4와 myeloid differentiation factor 88 (Myd88)에 의하여 크게 감소되었지만, dominant negative 형태의 TLR-2와 TIR-domain-containing adapter-inducing interferon-$\beta$ (TRIF)의 영향을 받지 않았다. 그리고 Extrcellular signal-related kinase (ERK) 억제 물질들은 GA에 의한 인터루킨-6의 분비 및 인터루킨-6 유전자 promoter 활성화를 억제하였다. 그리고 인터루킨-6 유전자의 promoter의 NF-${\kappa}B$-binding sequence에 변이는 GA에 의한 인터루킨-6 유전자의 promoter 활성화 억제하였다. 이러한 결과는 혈관평활근세포에서 GA에 의한 인터루킨-6 유전자 활성화에 TLR-4와 ERK 및 NF-${\kappa}B$가 관여함을 의미한다.

• The Korean Journal of Physiology and Pharmacology
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• 제13권5호
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• pp.385-392
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• 2009

Angiotensin II (Ang II) plays an important role in vascular hypertension. The role of the chemokine CCL5 on Ang II-induced activities in vascular smooth muscle cells (VSMCs) has not been studied. In this study, we elucidated the effect of CCL5 on Ang II-induced 12-lipoxygenase (LO) expression and cell proliferation in spontaneously hypertensive rats (SHR) VSMCs. CCL5 decreased Ang II-induced 12-LO mRNA expression and protein production, and it increased Ang II type 2 ($AT_2$) receptor expression in SHR VSMCs. The inhibitory effect of CCL5 on Ang II-induced 12-LO mRNA expression was mediated through the $AT_2$ receptor. Although treatment of CCL5 alone induced SHR VSMCs proliferation, CCL5 inhibited Ang II-induced VSMCs proliferation and PD123,319, an $AT_2$ receptor antagonist, blocked the inhibitory effect of CCL5 on Ang II-induced VSMCs proliferation. Phosphorylation of p38 was detected in VSMCs treated with Ang II or CCL5 alone. But, decrease of p38 phosphorylation was detected in VSMCs treated with Ang II and CCL5 simultaneously (Ang II/CCL5) and PD123,319 increased p38 phosphorylation in VSMCs treated with Ang II/CCL5. Therefore, these results suggest that the inhibitory effect of CCL5 on Ang II-induced VSMCs proliferation is mediated by the $AT_2$ receptor via p38 inactivation, and CCL5 may play a beneficial role in Ang II-induced vascular hypertension.

• The Korean Journal of Physiology and Pharmacology
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• 제28권1호
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• pp.39-48
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• 2024

Wogonin, extracted from the roots of Scutellaria baicalensis Georgi, has been shown to suppress collagen deposition in spontaneously hypertensive rats (SHRs). This study was performed to investigate the role and mechanism of wogonin underlying vascular remodeling in SHRs. After injection of SHRs with 40 mg/kg of wogonin, blood pressure in rats was measured once a week. Masson's trichrome staining was conducted to observe the changes in aortas and mesenteric arteries. Vascular smooth muscle cells (VSMCs) isolated from rat thoracic aortas were treated with Angiotensin II (Ang II; 100 nM) in the presence or absence of varying concentrations of wogonin. The viability and proliferation of VSMCs were examined using Cell Counting Kit-8 assay and 5-ethynyl-2'-deoxyuridine assay, respectively. The migration of VSMCs was examined using wound healing assay and transwell assay. We found that wogonin administration alleviated hypertension, increased lumen diameter, and reduced the thickness of the arterial media in SHRs. Ang II treatment enhanced the viability of VSMCs, which was inhibited by wogonin in a concentration-dependent manner. Wogonin reversed Ang II-induced increases in the viability, proliferation, and migration of VSMCs. Moreover, wogonin inhibited Ang II-induced activation of mitogen-activated protein kinase (MAPK) signaling in VSMCs. Overall, wogonin repressed the proliferative and migratory capacity of VSMCs by regulating the MAPK signaling pathway, thereby attenuating vascular remodeling in hypertensive rats, indicating that wogonin might be a therapeutic agent for the treatment of vascular diseases.

• Journal of Ginseng Research
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• 제23권4호
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• pp.235-238
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• 1999

[ $K_{ATP}$ ]채널은 세포내 ATP에 의해서 억제되는 포타슘 채널로서 혈관평활근, 골격근 및 체장의 ${\beta}$세포 막에 존재하여, 근세포의 막전압 조절을 통하여 근수축 및 이완을 조절할 뿐만 아니라 췌장의 ${\beta}$세포로부터 인슐린분비를 조절한다. 홍삼 복합사포닌 및 사포닌 $Rg_3$ 성분은 토끼 관상동맥 평활근세포의 칼슘의존성-포타슘채널$(BK_{Ca})$의 활성을 증가시켜 막전압의 과분극을 유발하여 혈관평활근을 이완시킨다. 사포닌 $Rg_3$성분은 홍삼의 복합사포닌 성분보다 $BK_{Ca}$에 더 높은 활성을 보이기 때문에 본 연구는 사포닌 $Rg_3$성분이 토끼 관상동맥 단일 평활근세포의 ${\beta}$채널의 활성도를 조절하는지를 팻치클램프 방법으로 기록하였다. 막전압 의존성과 함께 내향전류(inward rectification)특성을 보이는 ${\beta}$채널의 활성을 토끼 관상동맥 평활근 세포로부터 기록하였다. 이 ${\beta}$채널은 ATP와 giyburide에 의해서 억제되었으며 minoxidil에 의해서 활성이 증가되었다. 홍삼 사포닌 $Rg_3$성분은 $K_{ATP}$채널의 전류극대치에는 영향을 주지 않고 전류의 inactivation을 억제시켜 결과적으로 $K_{ATP}$채널의 활성을 증가시켰으며, 단일 KhTr채널이 열리는 시간도 증가시켰다. 따라서 본 실험 결과는 사포닌 $Rg_3$성분이 KATP채널의 활성을 증가시켜 막전압을 조절하여 관상동맥 평활근의 이완을 촉진한다고 여겨진다.

• The Korean Journal of Physiology
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• 제17권1호
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• pp.45-54
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• 1983

Contractile responses of myocardium and vascular smooth muscle to angiotensin II were studied in isolated rabbit papillary muscles and aortic helical strips, with respect to the sensitivity and the mechanism of action. All experiments were performed in $HCO-_3\;-buffered Tyrode solution which was aerated with $3%\;CO_2-97%\;O_2$ and kept pH 7.35 at $35^{\circ}C$. Action potentials were measured by conventional microelectrode technique in the papillary muscles. Helical strips of vascular smooth muscle were prepared from the descending thoracic aorta of the rabbit. Angiotensin II elicited a positive inotropic effect in doses from $10^{-8}$ to $10^{-6}\;M$, and this effect was dose-dependent and characterized by a symmetrical increase of maximum dP/dt during contraction and relaxation phase. Slow responses (or slow action potentials) were induced by A. II $(10^{-6}\;M)$ in the papillary muscle hypopolarized by 27 mM $K^+$. These A. II-induced slow action potentials were eliminated by verapamil (2 mg/l), but not affected by propranolol $(10^{-5}\;M)$. In aortic helical strips, contractile force was increased dose-dependently in the range of $10^{-10}{\sim}10^{-7}\;M$ A. II. $ED_{50}$ in aorta was $3{\times}10^{-9}\;M$ A. II, whereas that in paillary muscle was $2.5{\times}10^{-7}\;M$ A. II. A. II contracted vascular smooth muscle in depolarizing concentration of $K^+$ (100 mM $K^+$), and also produced a sustained contraction even in the presence of verapamil and regitine. The results of this experiment suggest that the primarily important physiological role of A. II is the action on the blood vessel, and the positive inotropic effect of A. II in papillary muscle results from the increase of slow inward $Ca^{++}$ current, and that A. II-induced contraction of aorta is independent of transmembrane potential and associated with promoting bet transmembrane $Ca^{++}\;-influx$ and the mobilization of cellular $Ca^{++}$.