http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
MiR-200c-3p inhibits LPS-induced M1 polarization of BV2 cells by targeting RIP2
Zhao Lei,Liu Xiaosong,Yang Jiankai,Wang Xiaoliang,Liu Xiaomeng,Wu Jianliang,Li Chen,Xu Donggang,Hu Yuhua 한국유전학회 2022 Genes & Genomics Vol.44 No.4
Background: Microglia are important immune cells, which can be induced by lipopolysaccharide (LPS) into M1 phenotype that express pro-inflammatory cytokines. Some studies have shown that microRNAs play critical roles in microglial activation. Objective: This study was designed to investigate the role of miR-200c-3p in regulating inflammatory responses of LPS-treated BV2 cells. Methods: The expression of miR-200c-3p in BV2 cells was detected by real-time PCR. Receptor-interacting protein 2 (RIP2) was predicted as a target gene of miR-200c-3p. Their relationship was verified by dual-luciferase reporter assay. The function of miR-200c-3p and RIP2 in microglial polarization and NF-κB signaling was further evaluated. Results: LPS treatment reduced miR-200c-3p expression in a dose-dependent and time-dependent manner in BV2 cells. LPS treatment increased the expression of M1 phenotype markers inducible nitric oxide synthase (iNOS) and major histocompatibility complex class (MHC)-II, promoted the release of pro-inflammatory cytokines interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α, and enhanced the nuclear translocation and phosphorylation of nuclear factor-kappaB (NF-κB) p65. Reversely, miR-200c-3p mimics down-regulated the levels of these inflammatory factors. Furthermore, RIP2 was identified to be a direct target of miR-200c-3p. RIP2 knockdown had a similar effect to miR-200c-3p mimics. Overexpression of RIP2 eliminated the inhibitory effect of miR-200c-3p on LPS-induced M1 polarization and NF-κB activation in BV2 cells. Conclusions: MiR-200c-3p mimics suppressed LPS-induced microglial M1 polarization and NF-κB activation by targeting RIP2. MiR-200c-3p/RIP2 might be a potential therapeutic target for the treatment of neuroinflammation-associated diseases.
Receptor Interacting Protein 2 (RIP2) Is Dispensable for OVA-Induced Airway Inflammation in Mice
김태현,박재학,박영민,류승욱,김동재,박종환 대한천식알레르기학회 2014 Allergy, Asthma & Immunology Research Vol.6 No.2
Purpose: Asthma is a pulmonary chronic inflammatory disease characterized by airway obstruction and hyperresponsiveness. Pattern recognitionreceptors are known to play a key role in the development of allergic diseases as well as host defenses against microbial infection. Receptor interactingprotein 2 (RIP2), a serine/threonine kinase, is an adaptor molecule of NOD1 and NOD2, and genetic variation in this receptor is known to beassociated with the severity of allergic asthma in children. In this study, we examined the role of RIP2 in the development of allergic airway inflammationin a mouse model. Methods: Airway inflammation was induced in mice through intranasal administration of ovalbumin (OVA) after 2 intraperitonealimmunizations with OVA. Lung inflammation and mucus hypersecretion were examined histologically and total cell infiltration in bronchoalveolar(BAL) fluids was determined. Levels of the Th2-related cytokines, IL-5 and IL-13, in lung extracts were measured by ELISA. Serum antigen-specific IgE and IgG1 levels were also assessed. Results: OVA-induced lung inflammation and mucus hypersecretion were not different betweenWT and RIP2-deficient mice. The IL-5 and IL-13 levels in the bronchoalveolar (BAL) fluids were also not impaired in RIP2-deficient mice comparedto WT mice. Moreover, RIP2 deficiency did not affect serum OVA-specific IgG1 and IgE levels. Conclusions: Our results suggest that RIP2 isnot associated with the development of allergic airway inflammation.
Koh, Yee Kan,Lyons, Austin S.,Bae, Myung-Ho,Huang, Bin,Dorgan, Vincent E.,Cahill, David G.,Pop, Eric American Chemical Society 2016 NANO LETTERS Vol.16 No.10
<P>heat transfer across interfaces of graphene and polar dielectrics (e.g.; SiO2) could be Mediated by direct: phonon coupling, as well as electronic coupling with remote interfacial phonons (RIPs). To understand-the relative contribution of each component, we develop a new pump probe technique called voltage-modulated thermorefleetance (VMTR) to accurately measure the change-of interfacial: thermal conductance under an electrostatic field. We employed VMTR on top gates of graphene field-,effect-transistors. and find that the thermal conductance of SiO2/graphene/SiO2 interfaces increases by up to Delta G approximate to 0.8 MW M-2 K-1 under electrostatic fields of <0.2 V nm(-1). We propose two possible explanations for-the small observed Delta G. First, because the applied electrostatic field induces charge carriers in graphene, out VMTR measurements could originate from heat transfer-between the charge carriers in graphene and RIPs in SiO2. Second, the increase in heat conduction could be caused by better conformity of graphene interfaces under electrostatic pressure exerted by the induced charge carriers. Regardless of the origins of the observed Delta G, our VMTR measurements eStablish, an upper limit for heat transfer from unbiased graphene to SiO2 substrates via RIP scattering; for example, only <2% of the interfacial heat transport is facilitated' y RIP scattering even at a carrier concentration of similar to 4 X 10(12) cm(-2).</P>
Jeong, Hyun-Ja,Han, Na-Ra,Kim, Kyu-Yeob,Choi, Il-Sook,Kim, Hyung-Min Informa Healthcare USA, Inc. 2014 IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY Vol.36 No.3
<P>Gomisin A (GA), a lignan component contained in the fruit of <I>Schisandra chinensis</I> Baillon, improves hepatic cell degeneration, vasodilatory activity and insulin sensitivity. These effects also impact the immune system, including various inflammatory mediators and cytokines. In this study, the anti-inflammatory effect of GA on lipopolysaccharide-stimulated mouse peritoneal macrophages was studied. Pretreatment with GA attenuated the expression of receptor-interacting protein 2 (RIP2) and IκB kinase-β (IKK-β) as well as IKK-β phosphorylation. The activation of nuclear factor-kappa B (NF-κB) in the nucleus, the phosphorylation of IκBα and degradation of IκBα in the cytosol were suppressed by GA. GA decreased the production and mRNA expression of the inflammatory cytokines tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-6. In addition, expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and production of nitric oxide were decreased by pretreatment with GA. In conclusion, these results show that the anti-inflammatory properties of GA potentially result from the inhibition of COX-2, iNOS, IL-6, TNF-α and NO through the down-regulation of RIP2 and NF-κB activation. These results impact the development of potential health products for preventing and treating inflammatory diseases.</P>
토사자 추출물이 MCF-7 유방암 세포의세포자멸사에 미치는 영향
김지현 ( Ji Hyun Kim ),정은혜 ( Eun Hye Jung ),유동열 ( Dong Youl Yoo ) 대한한방부인과학회 2014 大韓韓方婦人科學會誌 Vol.27 No.2
This study aimed to evaluate the effects of Cuscutae Semen waterextract (CS) on MCF-7 human breast cancer cells. Methods: To clarify the results, we cultivated MCF-7 cells in cell culture plates. And then we extracted each of 100 μg/ml, 300 μg/ml, 600 μg/ml CS, gave it toMCF-7 cell. After these process we performed MTT assay to elucidate the ability of apoptosis. The result of mRNA was analyzed by RT-PCR. Results: Each of concentrated extracts CS decreased the survival rate of MCF-7cells. CS decreased Bcl-2 which is known as a blocking cell apoptosis. Bax, caspase-3,P21 and RIP-1 that accelerate apoptogenic activity factors increased by CS. CSdid not change the condition of caspase-8, caspase-9, P53 factors on MCF-7 cells. Furthermore caspase-8, caspase-9, P53 factors on MCF-7 cells does not make itmore active but turn it on. Conclusions: According to the above results, we could suggest that CS can occurthe apoptosis on MCF-7 cells.