• Journal of Animal Science and Technology
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• 제49권6호
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• pp.719-728
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• 2007

CSRP3, APOBEC2, CAV1, CAV2 및 CAV3 유전자들은 포유동물에서 도체와 육질 형질에 중요한 역할을 하는 것으로 보고되고 있다. 따라서, 이 유전자들의 단일염기다형(Single nucleotide poly- morphism; SNP)을 8개의 다른 소의 품종에서 확인한 결과 coding region에서 caveolin family 유전자에서 9개의 SNP, CSRP3유전자에서 1개의 SNP 및 APOBEC2 유전자에서 3개의 SNP가 존재함을 확인하였다. 이 coding region의 SNP들은 PCR-RFLP 방법에 의해 재확인하였으며 이들 유전자의 intronic region에서도 9개의 SNP가 존재함을 확인할 수 있었다. 8개의 다른 품종 소에 각 유전자들의 SNP들을 이용하여 유전자 빈도를 확인한 결과 CAV2, CAV3, CSRP3 및 APOBEC2 유전자의 SNP 중에서 5개가 품종간에서 유의적으로 차이가 있음을 확인할 수 있었다. 이 SNP들은 차후 검증작업을 통하여 육질관련 형질 마커로 이용될 수 있을 것으로 사료된다.

• 동의생리병리학회지
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• 제20권1호
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• pp.174-180
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• 2006

We examine the effect of Geiji-Bokryung-Hwan(GBH) on erectile function in a rat model of hypercholesterolemic erectile dysfunction. GBH, a drug preparation consisting of five herbs of Cinnamomi Ramulus (Geiji), Poria Cocos (Bokryun), Mountan Cortex Radicis (Mokdanpi), Paeoniae Radix (Jakyak), and Persicae Semen (Doin) is a traditional Korean herbal medicine that is widely used in the treatment of atherosclerosis-related disorders. In this study, 3-month-old Sprague-Dawley rats were used. The 6 rats control animals were fed a normal diet and the other 18 rats were fed 1% cholesterol diet for 3 months. After 1 months, GBH was added to the drinking water of the treatment group of 12 rats but not the cholesterol only group of 6 rats. Of the 12 rats 6 received 30 mg/kg per day (group 1) and 6 received 60 mg/kg per day (group 2) of GBH. At 3 months erectile function was evaluated with cavernous nerve electrostimulation in all animals. Penile tissues were collected for electron microscopy, and to perform Western blot for endothelial nitric oxide synthase (eNOS), neuronal nitric oxide synthase (nNOS), basic fibroblast growth factor (bFGF) and caveolin-1. Systemic arterial pressure was not significantly different between the animals that were fed the 1% cholesterol diet and the controls. Conversely erectile function was not impaired in the herbal medicine treated rats. Electron microscopy showed many caveolae with fingerlike processes in the cavernous smooth muscle and endothelial cell membranes in control and treated rats but not in the cholesterol only group of rats. Western blot showed differences among groups in protein expression for eNOS, nNOS, caveolin-1 and bFGF protein expression in penile tissue. Increased eNOS and nNOS protein expressions dy high cholesterol diet were significantly decreased in group 1 and group 2. Interestingly, caveolin-1 and bFGF protein expression was significantly higher in groups 1 and 2 than in the cholesterol only and control groups.

• 한국생명과학회:학술대회논문집
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• 한국생명과학회 2002년도 제38회 학술심포지움
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• pp.3-12
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• 2002

• The Korean Journal of Physiology and Pharmacology
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• 제12권4호
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• pp.143-148
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• 2008

Caveolin-1 (CAV1) is an integral membrane protein that may function as a scaffold for plasma membrane proteins and acts as a tumor suppressor protein. One causative factor of chemotherapy-resistant cancers is P-plycoprotein (P-gp), the product of the multidrug resistance-1 gene (MDR1), which is localized in the caveolar structure. Currently, the interactive roles of CAV1 and MDR1 expression in the death of cancer cells remain controversial. In this study, we investigated the effects of indomethacin on the cell viability and the expression levels of MDR1 mRNA and protein in a CAV1-siRNA-mediated gene knockdown hepatoma cell line (SK-Hep1). Cell viability was significantly decreased in CAV1-siRNA-transfected cells compared with that of control-siRNA-transfected cells. Furthermore, the viability of cells pretreated with CAV1 siRNA was markedly decreased by treatment with indomethacin (400${\mu}$M for 24 h). However, the protein and mRNA levels of MDR1 were unchanged in CAV1-siRNA-transfected cells. These results suggest that CAV1 plays an important role as a major survival enzyme in cancer cells, and indomethacin can sensitively induce cell death under conditions of reduced CAV1 expression, independent of MDR1 expression.

• Molecules and Cells
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• 제45권12호
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• pp.950-962
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• 2022

Aging is a major risk factor for common neurodegenerative diseases. Although multiple molecular, cellular, structural, and functional changes occur in the brain during aging, the involvement of caveolin-2 (Cav-2) in brain ageing remains unknown. We investigated Cav-2 expression in brains of aged mice and its effects on endothelial cells. The human umbilical vein endothelial cells (HUVECs) showed decreased THP-1 adhesion and infiltration when treated with Cav-2 siRNA compared to control siRNA. In contrast, Cav-2 overexpression increased THP-1 adhesion and infiltration in HUVECs. Increased expression of Cav-2 and iba-1 was observed in brains of old mice. Moreover, there were fewer iba-1-positive cells in the brains of aged Cav-2 knockout (KO) mice than of wild-type aged mice. The levels of several chemokines were higher in brains of aged wild-type mice than in young wild-type mice; moreover, chemokine levels were significantly lower in brains of young mice as well as aged Cav-2 KO mice than in their wild-type counterparts. Expression of PECAM1 and VE-cadherin proteins increased in brains of old wild-type mice but was barely detected in brains of young wild-type and Cav-2 KO mice. Collectively, our results suggest that Cav-2 expression increases in the endothelial cells of aged brain, and promotes leukocyte infiltration and age-associated neuroinflammation.

• Journal of Applied Biological Chemistry
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• 제66권
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• pp.311-319
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• 2023

Caveolin-1 (Cav-1) is the main structural component of the caveolae on the plasma membrane, which regulates various cellular processes, including cell growth, differentiation, and endocytosis. Although a recent study demonstrated that Cav-1 might be involved in diabetes-associated inflammation, its exact role in the intestine was unclear. In this study, we examined the intestinal expression of Cav-1 in diabetic conditions. We also investigated its effect on lipopolysaccharide (LPS)-induced inflammation by expressing this protein in human intestinal Caco-2 cells lacking Cav-1. We observed that increased Cav-1 levels and decreased expression of tight junction proteins affected intestinal permeability in high-fat diet-induced diabetic mice. When Caco-2 cells were treated with LPS, Cav-1 enhanced the NF-κB signaling. Moreover, LPS reduced the expression of tight junction proteins while it increased cell-cell permeability and reactive oxygen species generation in Caco-2 cells and this effect was amplified by cav-1 overexpression. LPS treatment promoted phosphorylation of tyrosine-14 (Y14) on Cav-1, and the LPS-induced NF-κB signaling was suppressed in cells expressing non-phosphorylatable Cav-1 (tyrosine-14 to phenylalanine mutant), which reduced intestinal barrier permeability. These results suggest that Cav-1 expression promotes LPS-induced inflammation in Caco-2 cells, and phosphorylation of Y14 on Cav-1 might contribute to the anti-inflammatory response in LPS-induced NF-κB signaling and cell permeability.

• Asian Pacific Journal of Cancer Prevention
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• 제14권4호
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• pp.2295-2299
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• 2013

Background: To explore the role of caveolin-1(CAV-1) gene silencing on MAPK activation in lipopolysaccharide (LPS)-challenged human mammary epithelial cells. Methods: We established a MCF-10ACE of CAV-1 gene silencing from human mammary epithelial cell line MCF-10A by RNAi technology. DNA Microarray were used to detect the expression of inflammation-associated genes in MCF10ACE. Western blotting was used to examine the activation of MAPK in lipopolysaccharide(LPS)-challenged MCF-10A and MCF-10ACE. Moreover, immunofluorescence and Western bloting were performed to detect the co-localization of CAV-1 and toll-like receptor 4 (TLR4) in human mammary epithelial cells. Results: MCF-10ACE exhibited significant increases in inflammation-associated gene expression, especially IL-6 (~7-fold) and IL6R (~17-fold). In addition, LPS-induced p38 MAPK and JNK MAPK activation was significantly increased in MCF-10ACE. Furthermore, CAV-1 co-localized with TLR4 and appeared a negative correlation trend. Conclusion: CAV-1 gene silencing promotes MAPK activation via TLR4 signaling in human mammary epithelial cells response to LPS.

• Asian Pacific Journal of Cancer Prevention
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• 제15권19호
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• pp.8367-8370
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• 2014

The relationship between caveolin-1 (Cav-1) and clinicopathological characteristics of gastric cancer is controversial, although Cav-1 plays an important role in tumor metastasis. To evaluate the clinicopathological and prognostic value of expression in patients with gastric cancer, a meta-analysis was performed to investigate the impact on clinicopathological parameters and prognosis in gastric cancer cases. Studies assessing these parameters for Cav-1 in gastric cancer were identified up to June 2014. Finally, a total of six studies met the inclusion criteria. Our combined results showed that Cav-1 expression was significantly associated with the Lauren classification (pooled OR=0.603, 95% CI: 0.381-0.953, P=0.030). Furthermore, we found that Cav-1 expression predicted a better overall survival in gastric cancer patients (pooled OR=0.590, 95% CI: 0.360-0.970, P=0.038, fixed-effect). In conclusion, the overall data of the present meta analysis showed that Cav-1 expression was not correlated with clinicopathological features except for the Lauren classification. Simultaneously, Cav-1 overexpression predicted a better overall survival in gastric cancer. Cav-1 expression in tumors is a candidate positive prognostic biomarker for gastric cancer patients.

• 한국환경과학회:학술대회논문집
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• 한국환경과학회 2008년도 추계학술발표회 발표논문집
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• pp.538-544
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• 2008

Activated protein C (APC) is thought to exert antiinflammatory activities through the endothelial protein C receptor (EPCR)-dependent cleavage of protease activated receptor 1 (PAR-1) in endothelial cells. Since thrombin cleaves PAR-1 with $\sim$3-4-orders of magnitude higher efficiency, and PAR-1 is a target for proinflammatory activities of thrombin, it is not understood how APC can elicit protective responses through the cleavage of PAR-1. In this study, we demonstrate that EPCR is associated with caveolin-1 in endothelial lipid rafts, but its occupancy by protein C leads to its dissociation from caveolin-1 and subsequent recruitment of PAR-1 to protective signaling pathways through the coupling of PAR-1 to Gi-protein. When EPCR is bound by protein C, the PAR-1-dependent protective response in endothelial cells can be mediated by either thrombin or APC. These results provide a new paradigm for understanding the mechanism through which PAR-1 and EPCR participate in cellular signaling events in endothelial cells.

• 생명과학회지
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• 제16권6호
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• pp.955-959
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• 2006

단백질의 serine 및 threonine 잔기에 O-linked N-acetylglucosamine (O-GlcNAc)의 수식은 핵단백질과 세포질 단백질의 주요 조절인자로 부각되고 있다. 본 연구에서는 GlcNAc를 인산화시켜 GlcNAc 6-phosphate로 만드는 GlcNAc kinase (NAGK, EC2.7.1.59)의 세포내 표현을 면역화학적 방법으로 조사하였다. 배양한 해미신경세포에서 NAGK는 가지돌기를 따라 점박이(punctae)를 형성하였으며, 이 점박이들은 caveolin-1 혹은 flotillin 항체에도 염색이 되었다. 이들은 각각 caveolac와 lipid raft의 표지단백질이기 때문에 본 연구결과는 NAGK가 세포막의 이러한 특수 미세부분(microdomain)에 존재함을 의미하며, 이 미세부분에서 아직 알려지지 않은 어떤 기능을 할 것을 시사한다.