• 제목/요약/키워드: Micro-Targeting

검색결과 132건 처리시간 0.026초

microRNA-200a-3p enhances mitochondrial elongation by targeting mitochondrial fission factor

  • Lee, Heejin;Tak, Hyosun;Park, So Jung;Jo, Yoon Kyung;Cho, Dong Hyung;Lee, Eun Kyung
    • BMB Reports
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    • 제50권4호
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    • pp.214-219
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    • 2017
  • Mitochondria play pivotal roles in the ATP production, apoptosis and generation of reactive oxygen species. Although dynamic regulation of mitochondria morphology is a critical step to maintain cellular homeostasis, the regulatory mechanisms are not yet fully elucidated. In this study, we identified miR-200a-3p as a novel regulator of mitochondrial dynamics by targeting mitochondrial fission factor (MFF). We demonstrated that the ectopic expression of miR-200a-3p enhanced mitochondrial elongation, mitochondrial ATP synthesis, mitochondrial membrane potential and oxygen consumption rate. These results indicate that miR-200a-3p positively regulates mitochondrial elongation by downregulating MFF expression.

지능정보기술과 민주주의: 알고리즘 정보환경과 정치의 문제 (Intelligent Information Technology and Democracy : Algorithm-driven Information Environment and Politics)

  • 민희;김정연
    • 정보화정책
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    • 제26권2호
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    • pp.81-95
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    • 2019
  • 최근 선거캠페인에서 수집되는 유권자 모델링 및 맞춤형 커뮤니케이션에 관한 데이터는 양적 확장성과 질적 유용성 측면에서 새롭다. 본 연구는 지능정보기술을 활용한 고도의 데이터 분석 능력이 정치에 어떻게 활용되고 있는지에 주목한다. 그 중에서도 선거캠페인에서의 유권자 행동 타게팅이 다양한 측면에서 민주주의 과정과 충돌할 수 있다는 점에 초점을 맞춘다. 이를 위해 마이크로 타게팅과 정치 봇을 살펴본다. 본 연구는 이러한 기술 기반의 캠페인 기법들이 민주주의의 핵심인 자유로운 의견 표출과 논쟁을 방해하는 요인으로 작동하는 양상을 보여준다. 동시에 이에 영향을 미치는 알고리즘의 속성을 파악한다. 본 연구는 지능정보기술 기반의 정치와 민주주의에서 다음과 같은 문제가 발생할 수 있음을 제시한다. 첫째, 정치참여의 불평등이 심화된다. 둘째, 유권자 간 공적 논쟁이 어려워진다. 셋째, 피상적인 정치가 만연한다. 넷째, 단일 이슈 정치와 배제의 정치 현상이 증가한다. 마지막으로 정치적 프라이버시가 침해될 수 있다. 요컨대, 지능정보시대 우리의 역할은 점점 고도화되고 있는 지능정보기술과 민주주의가 공존할 수 있는 방법을 모색하는 것이다.

MicroRNA-802 Promotes Osteosarcoma Cell Proliferation by Targeting p27

  • Cao, Zhong-Qing;Shen, Zan;Huang, Wei-Yi
    • Asian Pacific Journal of Cancer Prevention
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    • 제14권12호
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    • pp.7081-7084
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    • 2013
  • MicroRNAs have been demonstrated to regulate proliferation and apoptosis in many types of cancers, but biological functions in osteosarcomas remain relatively unknown. Here, we found expression of miR-802 to be up-regulated in osteosarcoma tissues in comparison with adjacent normal tissues. Enforced expression of miR-802 was able to promote cell proliferation in U2OS and MG63 cells, while miR-802 antisense oligonucleotides (antisense miR-802) inhibited cell proliferation. At the molecular level, our results further revealed that expression of p27, a negative cell-cycle regulator, was negatively regulated by miR-802. Therefore, the data reported here indicate that miR-802 is an important regulator in osteosarcoma, our findings contributing to a better understanding of important mis-regulated miRNAs in this tumour type.

Microfinance Outreach and the Microfinance Institutions(MFIs) Sustainability: Evidence from Vietnam

  • Chinomona, Richard;Le, Thanh Tam
    • Asian Journal of Business Environment
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    • 제3권1호
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    • pp.5-16
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    • 2013
  • Purpose - Micro-finance institutions (MFIs) are critical to Vietnam's quest for poverty alleviation among the poor in the rural and agrarian communities. The current study attempts to investigate the impact of microfinance outreach programs undertaken by formal and semi-formal MFIs in Vietnam targeting the poor rural and agrarian communities. Research design, data, methodology - An enquiry was made as to whether the poor and rural communities accessed the micro credit offered by Government supported MFIs and NGOs through their microfinance outreach programs. Furthermore, the current study attempted to explore if the current mode of operations adopted by MFIs in Vietnam is sustainable. Results -The findings indicate that significant progress has been made in Vietnam to alleviate poverty among the poor rural communities through micro finance outreach programs. Conclusions - There are also pointers of MFIs sustainability in Vietnam. However, it still remains to be seen if the current sustainability pointers are long lasting without government subsidies or some international organizations financial support to microfinance outreach programs.

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MicroRNA-16 Inhibits Bladder Cancer Proliferation by Targeting Cyclin D1

  • Jiang, Qi-Quan;Liu, Bin;Yuan, Tao
    • Asian Pacific Journal of Cancer Prevention
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    • 제14권7호
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    • pp.4127-4130
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    • 2013
  • MicroRNA-16 (miR-16) has been demonstrated to regulate proliferation and apoptosis in many types of cancers, but its biological function in bladder cancer remains unknown. Here, we found expression of miR-16 to be downregulated in bladder cancer in comparison with the adjacent normal tissues. Enforced expression of miR-16 was able to inhibit cell proliferation in TCHu-1 cells, in line with results for miR-16 antisense oligonucleotides (antisense miR-16). At the molecular level, our results further revealed that cyclin D1 expression was negatively regulated by miR-16. Therefore, the data reported here demonstrate that miR-16 is an important regulator in bladder cancer, which will contribute to better understanding of important mis-regulated miRNAs.

Down-Regulation of MicroRNA-210 Confers Sensitivity towards 1'S-1'-Acetoxychavicol Acetate (ACA) in Cervical Cancer Cells by Targeting SMAD4

  • Phuah, Neoh Hun;Azmi, Mohamad Nurul;Awang, Khalijah;Nagoor, Noor Hasima
    • Molecules and Cells
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    • 제40권4호
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    • pp.291-298
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    • 2017
  • MicroRNAs (miRNAs) are short non-coding RNAs that regulate genes posttranscriptionally. Past studies have reported that miR-210 is up-regulated in many cancers including cervical cancer, and plays a pleiotropic role in carcinogenesis. However, its role in regulating response towards anti-cancer agents has not been fully elucidated. We have previously reported that the natural compound 1'S-1'-acetoxychavicol acetate (ACA) is able to induce cytotoxicity in various cancer cells including cervical cancer cells. Hence, this study aims to investigate the mechanistic role of miR-210 in regulating response towards ACA in cervical cancer cells. In the present study, we found that ACA down-regulated miR-210 expression in cervical cancer cells, and suppression of miR-210 expression enhanced sensitivity towards ACA by inhibiting cell proliferation and promoting apoptosis. Western blot analysis showed increased expression of mothers against decapentaplegic homolog 4 (SMAD4), which was predicted as a target of miR-210 by target prediction programs, following treatment with ACA. Luciferase reporter assay confirmed that miR-210 binds to sequences in 3'UTR of SMAD4. Furthermore, decreased in SMAD4 protein expression was observed when miR-210 was overexpressed. Conversely, SMAD4 protein expression increased when miR-210 expression was suppressed. Lastly, we demonstrated that overexpression of SMAD4 augmented the anti-proliferative and apoptosis-inducing effects of ACA. Taken together, our results demonstrated that down-regulation of miR-210 conferred sensitivity towards ACA in cervical cancer cells by targeting SMAD4. These findings suggest that combination of miRNAs and natural compounds could provide new strategies in treating cervical cancer.

MicroRNA-206 Protects against Myocardial Ischaemia-Reperfusion Injury in Rats by Targeting Gadd45β

  • Zhai, Changlin;Qian, Qang;Tang, Guanmin;Han, Bingjiang;Hu, Huilin;Yin, Dong;Pan, Haihua;Zhang, Song
    • Molecules and Cells
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    • 제40권12호
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    • pp.916-924
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    • 2017
  • MicroRNAs are widely involved in the pathogenesis of cardiovascular diseases through regulating gene expression via translational inhibition or degradation of their target mRNAs. Recent studies have indicated a critical role of microRNA-206 in myocardial ischaemia-reperfusion (I/R) injury. However, the function of miR-206 in myocardial I/R injury is currently unclear. The present study was aimed to identify the specific role of miR-206 in myocardial I/R injury and explore the underlying molecular mechanism. Our results revealed that the expression level of miR-206 was significantly decreased both in rat I/R group and H9c2 cells subjected to hypoxia/reoxygenation (H/R) compared with the corresponding control. Overexpression of miR-206 observably decreased infarct size and inhibited the cardiomyocyte apoptosis induced by I/R injury. Furthermore, bioinformatics analysis, luciferase activity and western blot assay proved that $Gadd45{\beta}$ (growth arrest DNA damage-inducible gene $45{\beta}$) was a direct target gene of miR-206. In addition, the expression of pro-apoptotic-related genes, such as p53, Bax and cleaved caspase3, was decreased in association with the down-regulation of $Gadd45{\beta}$. In summary, this study demonstrates that miR-206 could protect against myocardial I/R injury by targeting $Gadd45{\beta}$.

MicroRNA-27a Inhibits Cell Migration and Invasion of Fibroblast-Like Synoviocytes by Targeting Follistatin-Like Protein 1 in Rheumatoid Arthritis

  • Shi, Dong-liang;Shi, Gui-rong;Xie, Jing;Du, Xu-zhao;Yang, Hao
    • Molecules and Cells
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    • 제39권8호
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    • pp.611-618
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    • 2016
  • Fibroblast-like synoviocytes (FLS) with aberrant expression of microRNA (miRNA) are critical pathogenic regulators in rheumatoid arthritis (RA). Previous studies have found that overexpression or silencing of miRNA can contribute to the development of miRNA-based therapeutics in arthritis models. In this study, we explored the effects of miR-27a on cell migration and invasion in cultured FLS from RA patients. We found that miR-27a was markedly downregulated in the serum, synovial tissue, and FLS of RA patients. Meanwhile, the expression of follistatin-like protein 1 (FSTL1) was upregulated, which suggests that FSTL1 plays a key role in RA development. The results of a Transwell assay showed that miR-27a inhibited FLS migration and invasion. However, miR-27a inhibition promoted the migration and invasion of FLS. In addition, the down-regulated expression of matrix metalloproteinases (MMP2, MMP9, and MMP13) and Rho family proteins (Rac1, Cdc42, and RhoA) was detected after treatment with miR-27a in RA-FLS by quantitative reverse transcription-PCR and western blot analysis. Then, a luciferase reporter assay validated that miR-27a targeted the 3-untranslated region (3'-UTR) of FSTL1. Moreover, miR-27a caused a significant decrease of FSTL1. In addition, the expression of TLR4 and $NF{\kappa}B$ was inhibited by miR-27a but increased by FSTL1 overexpression. In conclusion, we found that miR-27a inhibited cell migration and invasion of RA-FLS by targeting FSTL1 and restraining the $TLR4/NF{\kappa}B$ pathway.

FOLED를 이용한 마이크로 모빌리티 사용자용 의류의 거리에 따른 시그널 가시성 연구 (A Study of Signal Visibility according to the Distance of Clothing for Micro-mobility Users using FOLED)

  • 최현석;이지혜;장현미;홍성민
    • 한국염색가공학회지
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    • 제33권4호
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    • pp.288-301
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    • 2021
  • The purpose of this study was to verify the degree of visibility of FOLED (fiber optic light-emitting diode) materials applied to safety-enhancing clothes of micro-mobility users during the day and night by conducting an empirical test targeting 50 people in their teens, 20's, 30's, 40's, and 50's or older. First, the results of the visibility test at 10 m-intervals from 10 to 70 m based on the clothes sample showed that the light detection of FOLED material was very good without daytime or night-time distinction. Second, the results of directional sign detection of FOLED were confirmed to be very high without any daytime or night. Third, the results of identifying a pictogram design showed that the distance was shorter than that of light detection or directional indication. However, the FOLED pictogram design could be confirmed at a distance of 50 m or less. Therefore, if a clothes product using FOLED material is worn and micro-mobility is used, the experimental results indicate that safety will be sufficiently secured due to the excellent visibility.

MicroRNA-21 promotes epithelial-mesenchymal transition and migration of human bronchial epithelial cells by targeting poly (ADP-ribose) polymerase-1 and activating PI3K/AKT signaling

  • Zhang, Shiqing;Sun, Peng;Xiao, Xinru;Hu, Yujie;Qian, Yan;Zhang, Qian
    • The Korean Journal of Physiology and Pharmacology
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    • 제26권4호
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    • pp.239-253
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    • 2022
  • Epithelial-mesenchymal transition (EMT) is known to be involved in airway remodeling and fibrosis of bronchial asthma. However, the molecular mechanisms leading to EMT have yet to be fully clarified. The current study was designed to reveal the potential mechanism of microRNA-21 (miR-21) and poly (ADP-ribose) polymerase-1 (PARP-1) affecting EMT through the PI3K/AKT signaling pathway. Human bronchial epithelial cells (16HBE cells) were transfected with miR-21 mimics/inhibitors and PARP-1 plasmid/small interfering RNA (siRNA). A dual luciferase reporter assay and biotin-labeled RNA pull-down experiments were conducted to verify the targeting relationship between miR-21 mimics and PARP-1. The migration ability of 16HBE cells was evaluated by Transwell assay. Quantitative real-time polymerase chain reaction and Western blotting experiments were applied to determine the expression of Snail, ZEB1, E-cadherin, N-cadherin, Vimentin, and PARP-1. The effects of the PI3K inhibitor LY294002 on the migration of 16HBE cells and EMT were investigated. Overexpression of miR-21 mimics induced migration and EMT of 16HBE cells, which was significantly inhibited by overexpression of PARP-1. Our findings showed that PARP-1 was a direct target of miR-21, and that miR-21 targeted PARP-1 to promote migration and EMT of 16HBE cells through the PI3K/AKT signaling pathway. Using LY294002 to block PI3K/AKT signaling pathway resulted in a significant reduction in the migration and EMT of 16HBE cells. These results suggest that miR-21 promotes EMT and migration of HBE cells by targeting PARP-1. Additionally, the PI3K/AKT signaling pathway might be involved in this mechanism, which could indicate its usefulness as a therapeutic target for asthma.