Ets-1 enhances tumor migration through regulation of CCR7 expression

( Li-wen Fang ),( Ying-hsien Kao ),( Ya-ting Chuang ),( Huey-lan Huang ),( Tzong-shyuan Tai ) 생화학분자생물학회 2019 BMB Reports Vol.52 No.9

Ets-1 is a prototype of the ETS protein family. Members of the ETS protein family contain a unique ETS domain. Ets-1 is associated with cancer progression and metastasis in many types of cancer. Many studies have shown a link between elevated expression of Ets-1 in cancer biopsies and poor survival. CCR7 is a chemokine that binds to specific ligand CCL21/CCL19. CCR7 expression is associated with tumor metastasis and infiltration into lymph nodes. The objective of this study was to test whether Ets-1 could regulate CCR7 expression and enhance tumor metastasis. Our data showed that CCR7 expression was downregulated in Ets-1-deficient T cells upon T-cell stimulation. Overexpression of Ets-1 increased CCR7 expression in breast cancer cell lines. In contrast, knockdown of Ets-1 reduced CCR7 expression. Ets-1 could directly bind to CCR7 promoter and mediate CCR7 expression in luciferase reporter assays and chromatin immunoprecipitation assays. Transactivation activity of Ets-1 was independent of the Pointed domain of Ets-1. Ets-1 could also enhance NF- κB and CBP transactivation of CCR7 promoter. Our results also showed that Ets-1 could modulate cancer cell transmigration by altering CCR7 expression in transwell assay and wound healing assay. Taken together, our data suggest that Ets-1 can enhance CCR7 expression and contribute to tumor cell migration. [BMB Reports 2019; 52(9): 548-553]

댄스스포츠 활동이 비만 아동의 혈류속도 및 혈관 조절인자에 미치는 영향

장용우,송지환 한국초등체육학회 2020 한국초등체육학회지 Vol.26 No.2

본 연구는 16주간의 댄스스포츠활동이 동맥의 혈류속도와 혈관 조절인자에 미치는 영향을 분석하는 것이 목적이다. 대 상자들은 실험군 10명, 통제군 10명으로 분류하였다. 비만여자아동들은 체성분 분석기인 Inbody 3.0을 이용하여 체 지방을 측정하고 초음파도플러(Ultrasound Doppler)를 이용한 쇄골하동맥혈관(subclavian artery blood vessels)의 혈류속도 측정과 산회질소(NO) 및 엔도텔린1(ET-1)을 분석하였다. 혈류속도의 경우 실험군, 통제군의 쇄골하동맥 최 대 혈류속도는 통계적인 유의한 변화는 없었다. 평균 혈류속도는 실험군의 경우 통재군에 비해 –28.6%의 유의한 감소 비율로 나타났다. NO의 경우 실험군은 통제군에 비해 16.3%의 유의하게 높은 증가비율을 나타냈다. ET-1의 경우 실 험군은 통제군에 비해 –28.6%의 유의하게 낮은 감소비율로 나타났다. 요약하면, 비만여자아동의 혈류속도의 감소 비율 과 연계된 NO의 증가와 ET-1의 감소를 통해 장기간의 댄스스포츠활동에 적응된 평균 혈류속도와 NO 및 ET-1의 민 감성에 대한 변화를 관찰할 수 있었다. 따라서 본 연구에서 제시된 댄스스포츠 프로그램은 여자아동들의 비만의 해소 와 혈관계의 기능적 향상 및 NO와 ET-1의 변화에 긍정적인 영향을 미친 것으로 풀이되며, 추후 비만 여자아동의 체 지방 감소, 혈류속도의 개선과 혈관조절인자의 조절을 위한 효과적인 유산소성 운동프로그램으로 제시하고자 한다. The purpose of this study is to analyze the effect of 16-week dance sports activity on the blood flow velocity and vascular control factor of the artery. To carry out this study, the group was classified into 10 subjects and 10 control groups. Obese children used Inbody 3.0 to measure body fat, measure blood flow velocity of subclavian artery blood vessels using Ultrasound Doppler, and nitric oxygen(NO) and endotheline 1(ET-1). For blood flow velocity, there was no statistically significant change in the maximum blood flow velocity of the subclavian artery of the experimental and control groups. The average blood flow velocity was shown to be a significant reduction rate of –28.6% compared to the control group for the experimental group. For NO, the experimental group showed a significantly higher rate of increase of 16.3% compared to the control group. For ET-1, the experimental group showed a significantly lower reduction rate of –28.6% compared to the control group. In summary, the increase in NO linked to the decrease in blood flow rate of obese children and the decrease in ET-1 enabled us to observe changes in the average blood flow velocity and sensitivity of NO and ET-1 adapted to long-term dance sports activities. Therefore, the dance sports program presented in this study is believed to have had a positive effect on the elimination of obesity in girls, the functional improvement of blood relations, and the change in NO and ET-1, and is intended to be presented as an effective aerobic exercise program for reducing body fat, improving blood flow velocity and regulating vascular control factors in later years.

Reactive Oxygen Species Mediate ET-1-Induced Activation of ERK1/2 Signaling in Cultured Feline Esophageal Smooth Muscle Cells

Hyun Ju Song,Ji Soo Kim,Myong Jae Lee,Yoon Sung Nam,손의동 대한약학회 2007 Archives of Pharmacal Research Vol.30 No.9

Reactive oxygen species (ROS) have been shown to play a critical role in propagating the signals of several growth factors, peptide hormones, and cytokines, such as epidermal growth factor, insulin, and interleukin-1. We investigated a possible role for ROS generation in mediating the action of ET-1 on activation of ERK1/2 in cultured feline esophageal smooth muscle cells (ESMC). Confluent layers of ESMC were stimulated by 10nM ET-1; activation of ERK was examined by western blot analysis with phospho-specific antibodies of ERKs. ET-1 induced ERK1/2 phosphorylation in a dose- and time- dependent manner. ERK1/2 activation by ET-1 reached the maximal levels at 5min showing slight activation up to 20min, and then slowly declined. It was confirmed that the activation of ERK1/2 was reduced by MEK inhibitor PD98059. We observed the dose-dependent inhibitory effect of diphenyleneiodonium (DPI), an inhibitor of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase on the ET- 1-enhanced ERK1/2 phosphorylation in ESMC. Pretreatment of ESMC with N-acetylcysteine, a ROS scavenger, also attenuated the ET-1-induced ERK1/2 activation. In addition, DPI significantly inhibited the ET-1- induced ROS production when ROS was measured as a function of DCF fluorescence. The results suggest that ROS might be critical mediators of the ET-1- induced ERK1/2 signaling events in ESMC.

고 반복 저항성 운동이 비만 남성의 혈관내피 기능 및 산화질소(NO), 엔도텔린1(ET-1)에 미치는 영향

장용우 한국융합과학회 2023 한국융합과학회지 Vol.12 No.1

Purpose: This study aims to analyze the effects of high-repetitive resistance exercise on vascular endothelial function and nitric oxide(NO) and endocelin1(ET-1) in obese men. Methods: Body fat percentage was examined using a body composition analyzer(in body3.0) for obese males consisting of 10 obese experimental groups and 10 control groups, and obesity status was examined using body mass index(BMI). Blood pressure was measured using a mercury sphygmomanometer. For vascular endothelial cell function tests, blood flow velocity, vascular resistance and vascular stenosis of the subclavian artery were measured using an ultrasound doppler device, and maximum vessel diameter(PVD) and flow-mediated diastolic response(FMD) were measured using a pulse wave doppler device and vascular endothelial regulatory variables NO and ET-1 were measured through blood analysis. Result: In the case of systolic blood pressure, a vascular endothelial function variable, the experimental group showed a significant(p<.01) difference of -10.7% by treatment period, and the blood flow rate in the experimental group showed a significant(p<.01) difference of –20.4%. Vascular resistance showed a significant(p<.01) difference of -24.8% by treatment period in the experimental group, and a significant(p<.01) difference of -12.6% in the experimental group by treatment period in the case of vascular stenosis. PVD did not show a significant difference at -2.12% by treatment period in the experimental group. In the case of FMD, the experimental group showed a significant (p<.001) difference of 43.4% by treatment period compared to the control group. In the case of NO, a vascular modulator, the experimental group showed a significant (p<.001) difference of 32.1% by treatment period, and ET-1 showed a significant(p<.001) difference of -46.7% in the experimental group. There was no statistical change in the control group for each variable. Conclusion: High- repetitive resistance exercise is interpreted to have a positive effect on vascular endothelial function and vascular endothelial control of NO and ET-1 along with relieving obesity in men, and through the advantages of resistance exercise that will be set variously in the future, we would like to propose the efficiency of high-repetitive resistance exercise for body fat control, improvement of vascular endothelial function, and improvement of endothelial regulation variables in obese men. 연구목적: 본 연구는 16주간의 고 반복형 저항성 운동이 비만 남성의 혈관내피 기능 및 산화질소(NO), 엔도셀린1(ET-1) 미치는 영향을 분석하는 것이 목적이다. 연구방법: 비만 실험군 10명, 통제군10명으로 구성된 비만 남성을 대상으로 체성분분석기(in body3.0)를 사용하여 체지방률을 검사하였으며, 체질량지수(BMI)를 이용하여 비만 상태를 검사하였다. 혈압은 수은혈압계를 이용하여 측정하였다. 혈관내피세포 기능 검사는 ultrasound doppler 기기를 통해 쇄골하동맥의 혈류속도, 혈관저항 및혈관협착의 측정과 pulse wave doppler 기기를 이용하여 최대혈관직경(PVD)과 혈류매개 확장 반응(FMD)을 측정하였으며, 혈관내피 조절변인 인 NO와 ET-1은 혈액분석을 통해 측정하였다. 결과: 혈관내피 기능변인 인 수축기 혈압의 경우 실험군은 처치시기별 –10.7%의 유의한(p<.01) 차를 나타냈고, 혈류속도는 실험군의 경우 처치시기별 –20.4%의 유의한(p<.01) 차를 나타냈다. 혈관저항은 실험군의경우 처치시기별 –24.8%의 유의한(p<.01) 차를 나타냈으며, 혈관협착의 경우 실험군은 처치시기별 – 12.6%의 유의한(p<.01) 차를 나타냈다. PVD는 실험군의 경우 처치시기별 –2.12%로 유의한 차는 나타나지 않았다. FMD의 경우 실험군은 통제 군에 비해 처치시기별 43.4%의 유의한(p<.001) 차를 나타냈다. 혈관조절물질 인 NO의 경우 실험군은 처치시기 별 32.1%의 유의한(p<.001) 차를 나타냈으며, ET-1 은 실험군의 경우 –46.7%의 유의한(p<.001) 차를 나타냈다. 각 변인별 통제군은 전반적인 통계적인변화는 없었다. 결론: 고 반복형 저항성 운동은 남성들의 비만 해소와 함께 혈관내피 기능과 NO와ET-1의 혈관내피 조절에 긍정적인 영향을 미친 것으로 해석되며, 추후 다양하게 설정되는 저항성 운동의 장점을 통해 비만 남성의 체지방 조절, 혈관내피 기능의 향상과 내피 조절변인의 개선을 위한고 반복 개념의 저항성 운동 프로그램의 효율성을 제안하고자 한다.

Reactive Oxygen Species Mediate ET-1-Induced Activation of ERK1/2 Signaling in Cultured Feline Esophageal Smooth Muscle Cells

Song, Hyun-Ju,Kim, Ji-Soo,Lee, Myong-Jae,Nam, Yun-Sung,Sohn, Uy-Dong 대한약학회 2007 Archives of Pharmacal Research Vol.30 No.9

Reactive oxygen species (ROS) have been shown to play a critical role in propagating the signals of several growth factors, peptide hormones, and cytokines, such as epidermal growth factor, insulin, and interleukin-1. We investigated a possible role for ROS generation in mediating the action of ET-1 on activation of ERK1/2 in cultured feline esophageal smooth muscle cells (ESMC). Confluent layers of ESMC were stimulated by 10nM ET-1; activation of ERK was examined by western blot analysis with phospho-specific antibodies of ERKs. ET-1 induced ERK1/2 phosphorylation in a dose- and time- dependent manner. ERK1/2 activation by ET-1 reached the maximal levels at 5min showing slight activation up to 20min, and then slowly declined. It was confirmed that the activation of ERK1/2 was reduced by MEK inhibitor PD98059. We observed the dose-dependent inhibitory effect of diphenyleneiodonium (DPI), an inhibitor of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase on the ET-1-enhanced ERK1/2 phosphorylation in ESMC. Pretreatment of ESMC with N-acetylcysteine, a ROS scavenger, also attenuated the ET-1-induced ERK1/2 activation. In addition, DPI significantly inhibited the ET-1- induced ROS production when ROS was measured as a function of DCF fluorescence. The results suggest that ROS might be critical mediators of the ET-1-induced ERK1/2 signaling events in ESMC.

양 태아의 산소 환기 중 Endothelin B 수용체 차단제가 폐동맥 확장에 미치는 영향

김나연,이동석,Ivy, D. Dunbar 東國大學校醫學硏究所 2004 東國醫學 Vol.11 No.2

Endothelin-1 (ET-1)은 정상 양 태아와 주산기 폐동맥 고혈압 모델에서 폐혈관 긴장도를 유지하는데 관여하고 있다. ET-1의 효과는 적어도 두개의 수용체 아형인 ET_(A)와 ET_(B)의 균형에 의한다. ET_(A) 수용체는 주로 평활근 세포에 존재하며 혈관의 수축과 평활근 세포의 증식에 기여한다. 혈관 내피 세포에 존재하는 ET_(B) 수용체의 자극은 산화질소의 분비를 통해 혈관을 확장시키고 혈중의 ET-1을 제거하는 역할을 한다. 그러나 출생 시 ET_(B) 수용체의 자극이 폐혈관 긴장도의 감소를 유도하는지에 대하여서는 잘 알려져 있지 않다. 출생과 관련된 자극에서 단기간 동안의 ET_(B) 수용체 차단제의 사용이 폐혈관 저항에 미치는 영향을 알아보기 위하여 출산이 임박한 만삭 양 태아에게 저농도(FiO₂<10%)와 고농도(FiO₂100%)로 기계적 환기를 시키는 동안, 선택적인 ET_(B) 수용체 차단제인 BQ-788가 혈류역학에 미치는 영향을 알아보기로 하였다. 정상적인 양 태아에서 BQ-788의 투여는 기저 좌폐동맥 혈류량과 폐혈관저항에는 영향을 미치지는 않았다. 대조군과 비교하여 저농도와 고농도의 산소 호흡중 BQ-788의 투여는 좌 폐동맥 혈류량의 증가를 현저하게 약화시켰다(P<0.01). 폐혈관 저항은 저농도와 고농도의 기계적산소 환기시 양군에서 모두 점차적으로 감소하였으나, BQ-788의 투여는 실험 기간 동안 내내 폐혈관저항을 높게 유지시켰다(P<0.01). 본 실험의 결과로 미루어 볼 때 선택적인 ET_(B) 수용체의 차단은 분만시 폐혈관 확장을 약화시키며, 선택적인 ET_(B) 수용체의 자극은 양 태아의 분만 시 폐혈관 확장에 기여하리라 생각된다. Endothelin-1 (ET-1) contributes to regulation of pulmonary vascular tone in the normal ovine fetus and in models of perinatal pulmonary hypertension. In utero, the effects of ET-1 depend on the balance of at least two receptor subtypes: ET_(A) and ET_(B). ET_(A) receptors are located on smooth muscle cells and mediate vasoconstriction and smooth muscle proliferation. Stimulation of endothelial ET_(B) receptors causes vasodilation through release of nitric oxide and also functions to remove ET-1 from the circulation. However, whether activation of ET_(B) receptors contributes to the fall in pulmonary vascular tone at birth is unknown. To determine the role of acute ET_(B) receptor blockade in pulmonary vasodilation to birth related stimuli, we studied the hemodynamic effects of selective ET_(B) receptor blockade with BQ-788 during mechanical ventilation with low (<10%) and high FiO₂(100%) in near term fetal sheep. Intrapulmonary infusion of BQ-788 did not change left pulmonary artery (LPA) blood flow and pulmonary vascular resistance (PVR) at baseline. Comparison with controls, BQ-788 treatment attenuated the rise in LPA flow with low and high FiO₂ ventilation (P<0.01). PVR progressively decreased during mechanical ventilation with low and high FiO₂in both groups, but PVR remained higher after BQ-788 treatment throughout the study period (P<0.01). We conclude that selective ET_(B) receptor blockade attenuates pulmonary vasodilation at birth. We speculate that ET_(B) receptor stimulation contributes to pulmonary vasodilation at birth in the ovine fetus.

Activation of p38 MAPK Is Involved in Endothelin-1-stimulated COX-2 Expression in Cultured Feline Esophageal Smooth Muscle Cells

손의동,Hyun Ju Song,민영실,Chang Yell Shin,정지훈 한국분자세포생물학회 2006 Molecules and cells Vol.22 No.1

We investigated the possible role of p38 MAPK and ETB receptors in ET-1 induction of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) in cultured feline esophageal smooth muscle cells (ESMC). Confluent layers of ESMC were stimulated with 10 nM ET-1 and expression of COX-1 and COX-2, involvement of receptors, and activation of p38 MAPK, were examined by Western blot analysis. Levels of PGE2 induced by ET-1 were measured by Elisa. Using ETA and ETB antagonists (BQ-123 and BQ-788, respectively), the contribution of the ET receptors to COX-1 and COX-2 expression induced by ET-1 was determined. Western blot analysis revealed that treatment of ESMC with ET-1 resulted in transient expression of COX-2 and activation of p38 MAPK. Activation of p38 MAPK was maximal after 1 h. SB202190, a p38 MAPK inhibitor, reduced expression of COX-2, but not COX-1. ET-1induced release of PGE2 was also blocked by SB202190. COX-2 expression was upregulated only via the ETB receptor, and COX-1 expression was not affected by either antagonist. Taken together, our data suggest that ET-1 causes p38 MAPK-dependent expression of COX-2 by interacting with ETB receptors on ESMC

Influence of Nitric Oxide Synthesis Inhibition on Endothelin-1 and Its Receptor Expression in Rat Kidney

Lee, Jong Un,Kim, Soo Wan,Kim, Sun Mi,Oh, Yoon Wha,Li, Ying Shun,Kim, Nam Ho,Choi, Ki Chul 대한신장학회 2002 Kidney Research and Clinical Practice Vol.21 No.2

배 경 : 본 연구는 산화질소 합성억제 흰쥐 모델에서신장 endothelin(ET)계의 변화를 알아보고자 하였다. 방 법 : 수컷 Sprague-Dawley 흰쥐를 이용하여 실험하였다. 실험군은 내인성 산화질소 합성을 억제하고자 NG-nitro-L-arginine methyl ester(L-NAME, 100mg/L)을 4주간 음용수로 공급하였다. 대조군은 약물이 포함되지 않은 수돗물을 공급하였다. 신장에서 ET-1,ETA 및 ETB 수용체 mRNA 발현 변화는 역전사-중합효소 연쇄반응을 이용하였다. 혈장 및 신장에서 산화질소 대사물 함량을 측정하였다. 결 과 : 산화질소 합성억제제인 L-NAME 투여군에서 유의한 혈압의 상승을 보였으며, 혈장 및 신장에서 산화질소 대사물은 감소하였다. ET-1 mRNA 발현은 신피질에서 증가하였으나, 신수질에서는 유의한 변화를 보이지 않았다. 신장에서 ETA 및 ETB 수용체 발현 또한 유의한 차이를 보이지 않았다. L-NAME(200 μg/kg per min, iv)를 60분간 주사한 흰쥐에서 유의한 혈압의 증가와 함께 혈장 ET-1 농도가 증가하였다. 또한, 이때 신피질 ET-1 mRNA 발현은 증가하였으나, ETA 및 ETB 수용체 발현 또한 유의한 차이를 보이지 않았다. 결 론 : 이상의 결과는 산화질소 합성 억제에 의한 고혈압의 발생에 ET계의 활성증가가 일부 관여함을 시사한다. Background : The present study was aimed to evaluate the influence of nitric oxide( NO) synthesis inhibition on endothelin(ET) expression in rat kidney. Methods : Male Sprague-Dawley rats were treated with NG-nitro-L-arginine methyl ester(L-NAME, 100 mg/L drinking water) for 4 weeks to inhibit the endogenous synthesis of NO. The tissue expression of ET-1, ETA receptor, and ETB receptor mRNA in the kidney was determined by reverse transcription-polymerase chain reaction. Results : Tissue levels of NO metabolites were significantly decreased in the plasma and the kidney, along with the increased blood pressure. The expression of ET-1 mRNA was increased in the cortex, but not in the medulla. The expression of ETA and ETB receptor mRNA was not significantly altered either in the cortex or in the medulla. The plasma level of ET-1 peptide was significantly increased, along with the increased blood pressure, when L-NAME(200 μg/kg per min, iv) was administered in an acute preparation of animals. Accordingly, the expression of ET-1 mRNA was increased in the cortex, whereas that of ETA and ETB receptor mRNA was not altered. Conclusion : These results suggest that enhanced activity of ET system induced by NO synthesis inhibition may be associated with hypertension although direct association between two factors is not confirmed. (Korean J Nephrol 2002;21(2):205-212)

New Therapeutic Schedule for Prostatic Cancer-3 Cells with ET-1 RNAi and Endostar

Zhang, Hao-Jie,Qian, Wei-Qing,Chen, Ran,Sun, Zhong-Quan,Song, Jian-Da,Sheng, Lu Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.23

Background: Endothelin-1 and Endostar are both significant for the progression, proliferation, metastasis and invasion of cancer. In this paper, we studied the effect of ET-1 RNAi and Endostar in PC-3 prostatic cancer cells. Materials and Methods: The lentiviral vector was used in the establishment of ET-1 knockdown PC-3 cells. Progression and apoptosis were assessed by CKK-8 and flow cytometry, respectively. Transwell assay was used to estimate invasion and signaling pathways were studied by Western blotting. Results: ET-1 mRNA and protein in ET-1 knockdown PC-3 cells were reduced to 26.4% and 22.4% compared with control group, respectively. ET-1 RNAi and Endostar both were effective for the suppression of progression and invasion of PC-3 cells. From Western blotting results, the effects of ET-1 regulation and Endostar on PC-3 cells were at least related to some signaling pathways involving PI3K/Akt/Caspase-3, Erk1/2/Bcl-2/Caspase-3 and MMPs (MMP-2 and MMP-9). Furthermore, combined treatment of ET-1RNAi and Endostar was found to be more effective than single treatment. Conclusions: Both ET-1 RNAi and Endostar can inhibit the progression and invasion of PC-3 cells, but combined treatment might be a better therapeutic schedule.

16주간의 웨이트트레이닝이 비만 여성의 동맥혈류 및 혈관조절변인에 미치는 영향

장용우 한국웰니스학회 2022 한국웰니스학회지 Vol.17 No.1

This study analyzes the effect of 16-week weight training on blood flow and vascular control variables in arteries. It was classified into 10 experimental groups and 10 control groups for each group. Body fat percentage was mea- sured in obese women using Inbody 3.0, and arterial blood flow was measured using ultrasonic doppler to measure blood flow velocity and blood flow resistance of subclavicular artery vessels, and nitric oxide(NO) and endoteline1 (ET-1), which are vascular variables. In the case of blood flow rate, there was no significant change in the control group, and the experimental group showed a significant(p<.001) reduction rate of -10.7%. There was no significant change in blood flow resistance in the control group, and the experimental group showed a signif- icant(p<.001) reduction rate of -21.5%. In the case of NO, there was no significant change in the control group, and the expe- rimental group showed a significant(p<.001) increase rate of 14.2%. There was no significant change in ET-1 in the control group, and considering that the experimental group showed a significant(p<.001) reduction rate of –26.1 %, changes in average blood flow rate and blood flow resistance adapted to long-term weight training and sensitivity of NO and ET-1 could be observed. Therefore, the weight training presented in this study is interpreted as having a positive effect on the relaxation of arterial blood flow and changes in NO and ET-1, which are vascular control variables, and is intended to be presented as an efficient training program for obesity women's body fat control and blood flow. 본 연구는 16주간의 웨이트트레이닝이 동맥의 혈류와 혈관조절변인에 미치는 영향을 분석하는 것이다. 각 집단별 실험군 10명, 통제군 10명으로 분류하였다. 비만 여성을 대상으로 In body 3.0을 이용하여 체지방률의 측정하였으며, 동맥혈류는 초음파도플러를 이용한 쇄골하동맥 혈관의 혈류속도 및 혈류저항의 측정과 혈관조절변인인 산화질소(NO) 및 엔도텔린1(ET-1)을 측정 분석하였다. 혈류속도의 경우 통제군은 유의한 변화는 없었으며, 실험군은 –10.7%의 유의한(p<.001) 감소 비율로 나타났다. 혈류저항은 통제군의 경우 유의한 변화는 없었으며, 실험군은 –21.5%의 유의한(p<.001) 감소 비율을 나타냈다. NO의 경우 통제군은 유의한 변화는 없었으며, 실험군은 14.2%의 유의한(p<.001) 증가 비율로 나타났다. ET-1은 통제군의 경우 유의한 변화는 없었으며, 실험군은 –26.1%의 유의한(p<.001) 감소 비율을 나타낸 것으로 비추어볼 때 비만 여성의 혈류속도와 혈류저항의 감소 비율과 연계된 NO의 증가와 ET-1의 감소를 통해 장기간의 웨이트트레이닝에 적응된 동맥의 혈류와 혈관조절변인의 민감성에 대한 변화를 관찰 할 수 있었다. 따라서 본 연구에서 제시된 웨이트트레이닝은 여성들의 비만 해소와 더불어 동맥 혈류 유속의 완화적인 개선과 혈관조절변인인 NO와 ET-1의 변화에 긍정적인 영향을 미친 것으로 해석되며, 추후 비만 여성의 체지방 조절 및 혈류의 흐름과 혈관조절변인의 개선을 위한 효율적인 트레이닝 프로그램으로 제시하고자 한다.