• 제목/요약/키워드: Signalling

검색결과 560건 처리시간 0.033초

Beneficial effects of naringenin and morin on interleukin-5 and reactive oxygen species production in BALB/c mice with ovalbumin-induced asthma

  • Qi, Peng;Wei, Chunhua;Kou, Dianbo
    • The Korean Journal of Physiology and Pharmacology
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    • 제25권6호
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    • pp.555-564
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    • 2021
  • We investigated the effects of naringenin and morin on IL-5 and ROS production in PMA+ionomycin-treated EL-4 cells with the corroboration of their antioxidant and anti-inflammatory properties using an asthma-induced mouse model. The EL-4 cell line was used to study the outcomes of naringenin or morin, followed by cell viability studies. Western blot analysis and ELISA test were used to determine Th2 mediated cytokines. In vivo studies were carried out on BALB/c mice to induce allergic asthma using ovalbumin administered intraperitoneally. Intracellular ROS was determined using 2',7'-dichlorodihydrofluorescein diacetate, followed by serum enzymatic (AST and ALT) estimations and inflammatory cell count in the bronchoalveolar lavage fluid (BALF) and lung tissues. Histopathological studies were conducted to examine lung tissue-stained architecture. Our findings suggested that naringenin and morin significantly suppressed IL-5 and ROS production via various pathways. Interestingly, by reducing NFAT activity, naringenin and morin stimulated HO-1 expression, thereby suppressing IL-5 secretion due to regulating the transcription factor Nrf2 via P13/Akt or ERK/JNK signalling pathways in EL-4 cells, demonstrating the involvement of HO-1 expression in inhibiting asthmatic inflammation. The increased inflammatory cells in the BALF were substantially decreased by both naringenin and morin, followed by inhibition in the elevated Th-2 cytokines levels. The TNF-α protein levels in an allergic asthma mouse model were significantly reduced by suppressing Akt phosphorylation and eosinophil formation. Recent findings confirmed that naringenin and morin possess the potential to control asthma-related immune responses through antioxidant and anti-inflammatory properties, indicating potential therapeutic agents or functional foods.

Knockdown of LKB1 Sensitizes Endometrial Cancer Cells via AMPK Activation

  • Rho, Seung Bae;Byun, Hyun Jung;Kim, Boh-Ram;Lee, Chang Hoon
    • Biomolecules & Therapeutics
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    • 제29권6호
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    • pp.650-657
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    • 2021
  • Metformin is an anti-diabetic drug and has anticancer effects on various cancers. Several studies have suggested that metformin reduces cell proliferation and stimulates cell-cycle arrest and apoptosis. However, the definitive molecular mechanism of metformin in the pathophysiological signaling in endometrial tumorigenesis and metastasis is not clearly understood. In this study, we examined the effects of metformin on the cell viability and apoptosis of human cervical HeLa and endometrial HEC-1-A and KLE cancer cells. Metformin suppressed cell growth in a dose-dependent manner and dramatically evoked apoptosis in HeLa cervical cancer cells, while apoptotic cell death and growth inhibition were not observed in endometrial (HEC-1-A, KLE) cell lines. Accordingly, the p27 and p21 promoter activities were enhanced while Bcl-2 and IL-6 activities were significantly reduced by metformin treatment. Metformin diminished the phosphorylation of mTOR, p70S6K and 4E-BP1 by accelerating adenosine monophosphate-activated kinase (AMPK) in HeLa cancer cells, but it did not affect other cell lines. To determine why the anti-proliferative effects are observed only in HeLa cells, we examined the expression level of liver kinase B1 (LKB1) since metformin and LKB1 share the same signalling system, and we found that the LKB1 gene is not expressed only in HeLa cancer cells. Consistently, the overexpression of LKB1 in HeLa cancer cells prevented metformin-triggered apoptosis while LKB1 knockdown significantly increased apoptosis in HEC-1-A and KLE cancer cells. Taken together, these findings indicate an underlying biological/physiological molecular function specifically for metformin-triggered apoptosis dependent on the presence of the LKB1 gene in tumorigenesis.

드론 기반의 무선 통신 시스템에서 주파수 효율 향상을 위한 확률적 핸드오버 기법 (A Probabilistic Handover Scheme for Enhancing Spectral Efficiency in Drone-based Wireless Communication Systems)

  • 장환원;우동혁;황호영
    • 한국정보통신학회논문지
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    • 제25권9호
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    • pp.1220-1226
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    • 2021
  • 본 논문에서는 기지국의 역할을 수행하는 드론을 기반으로 하는 무선 통신 시스템에서 주파수 효율 성능 향상을 위한 확률적 핸드오버 기법을 제안한다. 제안하는 기법은 이동하는 드론 기지국이 지상에 위치한 사용자 단말에게 서비스를 제공하는 무선 네트워크 환경에서 드론 기지국과 사용자 단말 간 거리 및 소규모 페이딩을 고려하여 드론기지국들 간의 핸드오버를 수행한다. 또한, 제안하는 기법은 빈번한 핸드오버 수행 시 발생할 수 있는 시그널링 오버헤드를 완화하기 위해 드론 기지국들 간 핸드오버를 수행할 확률을 고려한다. 드론 기반 무선 통신 시스템에서의 시뮬레이션을 통해 제안하는 핸드오버 기법 및 기존 핸드오버 기법의 주파수 효율 성능 및 핸드오버 확률을 평가한다. 시뮬레이션 결과를 통해 드론 기지국과 사용자 단말 간의 거리만을 고려한 기존의 핸드오버 기법보다 제안하는 핸드오버 기법에서 더 높은 평균 주파수 효율 성능이 나타남을 보인다.

Overexpression of CXCL2 inhibits cell proliferation and promotes apoptosis in hepatocellular carcinoma

  • Ding, Jun;Xu, Kangdi;Zhang, Jie;Lin, Bingyi;Wang, Yubo;Yin, Shengyong;Xie, Haiyang;Zhou, Lin;Zheng, Shusen
    • BMB Reports
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    • 제51권12호
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    • pp.630-635
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    • 2018
  • C-X-C motif chemokine ligand 2 (CXCL2) is a small secreted protein that exhibits a structure similar to the proangiogenic subgroup of the CXC chemokine family. Recently, accumulating evidence suggests that chemokines play a pivotal role in cancer progression and carcinogenesis. We examined the expression levels of 7 types of $ELR^+$ CXCLs messenger RNA (mRNA) in 264 clinical samples. We found that CXCL2 expression was stably down-regulated in 94% of hepatocellular carcinoma (HCC) specimens compared with paired adjacent normal liver tissues and some HCC cell lines. Moreover, CXCL2 overexpression profoundly attenuated HCC cell proliferation and growth and induced apoptosis in vitro. In animal studies, we found that overexpressing CXCL2 by lentivirus also apparently inhibited the size and weight of subcutaneous tumours in nude mice. Furthermore, we demonstrated that CXCL2 induced HCC cell apoptosis via both nuclear and mitochondrial apoptosis pathways. Our results indicate that CXCL2 negatively regulates the cell cycle in HCC cells via the ERK1/2 signalling pathway. These results provide new insights into HCC and may ultimately lead to the discovery of innovative therapeutic approaches of HCC.

렌티큘러 기법을 적용한 새로운 녹색점멸신호 시스템 디자인 (Design of new green flashing signal system using the Lenticular technique)

  • 이현욱;오광명
    • 한국융합학회논문지
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    • 제10권9호
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    • pp.111-117
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    • 2019
  • 본 연구에서는 렌티큘러 기법을 사용하여 새로운 신호등을 제안하는 것으로 녹색점멸신호일 때, 횡단보도에 진입한 보행자와 진입하지 않은 보행자의 신호를 달리 보이게 하여 무분별하고 무리한 횡단으로 인해 일어나는 인사사고를 예방하고자 한다. 연구는 렌티큘러 신호등의 도입 가능성을 검토하고자 렌티큘러 기법을 적용시킨 프로토타입을 제작하고, 소수의 피실험자로 횡단보도 내에서 가상 상황을 통해 렌티큘러 신호등 인지 실험을 진행하였다. 실험결과로 피실험자들은 거리에 따라 적색점멸신호와 녹색점멸신호를 정상적으로 구분할 수 있었다. 이를 바탕으로 렌티큘러 신호 등의 도입 가능성을 발견하였고, 이는 차후 횡단보도 내에서 보행자의 무분별한 횡단을 막을 수 있고, 인사사고를 감소시킬 수 있을 것이다. 또한 조금 더 심도 깊은 연구를 통해 향후 실제 신호등으로 제작하고, 실험하여 도입방안에 대해 적극적으로 검토할 것이다.

Soybean Fermented with Bacillus amyloliquefaciens (Cheonggukjang) Ameliorates Atopic Dermatitis-Like Skin Lesion in Mice by Suppressing Infiltration of Mast Cells and Production of IL-31 Cytokine

  • Cho, Byoung Ok;Shin, Jae Young;Kim, Ji-su;Che, Denis Nchang;Kang, Hyun Ju;Jeong, Do-Youn;Jang, Seon Il
    • Journal of Microbiology and Biotechnology
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    • 제29권5호
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    • pp.827-837
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    • 2019
  • The present study was conducted with the aim to investigate the ameliorative effects of a new soybean product (cheonggukjang) fermented with Bacillus amyloliquefaciens SCGB1 (SFBA) in atopic dermatitis (AD) mouse model. Visual evaluation of AD induction in the mice indicated the remarkable control of SFBA in reducing the pathological severity of AD-like skin lesions reported as the SCORAD score of AD clinical symptoms. The results revealed that SFBA reduced dorsal skin and epidermal thickness to a similar extent with prednisolone. Further analysis revealed the dominance of SFBA in restraining mast cell infiltration in the dermis; immunoglobulin-E expression in serum; and TH2 IL-4 cytokine and itch-related IL-31 cytokine in the mice skin and serum. SFBA also suppressed scratching behaviours in mice induced by compound 48/80. Further histological findings also revealed the alleviation of collagen fiber deposition in dermal skin of the AD mice model. These actions of SFBA were examined to be mediated by its suppression of the phosphorylation activation of key signalling molecules such as $NF-{\kappa}B$ and MAPK responsible for the induction of cytokine production. Thus, SFBA can be considered as a promising functional food for managing clinical, histological and immunological spectra associated with AD.

An Enhanced Control Protocol Design for LADN in 5G Wireless Networks

  • Kim, Jae-Hyun
    • 한국컴퓨터정보학회논문지
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    • 제25권12호
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    • pp.109-117
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    • 2020
  • 본 논문에서는 5G 무선 네트워크에서 높은 처리율, 저지연 및 서비스 영역화를 제공하기 위한 LADN(로컬 영역 데이터망)을 살펴보고, LADN을 위한 향상된 제어 프로토콜 설계 방안을 제안한다. LADN은 3GPP 5G 통신 시스템에서 새롭게 도입된 개념으로써, 단말(UE)이 특성 서비스 영역에 위치해 있을 때, 특정 LADN 세션을 연결할 수 있는 데이터 네트워크를 의미한다. 5G 무선 네트워크에서 단말과 핵심 망의 LADN 정보가 동일하지 않은 경우가 발생했을 때, 단말의 LADN 세션 설정이 실패하게 된다. 본 논문에서 제안하는 기법은 특정 등록 절차 수행을 통하여 단말과 5G 핵심 망의 LADN 정보를 신속하게 갱신하여 일치시키고 곧바로 LADN 세션을 적절하게 설정한다. 결과적으로, 제안하는 ECP 기법은 5G 무선 네트워크에서 LADN 서비스 제공을 위한 세션 연결 수행 시, 불필요한 제어 신호 오버헤드 및 통신 지연 발생을 방지할 수 있다.

Access Control for D2D Systems in 5G Wireless Networks

  • Kim, Seog-Gyu;Kim, Jae-Hyun
    • 한국컴퓨터정보학회논문지
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    • 제26권1호
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    • pp.103-110
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    • 2021
  • 본 논문에서는 5G 무선 네트워크 D2D 시스템에서 수행될 수 있는 두 가지 액세스 제어 메커니즘들을 비교해 보고 효과적인 액세스 제어 기법을 제안한다. 현재 5G D2D 시스템에서는 액세스 제어 기법이 표준 규격에 제정 되어 있지 않고 있으나, 두 가지 액세스 제어 기법들이 가능하다. 하나의 방식으로는 UE-to-Network Relay 기반의 액세스 제어 기법이고, 다른 하나의 방식으로는 Remote UE 기반의 액세스 제어 기법이다. 전자의 경우는 UE-to-Network Relay가 액세스 제어 검사를 수행하는 것이며, 후자의 경우는 Remote UE가 액세스 제어 검사를 직접 수행하는 방식이다. 실험 평가 결과, 본 논문에서는 5G 무선 네트워크 D2D 시스템에서 효율적인 액세스 제어 방안으로써 Remote UE 기반의 액세스 제어 기법을 최종 제안한다. Remote UE 기반의 액세스 제어 기법은 UE-to-Network Relay 기반의 액세스 제어 기법이 비하여, 신호 오버헤드를 최소화하고, 서로 액세스 제어 기능들이 다른 경우 보다 효율적인 액세스 제어 검사를 수행할 수 있다.

Novel Anti-Angiogenic and Anti-Tumour Activities of the N-Terminal Domain of NOEY2 via Binding to VEGFR-2 in Ovarian Cancer

  • Rho, Seung Bae;Lee, Keun Woo;Lee, Seung-Hoon;Byun, Hyun Jung;Kim, Boh-Ram;Lee, Chang Hoon
    • Biomolecules & Therapeutics
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    • 제29권5호
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    • pp.506-518
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    • 2021
  • The imprinted tumour suppressor NOEY2 is downregulated in various cancer types, including ovarian cancers. Recent data suggest that NOEY2 plays an essential role in regulating the cell cycle, angiogenesis and autophagy in tumorigenesis. However, its detailed molecular function and mechanisms in ovarian tumours remain unclear. In this report, we initially demonstrated the inhibitory effect of NOEY2 on tumour growth by utilising a xenograft tumour model. NOEY2 attenuated the cell growth approximately fourfold and significantly reduced tumour vascularity. NOEY2 inhibited the phosphorylation of the signalling components downstream of phosphatidylinositol-3'-kinase (PI3K), including phosphoinositide-dependent protein kinase 1 (PDK-1), tuberous sclerosis complex 2 (TSC-2) and p70 ribosomal protein S6 kinase (p70S6K), during ovarian tumour progression via direct binding to vascular endothelial growth factor receptor-2 (VEGFR-2). Particularly, the N-terminal domain of NOEY2 (NOEY2-N) had a potent anti-angiogenic activity and dramatically downregulated VEGF and hypoxia-inducible factor-1α (HIF-1α), key regulators of angiogenesis. Since no X-ray or nuclear magnetic resonance structures is available for NOEY2, we constructed the three-dimensional structure of this protein via molecular modelling methods, such as homology modelling and molecular dynamic simulations. Thereby, Lys15 and Arg16 appeared as key residues in the N-terminal domain. We also found that NOEY2-N acts as a potent inhibitor of tumorigenesis and angiogenesis. These findings provide convincing evidence that NOEY2-N regulates endothelial cell function and angiogenesis by interrupting the VEGFR-2/PDK-1/GSK-3β signal transduction and thus strongly suggest that NOEY2-N might serve as a novel anti-tumour and anti-angiogenic agent against many diseases, including ovarian cancer.

Apolipoprotein H: a novel regulator of fat accumulation in duck myoblasts

  • Ziyi, Pan;Guoqing, Du;Guoyu, Li;Dongsheng, Wu;Xingyong, Chen;Zhaoyu, Geng
    • Journal of Animal Science and Technology
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    • 제64권6호
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    • pp.1199-1214
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    • 2022
  • Apolipoprotein H (APOH) primarily engages in fat metabolism and inflammatory disease response. This study aimed to investigate the effects of APOH on fat synthesis in duck myoblasts (CS2s) by APOH overexpression and knockdown. CS2s overexpressing APOH showed enhanced triglyceride (TG) and cholesterol (CHOL) contents and elevated the mRNA and protein expression of AKT serine/threonine kinase 1 (AKT1), ELOVL fatty acid elongase 6 (ELOVL6), and acetyl-CoA carboxylase 1 (ACC1) while reducing the expression of protein kinase AMP-activated catalytic subunit alpha 1 (AMPK), peroxisome proliferator activated receptor gamma (PPARG), acyl-CoA synthetase long chain family member 1 (ACSL1), and lipoprotein lipase (LPL). The results showed that knockdown of APOH in CS2s reduced the content of TG and CHOL, reduced the expression of ACC1, ELOVL6, and AKT1, and increased the gene and protein expression of PPARG, LPL, ACSL1, and AMPK. Our results showed that APOH affected lipid deposition in myoblasts by inhibiting fatty acid beta-oxidation and promoting fatty acid biosynthesis by regulating the expression of the AKT/AMPK pathway. This study provides the necessary basic information for the role of APOH in fat accumulation in duck myoblasts for the first time and enables researchers to study the genes related to fat deposition in meat ducks in a new direction.