• 운동영양학회지
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• 제24권3호
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• pp.13-18
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• 2020

[Purpose] In vivo studies have demonstrated the ergogenic benefits of eleutherococcus senticosus (ES) supplementation. ES has been observed to enhance endurance capacity, improve cardiovascular function, and alter metabolic functions (e.g., increased fat utilization); however, the exact mechanisms involved remain unknown. We aimed to determine whether ES could effectively induce fat loss and improve muscle metabolic profiles through increases in lipolysis- and lipid metabolism-associated protein expression in 3T3-L1 adipocytes and C2C12 skeletal muscle cells, respectively, to uncover the direct effects of ES on adipocytes and skeletal muscle cells. [Methods] Different doses of ES extracts (0.2, 0.5, and 1.0 mg/mL) were added to cells (0.2 ES, 0.5 ES, and 1.0 ES, respectively) for 72 h and compared to the vehicle control (control). [Results] The intracellular triacylglycerol (TG) content significantly decreased (p < 0.05 for 0.2 ES, p < 0.01 for 0.5 ES and 1.0 ES) in 3T3-L1 cells. Adipose triglyceride lipase, which is involved in active lipolysis, was significantly higher in the 1.0 ES group than in the control group (p < 0.01) of 3T3-L1 adipocytes. In C2C12 cells, the mitochondrial protein voltage-dependent anion channel (VDAC) was significantly increased in the 1.0 ES group (p < 0.01). Furthermore, we found that 1.0 ES activated both 5' AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) in skeletal muscle cells (p < 0.01). [Conclusion] These findings suggest that ES extracts decreased TG content, presumably by increasing lipase in adipocytes and metabolism-associated protein expression as well as mitochondrial biogenesis in muscle cells. These effects may corroborate previous in vivo findings regarding the ergogenic effects of ES supplementation.

• PNF and Movement
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• 제2권1호
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• pp.35-47
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• 2004

Purpose : The purpose of this article was to review the literature on contractile properties of skeletal muscle with reference to its molecular and functional diversity. Method : This review outlines scientific findings regarding different contractile properties in skeletal muscle fibers, and discusses their involvement in functional diversity. Result & Conclusions: Muscle fibers possess distinct mechanical and energetic properties. Myosis, one of the primary contractile muscle proteins, displays structural, functional variability and plays the role of the molecular motor of muscle contraction. Muscle satellite cells are normally mitotically quiescent, but initiate proliferation and give rise to daughter myogenic precursor cells as required for the postnatal growth and regeneration of adult muscle. Passive extensibility is an important component of total muscle function because it allows for the maximal length of skeletal muscles. Proprioceptive neuromuscular facilitation(PNF) stretching can help to restore or improve flexibility and coordination, thereby improving overall muscle function.

• The Journal of Korean Physical Therapy
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• 제20권3호
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• pp.53-59
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• 2008

Purpose: The non-receptor-type protein tyrosine kinase Syk (636 amino acids, 72 kDa) is ubiquitously expressed in hematopoietic stem cells and has been widely studied as a regulator and effector of B cell receptor signaling that occurs in processes such as differentiation, proliferation and apoptosis. However, the mechanism relating Syk and p38 mitogen-activated protein kinases (p38MAPK) by endothelin-1 (ET-1, 21 amino acids) stimulation in muscle cells, especially in the volume-dependent hypertensive state, remains unclear. Methods: In this study, we investigated the relationship between Syk and p38MAPK for isometric contraction and enzymatic activity by ET-1 from rat aortic smooth muscle cells and aldosterone-analogue deoxycorticosterone acetate (DOCA) hypertensive state rats (ADHR). Results: The systolic blood pressure was significantly increased in ADHR than in a control group of animals. ET-1 induced isometric contraction and phosphorylation of p38MAPK, which was increased in muscle strips from ADHR. Increased vasoconstriction and phosphorylation of p38MAPK induced by treatment with 30 nM ET-1 were inhibited by the use of 10${\mu}M$ SB203580, an inhibitor of p38MAPK from ADHR. Furthermore, ET-1 induced isometric contraction and phosphorylation of Syk and p38MAPK, which were increased in the aortic smooth muscle cells. Increased tension and phosphorylation of Syk and p38MAPK induced by ET-1 were inhibited by SB203580 from rat aortic smooth muscle cells. Conclusion: These results, suggest that the Syk activity affects ET-1-induced contraction through p38MAPK in smooth muscle cells and that the same pathway directly or indirectly is associated with volume dependent hypertension. The findings suggest the need to develop cardiovascular disease-specialized physical therapy.

• International Journal of Oral Biology
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• 제41권4호
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• pp.217-223
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• 2016

Porphyromonas gingivalis, a foremost periodontal pathogen, has been known to cause periodontal diseases. Epidemiologic evidences have indicated the involvement of P. gingivalis in the development of cardiovascular diseases. In this study, we show that the P. gingivalis lipopolysaccharide increases the mRNA expression and protein secretion of interleukin-6 in vascular smooth muscle cells. We demonstrate that P. gingivalis LPS activates the extracellular signal-regulated kinase 1/2 (ERK1/2), p38 mitogen-activated protein kinase (MAPK), and Akt, which mediate the IL-6 expression in vascular smooth muscle cells. Also, P. gingivalis LPS stimulates the vascular smooth muscle cell migration, which is a critical step for the progression of atherosclerosis. Moreover, neutralization of the IL-6 function inhibits the migration of vascular smooth muscle cells induced by P. gingivalis LPS. Taken together, these results indicate that P. gingivalis LPS promotes the expression of IL-6, which in turn increases the migration of vascular smooth muscle cells.

• 동의생리병리학회지
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• 제19권5호
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• pp.1356-1362
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• 2005

The purpose of this study os to investigative the effect of Carrageenan-Induced Pain on lower limb muscle and ligament of rat. To evaluate pain mechanism in muscle and ligament, pain was induced by the injection of 2% $0.1m{\ell}$ carrageenan into the left lower limb muscle of rats after rats were anesthesized with 3% enflurane. Rats were killed on 72 hours after pain induction under the anesthesia. anterior rectus femoris muscle and its ligament were removed from rat hind limb. Morphological changes of them were peformed by the observation of light and electron microscopes. In the light microscopic findings, the muscle cells were polyheadral and situated with each other without small gap in control group. nucleus of cell was seen along the cell margin, and muscle cell groups were divided by regular narrow gap in cross section. In the pain-induced group, muscle cell groups were divided each other by the irregular gap, and some of groups formed larger than other cell groups by the fusion. Intercellular gap of most cell groups were increased compared with control groups. And also, perimysium of muscle cell groups was swollen in cross section. In control group, muscle cells contacted each other closely and each cell was divided by perimysium. The intracellular gaps were not seen between myofibrills, and also striations were well defined between muscle cells in longitudinal section. In pain-induced group, muscle cells were divided by the small intracellular gaps. And also, muscle cell showed many a short cross or longitudinal intercellular gaps in longitudinal section. In light microscopic findings of control group, tendon was composed with many tendon fibers contacted each other closely without gap. The free margin of tendon was fused, and apso the tendon fibers did not invaded between muscles. In pain-induced group, tendon was divided small groups by intertendinous gap, and also the margin of tendon divided by small groups. In the free margin, tendon invaded into muscle cells, and also fibroblasts between tendon fibers were long and lance-shaped. From these results, it is suggested that pain induction by carrageenan injured rat skeletal muscle and ligament by the morphological changes.

• Applied Microscopy
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• 제33권4호
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• pp.325-333
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• 2003

왕거미과 산왕거미(Araneus ventricosus)의 심관과 심근세포의 미세구조적 특성을 주사형 및 투과형 전자현미경으로 관찰하였다. 거미의 심관은 복부마디의 등쪽에 분포되어 있고, 심외막과 심근층으로 구성되어 있었다. 심근층의 근섬유들은 종축을 중심으로 나선상의 배열을 이루고 있었고, 내막이 없이 혈림프에 직접 노출되는 구조를 이루고 있었다. 심관의 외부 표면에서는 3쌍의 심문이 형성되어 있었고, 내강에서는 원형질혈구와 과립혈구, 그리고 편도혈구 등 다양한 유형의 혈구들이 관찰되었다. 특히 심관의 내강을 향해 돌출된 심근돌기 주위에서는 편도혈구들이 대부분을 차지하고 있었다. 편도혈구의 세포질에는 유리 리보조옴이 산재되어 있었고 핵에는 이질염색질과 인이 발달되어 있었으나, 심근층 조직과의 특이한 연접은 관찰되지 않았다. 심근층에는 횡문이 형성되어 있었고, Z-line을 중심으로 근절의 구조를 이룬 근원섬유의 주위에서는 미토콘드리아와 근소포체가 풍부하게 함유되어 있었다. 심관의 배면을 따라 뻗은 신경절의 축삭들이 심근세포와 신경근육간 연접부를 형성하고 있음이 관찰되었다.

• The Korean Journal of Physiology
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• 제28권2호
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• pp.151-157
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• 1994

Intracellular free $Ca^{2+}$ contributes to regulation of various events occurring in vascular smooth muscle cells. One of these events is modulating the membrane iou currents. Single smooth muscle cells were isolated from rabbit mesenteric artery. Three kinds of $Ca^{2+}-activated\;current$ were studied with the patch clamp method. $Ca^{2+}-activated\;K^+\;current$ with a large oscillation was recorded in the depolarized potential range. The single channel conductance of this current was about 250 pS. It was abolished by replacing intracellular $K^+\;with\;Cs^+$. A $Ca^{2+}-activated$ nonselective cation current was observed in both the depolarized and hyperpolarized potential ranges. And it was blocked by replacement of extracellular $Na^+$ with N-methylglucamine (NMG) or extracellular application of $Cd^{2+}$. $Ca^{2+}-activated\;Cl^-\;current$ was revealed in the whole voltage range and was blocked by niflumic acid. These results indicate that at least three kinds of $Ca^{2+}-activated$ ionic currents exist in smooth muscle cells from rabbit superior mesenteric artery.

• KSBB Journal
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• 제11권1호
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• pp.52-57
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• 1996

평활근 세포에 대한 shear stress의 영향을 알아보기 위해 슬라이드 글라스위에 배양된 牛 대통맥의 평활근 세포를 120시간 동안 0~26 dyn/$cm^2$의 각기 다른 일정한 shear stress의 유체에 노출하였다. 실험 장치를 순환하는 배지의 lactate dehydrogen­a ase의 농도측정 결과, 본 연구에서 적용된 shear stress 범위에서는 유체의 흐름으로 인하여 세포가 슬라이드 글라스 표면으로부터 이탈되는 현상은 없었다. 표면 $cm^2$ 당 존재하는 세포의 수를 측정한 결과, 평활근 세포는 정체배양시 가장 빨리 성장하였다. 표변에서의 shear stress가 증가할수록 i영활근 세포의 성장은 늦었으며, shear stress가 17 dyn/$cm^2$ 이상에서는 세포의 성장이 관찰되지 않았다.

• Molecules and Cells
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• 제27권4호
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• pp.403-408
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• 2009

Skeletal muscle regeneration is a highly orchestrated process initiated by activation of adult muscle satellite cells. Upon muscle injury, the inflammatory process is always accompanied by muscle regeneration. Leukotriene $B_4$ is one of the essential inflammatory mediators. We isolated and cultured primary satellite cells. RT-PCR showed that myoblasts expressed mRNA for $LTB_4$ receptors BLT1 and BLT2, and $LTB_4$ promoted myoblast proliferation and fusion. Quantitative real-time PCR and immunoblotting showed that $LTB_4$ treatment expedited the expression process of differentiation markers MyoD and M-cadherin. U-75302, a specific BLT1 inhibitor, but not LY2552833, a specific BLT2 inhibitor, blocked proliferation and differentiation of myoblasts induced by $LTB_4$, which implies the involvement of the BLT1 pathway. Overall, the data suggest that $LTB_4$ contributes to muscle regeneration by accelerating proliferation and differentiation of satellite cells.

• BMB Reports
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• 제56권3호
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• pp.160-165
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• 2023

Vascular calcification is common in cardiovascular diseases including atherosclerosis, and is associated with an increased risk of pathological events and mortality. Some semaphorin family members play an important role in atherosclerosis. In the present study, we show that Semaphorin 4D/Sema4D and its Plexin-B1 receptor were significantly upregulated in calcified aorta of a rat chronic kidney disease model. Significantly higher Sema4D and Plexin-B1 expression was also observed during inorganic phosphate-induced calcification of vascular smooth muscle cells. Knockdown of Sema4D or Plexin-B1 genes attenuated both the phosphate-induced osteogenic phenotype of vascular smooth muscle cells, through regulation of SMAD1/5 signaling, as well as apoptosis of vascular smooth muscle cells, through modulation of the Gas6/Axl/Akt survival pathway. Taken together, our results offer new insights on the role of Sema4D and Plexin-B1 as potential therapeutic targets against vascular calcification.