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RISS 인기검색어
- 검색키워드
- 주제어 : retinoic acid receptor ${\beta}$ (검색결과 4 건)
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Wang, Jing,Zhao, Shu-Lei,Li, Yan,Meng, Mei,Qin, Cheng-Yong Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.5
Overexpression of DNA methyltransferase 1 (DNMT1) has been detected in many cancers. Tobacco exposure is known to induce genetic and epigenetic changes in the pathogenesis of malignancy. 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is an important carcinogen present in tobacco smoke; however the detailed molecular mechanism of how NNK induces esophageal carcinogenesis is still unclear. We found that DNMT1 was overexpressed in ESCC tissues compared with paired non-cancerous tissues, the overexpression being correlated with smoking status and low expression of $RAR{\beta}$. The latter could be upregulated by NNK treatment in Het-1A cells, and the increased DNMT1 expression level reflected promoter hypermethylation and downregulation of retinoic acid receptor ${\beta}$($RAR{\beta}$). RNA interference mediated knockdown of DNMT1 resulted in promoter demethylation and upregulation of $RAR{\beta}$ in KYSE30 and TE-1 cells. 3-(4,5-Dimethyl-thiazol-2yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometric analysis demonstrated that NNK treatment in Het-1A cells could enhance cell proliferation and inhibit cell apoptosis in a dose-dependent manner. In conclusion, DNMT1 overexpression is correlated with smoking status and low expression of $RAR{\beta}$ in esophageal SCC patients. NNK could induce $RAR{\beta}$ promoter hypermethylation through upregulation of DNMT1 in esophageal squamous epithelial cells, finally leading to enhancement of cell proliferation and inhibition of apoptosis.
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Invited Mini Review : Innate immune recognition of respiratory syncytial virus infection
( Tae Hoon Kim ),( Heung Kyu Lee ) 생화학분자생물학회(구 한국생화학분자생물학회) 2014 BMB Reports Vol.47 No.4
Respiratory syncytial virus (RSV) is the leading cause of respiratory infection in infants and young children. Severe clinical manifestation of RSV infection is a bronchiolitis, which is common in infants under six months of age. Recently, RSV has been recognized as an important cause of respiratory infection in older populations with cardiovascular morbidity or immunocompromised patients. However, neither a vaccine nor an effective antiviral therapy is currently available. Moreover, the interaction between the host immune system and the RSV pathogen during an infection is not well understood. The innate immune system recognizes RSV through multiple mechanisms. The first innate immune RSV detectors are the pattern recognition receptors (PRRs), including toll-like receptors (TLRs), retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs), and nucleotide-biding oligomerization domain (NOD)-like receptors (NLRs). The following is a review of studies associated with various PRRs that are responsible for RSV virion recognition and subsequent induction of the antiviral immune response during RSV infection. [BMB Reports 2014; 47(4): 184-191]
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Adapalene induces adipose browning through the RARb-p38 MAPK-ATF2 pathway
Na Hyun Lee,Mi Jin Choi,Hana Yu,Jea Il Kim,Hyae Gyeong Cheon 대한약학회 2022 Archives of Pharmacal Research Vol.45 No.5
Adipose browning has recently been reportedto be a novel therapeutic strategy for obesity. Because theretinoic acid receptor (RAR) is a potential target involvedin browning, adapalene (AD), an anti-acne agent with RARagonism, was examined in detail for its eff ects on adiposebrowning and the underlying mechanisms in vitro andin vivo. AD upregulated the expression of adipose browning-related markers in a concentration-dependent manner,promoted mitochondrial biogenesis, increased oxygen consumptionrates, and lowered lipid droplet sizes in diff erentiated3T3/L1 white adipocytes. Among the three retinoicacid receptors (RARα, RARβ, and RARγ), knockdown ofthe gene encoding RARβ mitigated AD-induced adiposebrowning. Similarly, LE135 (a selective RARβ antagonist)attenuated AD action, suggesting that AD promotes adiposebrowning through RARβ. Sequential phosphorylation of p38mitogen-activated protein kinase (MAPK) and activatingtranscription factor 2 (ATF2) was critical for AD-inducedadipose browning, based on the observations that eitherSB203580 (a p38 MAPK inhibitor) or ATF2 siRNA reducedthe eff ects of AD. In vivo browning eff ects of AD were confirmed in C57BL/6J mice and high-fat diet-induced obese(DIO) mice after oral administration of AD either acutelyor chronically. This study identifi es new actions of AD as an adipose browning agent and demonstrates that RARβ activationfollowed by increased phosphorylation of p38 MAPKand ATF2 appears to be a key mechanism of AD action.
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Jang Young-Saeng,Park Sun-Hee,Kang Seung-Goo,Lee Jung-Shin,Ko Hyun-Jeong,Kim Pyeung-Hyeun 대한면역학회 2023 Immune Network Vol.23 No.5
Forkhead box P3-positive (Foxp3+)-inducible Tregs (iTregs) are readily generated by TGF-β1 at low TCR signaling intensity. TGF-β1–mediated Foxp3 expression is further enhanced by retinoic acid (RA) and lactoferrin (LF). However, the intensity of TCR signaling required for induction of Foxp3 expression by TGF-β1 in combination with RA and LF is unknown. Here, we found that either RA or LF alone decreased TGF-β1–mediated Foxp3 expression at low TCR signaling intensity. In contrast, at high TCR signaling intensity, the addition of either RA or LF strongly increased TGF-β1–mediated Foxp3 expression. Moreover, decreased CD28 stimulation was more favorable for TGF-β1/LF–mediated Foxp3 expression. Lastly, we found that at high signaling intensities of both TCR and CD28, combined treatment with TGF-β1, RA, and LF induced robust expression of Foxp3, in parallel with powerful suppressive activity against responder T cell proliferation. Our findings that TGFβ/RA/LF strongly generate high affinity Ag-specific iTreg population would be useful for the control of unwanted hypersensitive immune reactions such as various autoimmune diseases.
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