• Molecules and Cells
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• 제40권2호
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• pp.123-132
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• 2017

Insulin signaling is coordinated by insulin receptor substrates (IRSs). Many insulin responses, especially for blood glucose metabolism, are mediated primarily through Irs-1 and Irs-2. Irs-1 knockout mice show growth retardation and insulin signaling defects, which can be compensated by other IRSs in vivo; however, the underlying mechanism is not clear. Here, we presented an Irs-1 truncated mutated mouse ($Irs-1^{-/-}$) with growth retardation and subcutaneous adipocyte atrophy. $Irs-1^{-/-}$ mice exhibited mild insulin resistance, as demonstrated by the insulin tolerance test. Phosphatidylinositol 3-kinase (PI3K) activity and phosphorylated Protein Kinase B (PKB/AKT) expression were elevated in liver, skeletal muscle, and subcutaneous adipocytes in Irs-1 deficiency. In addition, the expression of IRS-2 and its phosphorylated version were clearly elevated in liver and skeletal muscle. With miRNA microarray analysis, we found miR-33 was down-regulated in bone marrow stromal cells (BMSCs) of $Irs-1^{-/-}$ mice, while its target gene Irs-2 was up-regulated in vitro studies. In addition, miR-33 was down-regulated in the presence of Irs-1 and which was up-regulated in fasting status. What's more, miR-33 restored its expression in re-feeding status. Meanwhile, miR-33 levels decreased and Irs-2 levels increased in liver, skeletal muscle, and subcutaneous adipocytes of $Irs-1^{-/-}$ mice. In primary cultured liver cells transfected with an miR-33 inhibitor, the expression of IRS-2, PI3K, and phosphorylated-AKT (p-AKT) increased while the opposite results were observed in the presence of an miR-33 mimic. Therefore, decreased miR-33 levels can up-regulate IRS-2 expression, which appears to compensate for the defects of the insulin signaling pathway in Irs-1 deficient mice.

• 생명과학회지
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• 제21권2호
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• pp.242-250
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• 2011

본 연구에서는 C2C12 근육 세포에서 IGF-I이 리간드 비의존적으로 엔드로젠 수용체 coactivator 유전자 발현에 미치는 영향에 대해 알아보았다. 그 결과 IGF-I 이 리간드 비의존적으로 엔드로젠 수용체의 coactivator인 GRIP-1, SRC-1, ARA70 유전자들의 단백질과 mRNA 발현을 증가시켰으며, p38 MAPK와 ERK1/2 신호전달 경로 억제제인 SB203580과 PD98059를 IGF-I과 함께 처리한 결과 IGF-I에 의한 엔드로젠 수용체 coactivator 유전자 발현의 증가를 감소시켰음을 알 수 있었다. 엔드로젠 수용체 coactivator가 엔드로젠 물질이 없이도 IGF-I에 의해 발현이 증가하였다는 사실은 운동에 의해 근육에서 분비가 증가하는 IGF-I이 리간드 비의존적으로 근육 세포에서 엔드로젠 수용체 활성화 안정에 기여하는 엔드로젠 수용체 coactivator를 활성화 시킬 수 있다는 사실을 증명 하였다는데 의의가 있다고 사료된다. 또한, IGF-I의 하부신호전달 경로로 잘 알려진 p38 MAPK와 ERK1/2 신호전달 경로를 차단하였을 때는 발현이 억제되었는데 이를 통해 IGF-I이 근육세포 내에서 p38 MAPK, ERK1/2 경로를 통해 엔드로젠 수용체 coactivator 발현에 중요한 역할을 한다는 사실을 확인할 수 있었다. 이러한 결과는 근육에서 중요한 기능을 담당하는 IGF-I이 엔드로젠 수용체 coactivator 유전자 발현을 조절하는 기능이 있으며 이러한 IGF-I에 의한 리간드 비의존적인 엔드로젠 수용체 coactivator 유전자 발현 조절에 있어 p38 MAPK와 ERK1/2는 필수적인 신호전달 경로임을 확인하였다는 데서 그 의의가 있다고 할 수 있겠다. 향후 다양한 성장인자들에 의한 coactivator 발현에 관한 연구를 비롯하여, corepressor의 발현 억제 기능 및 신호전달 경로에 관한 연구가 추가적으로 이루어져야 할 것이다.

• 대한의생명과학회지
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• 제18권3호
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• pp.227-236
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• 2012

Previous study showed that swimming improved obesity but was not through $PPAR{\alpha}$ activation in liver and skeletal muscle in high fat diet-fed female mice with functioning ovaries as an animal model of obese premenopausal women. Thus, this study was aimed at investigation of the effects of swimming on the promotion of health and its molecular mechanism in adipose tissue of high fat diet-fed female mice. Eight-week-old female C57BL/6J mice were randomly divided into two groups (a non-swim control group and a swim group, n=8/group). Mice in the swim group swam for 2 h daily for 6 weeks in water bath with temperature of $35{\pm}1^{\circ}C$. All the animals received high fat diet (45% kcal fat) for 6 weeks. Reverse transcription-polymerase chain reaction was used to elucidate the molecular mechanism. Female mice subjected to swimming had significantly decreased body weight gain and white adipose tissue mass compared with the female control mice. Histological studies illustrated that swimming decreases the hepatic lipid accumulation. As expected, swimming did not affect the expression of mRNA levels of peroxisome proliferator-activated receptor (PPAR) ${\alpha}$ and $PPAR{\alpha}$ target genes responsible for mitochondrial fatty acid ${\beta}$-oxidation, such as carnitine palmitoyltransgerase-1 and medium chain acyl-CoA dehydrogenase in the white adipose tissue. However, mice that underwent 6-weeks of swimming exercise had decreased the mRNA expression of lipogenic genes, such as sterol regulatory element-binding proteins-1C and fatty acid synthase in comparison to sedentary control mice, with decreased $PPAR{\gamma}$ target genes involved in adipocyte-specific marker genes, such as adipocyte fatty acid binding protein and leptin in the white adipose tissue. These results suggest that swimming can effectively prevent obesity induced by high fat diet-fed, in part through down-regulation of adipogenesis and lipogenesis in white adipose tissue of female obese mice. Moreover, these results suggest that swimming maybe contributing the promotion of health through regulation of adipogenesis and lipogenesis in overweight premenopausal women.

• 대한기계학회논문집A
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• 제35권12호
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• pp.1585-1591
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• 2011

본 연구에서는 사용자의 손에 장착하여 손의 움직임을 측정하고 힘의 반영이 가능한 새로운 형태의 데이터 글로브(data glove)를 제안한다. 본 연구의 데이터 글로브는 인간의 외골격 구조의 분석이 기반하고 있으며 하나의 손가락 모듈은 4절기구의 조합을 통하여 1자유도로 구동이 되도록 고안되어 있다. 데이터 글로브는 펴기(extension)와 구부리기(flexion)를 할 수 있으며 내전(adduction)/외전(abduction)을 위해서 두 개의 유니버설 관절을 이용한 새로운 metacarpal joint 메커니즘을 고안하였다. 동 데이터 글로브의 유효성을 평가하기 위하여 검지손가락을 위한 구동회로와 센서를 포함한 전체 시스템을 제작하였으며 가상공간에 동적 시뮬레이션을 통해서 나타낸 물체를 조작하는 실험을 수행하였다.

• 셀메드
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• 제4권4호
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• pp.27.1-27.5
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• 2014

Picrorhiza kurroa Royle ex Benth. (Scrophulariaceae) is a traditional Ayurvedic herb known as Kutki. It is used as a remedy for diabetes by tribes of North Eastern Himalayan region of India. Present study was conducted to explore the mechanism of antidiabetic activity of standardized aqueous extract of Picrorhiza kurroa (PkE). PkE (100 and 200 mg/kg/day) was orally administered to streptozotocin induced diabetic rats, for 14 consecutive days. Plasma insulin levels were measured and pancreas of rat was subjected to histopathological investigations. Glucose transporter type 4 (GLUT-4) protein content in the total membrane fractions of soleus muscle was estimated by Western blot analysis. Plasma insulin level was significantly increased along with concomitant increase in GLUT-4 content of total membrane fractions of soleus muscle of diabetic rats treated with extract. There was evidence of regeneration of ${\beta}$-cells of pancreatic islets of PkE treated group in histopathological examinations. PkE increased the insulin-mediated translocation of GLUT-4 from cytosol to plasma membrane or increased GLUT-4 expression, which in turn facilitated glucose uptake by skeletal muscles in diabetic rats.

• 대한핵의학회지
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• 제34권5호
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• pp.436-437
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• 2000

A 63-year-old male who had subtotal gastrectomy for early gastric cancer three months ago underwent Tc-99m bone scintigraphy for the evaluation of skeletal metastases. He had no symptoms such as fever, tenderness, or wound discharge. On physical examination, the surgical scat along the midline of the upper abdomen had keloid formation and there was no radiographic evidence of calcification. Bone scintigraphy (Fig. 1A & 1B) demonstrated all unusual linear increased uptake along the midline of the upper abdomen that corresponded to the,skin incision for subtotal gastrectomy. Usually, an incisional scar will not be visualized in Tc-99m methylene diphosphate (MDP) scintigraphy beyond two weeks after surgery.$^{1)}$ Upon reviewing the literature, there were only a few reports where localization of Tc-99m MDP in surgical scars were found two months after surgery.$^{2)}$ It was also reported that a few cases with Tc-99m MDP uptake in the keloid scar developed after surgery. Although there are several potential mechanisms that may explain the uptake of Tc-99m MDP in scar tissue, the primary mechanism in older scars is suggested to be a result of pathological calcification.$^{2)}$ Siddiqui et al$^{3)}$ suggested it could be due to microscopic calcification in small resolving hematomas. However, the primary mechanism in keloid scar is not well-known. We should obtain oblique or lateral views to differentiate the uptake in healing surgical scars from the artifactual uptake.

• Journal of Dental Anesthesia and Pain Medicine
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• 제19권2호
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• pp.91-99
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• 2019

Background: The imbalance between osteoblasts and osteoclasts can lead to pathological conditions such as osteoporosis. It has been reported that opioid adversely affect the skeletal system, but it is inconsistent. Remifentanil is currently used as an adjuvant analgesic drug in general anesthesia and sedation. The aim of the present study was to investigate the effect of remifentanil on the osteoblast differentiation and mechanism involved in this effect. Methods: The C2C12 cells (mouse pluripotent mesenchymal cell line) were used as preosteoblast. Osteoblastic differentiation potency was determined by alkaline phosphatase (ALP) staining. C2C12 cell migration by remifentanil was evaluated using Boyden chamber migration assay. The expression of Runx2 and osterix was evaluated by RT-PCT and western blot analysis to investigate the mechanism involved in remifentanil-mediated osteoblast differentiation. Results: ALP staining showed that remifentanil increased significantly osteoblast differentiation. In Boyden chamber migration assay, C2C12 cell migration was increased by remifentanil. RT-PCR and western blot analysis showed that the expression of Runx2 and osterix was upregulated by remifentanil. Conclusions: We demonstrated that remifentanil increased osteoblast differentiation in vitro by upregulation of Runx2 and osterix expression. Therefore, remifentanil has the potential for assisting with bone formation and bone healing.

• The Korean Journal of Physiology and Pharmacology
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• 제27권1호
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• pp.75-84
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• 2023

This study aimed to observe the protective effect of momordicine I, a triterpenoid compound extracted from momordica charantia L., on isoproterenol (ISO)-induced hypertrophy in rat H9c2 cardiomyocytes and investigate its potential mechanism. Treatment with 10 μM ISO induced cardiomyocyte hypertrophy as evidenced by increased cell surface area and protein content as well as pronounced upregulation of fetal genes including atrial natriuretic peptide, βmyosin heavy chain, and α-skeletal actin; however, those responses were markedly attenuated by treatment with 12.5 ㎍/ml momordicine I. Transcriptome experiment results showed that there were 381 and 447 differentially expressed genes expressed in comparisons of model/control and momordicine I intervention/model, respectively. GO enrichment analysis suggested that the anti-cardiomyocyte hypertrophic effect of momordicine I may be mainly associated with the regulation of metabolic processes. Based on our transcriptome experiment results as well as literature reports, we selected glycerophospholipid metabolizing enzymes group VI phospholipase A₂ (PLA2G6) and diacylglycerol kinase ζ (DGK-ζ) as targets to further explore the potential mechanism through which momordicine I inhibited ISO-induced cardiomyocyte hypertrophy. Our results demonstrated that momordicine I inhibited ISO-induced upregulations of mRNA levels and protein expressions of PLA2G6 and DGK-ζ. Collectively, momordicine I alleviated ISO-induced cardiomyocyte hypertrophy, which may be related to its inhibition of the expression of glycerophospholipid metabolizing enzymes PLA2G6 and DGK-ζ

• 대한소아치과학회지
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• 제50권4호
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• pp.483-494
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• 2023

이 논문은 저한성 외배엽 이형성증(Hypohidrotic Ectodermal Dysplasia, HED)으로 인한 부분무치증을 가진 소아 환자에게 의치의 유지력 증가 방법에 관한 두 가지 증례를 보고한다. 두 환자 모두 다수의 치아 결손 및 원추형의 견치와 치조골 위축, 골격적 III급 경향이 나타났다. 첫 번째 증례에서는, 변형된 형태의 Conical-Crown Retained Denture (CCRD)를 이용해 견치를 피개하였다. 이 방법은 치아를 삭제하거나 코핑 없이 진행되었다. 두 번째 증례에서는, 심한 치조제 흡수와 함께 하악 좌측 견치가 원심으로 경사지어 맹출한 상황에서, 하이브리드 세라믹 크라운을 사용하여 견치를 수복한 후, 흡착성 원리를 이용한 클라스프 유지 가철식 의치로 변경하였다. 두 환자는 현재 보철물 유지 관리 및 성장양상을 평가하기 위해 주기적으로 치료를 받고 있다. 이 증례는 HED로 인하여 의치의 유지력이 부족한 소아 환자에게 적용된 창의적인 보철 치료 방법을 제시하였다.

• Asian-Australasian Journal of Animal Sciences
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• 제22권10호
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• pp.1447-1460
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• 2009

Myogenic satellite cells have been isolated and identified by several recently elucidated molecular markers. Furthermore, knowledge about the precise function of these markers has provided insight into the early and terminal events of satellite cells during proliferation, differentiation, transdifferentiation, specification and activation. Recently, quiescent myogenic satellite cells have been associated with possession of Pax 3 and 7 that represent pluripotent stem cells capable of differentiating into other lineages. However, the mechanism by which myogenic satellite cells attain pluripotent potential remain elusive. Later, transdifferentiating ability of these cells to another lineage in the absence or presence of certain growth factor/ or agents has revolutionized the scope of these pluripotent myogenic satellite cells for manipulation of animal production (in terms of quality and quantity of muscle protein) and health (in terms of repair of skeletal muscle, cartilage or bone).