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Choi, Seunghwan,Kim, Joohwan,Kim, Ji-Hee,Lee, Dong-Keon,Park, Wonjin,Park, Minsik,Kim, Suji,Hwang, Jong Yun,Won, Moo-Ho,Choi, Yoon Kyung,Ryoo, Sungwoo,Ha, Kwon-Soo,Kwon, Young-Guen,Kim, Young-Myeong Nature Publishing Group 2017 Experimental and molecular medicine Vol.49 No.11
<P>Heme oxygenase-1-derived carbon monoxide prevents inflammatory vascular disorders. To date, there is no clear evidence that HO-1/CO prevents endothelial dysfunction associated with the downregulation of endothelial NO synthesis in human endothelial cells stimulated with TNF-α. Here, we found that the CO-releasing compound CORM-2 prevented TNF-α-mediated decreases in eNOS expression and NO/cGMP production, without affecting eNOS promoter activity, by maintaining the functional activity of the <I>eNOS</I> mRNA 3′-untranslated region. By contrast, CORM-2 inhibited MIR155HG expression and miR-155-5p biogenesis in TNF-α-stimulated endothelial cells, resulting in recovery of the 3′-UTR activity of <I>eNOS</I> mRNA, a target of miR-155-5p. The beneficial effect of CORM-2 was blocked by an NF-κB inhibitor, a miR-155-5p mimic, a HO-1 inhibitor and siRNA against HO-1, indicating that CO rescues TNF-α-induced eNOS downregulation through NF-κB-responsive miR-155-5p expression via HO-1 induction; similar protective effects of ectopic HO-1 expression and bilirubin were observed in endothelial cells treated with TNF-α. Moreover, heme degradation products, except iron and <I>N</I>-acetylcysteine prevented H<SUB>2</SUB>O<SUB>2</SUB>-mediated miR-155-5p biogenesis and eNOS downregulation. These data demonstrate that CO prevents TNF-α-mediated eNOS downregulation by inhibiting redox-sensitive miR-155-5p biogenesis through a positive forward circuit between CO and HO-1 induction. This circuit may play an important preventive role in inflammatory endothelial dysfunction associated with human vascular diseases.</P>
Choi, Seunghwan,Park, Minsik,Kim, Joohwan,Park, Wonjin,Kim, Suji,Lee, Dong-Keon,Hwang, Jong Yun,Choe, Jongseon,Won, Moo-Ho,Ryoo, Sungwoo,Ha, Kwon-Soo,Kwon, Young-Guen,Kim, Young-Myeong American Society for Biochemistry and Molecular Bi 2018 The Journal of biological chemistry Vol.293 No.38
<P>cGMP-dependent protein kinase 1 (PKG1) plays an important role in nitric oxide (NO)/cGMP-mediated maintenance of vascular smooth muscle cell (VSMC) phenotype and vasorelaxation. Inflammatory cytokines, including tumor necrosis factor-alpha(TNF alpha), have long been understood to mediate several inflammatory vascular diseases. However, the underlying mechanism of TNF alpha-dependent inflammatory vascular disease is unclear. Here, we found that TNF alpha treatment decreased PKG1 expression in cultured VSMCs, which correlated with NF-kappa B-dependent biogenesis of miR-155-5p that targeted the 3'-UTR of PKG1 mRNA. TNF alpha induced VSMC phenotypic switching from a contractile to a synthetic state through the down-regulation of VSMC marker genes, suppression of actin polymerization, alteration of cell morphology, and elevation of cell proliferation and migration. All of these events were blocked by treatment with an inhibitor of miR-155-5p or PKG1, whereas transfection with miR-155-5p mimic or PKG1 siRNA promoted phenotypic modulation, similar to the response to TNF alpha. In addition, TNF alpha-induced miR-155-5p inhibited the vasorelaxant response of de-endothelialized mouse aortic vessels to 8-Br-cGMP by suppressing phosphorylation of myosin phosphatase and myosin light chain, both of which are downstream signal modulators of PKG1. Moreover, TNF alpha-induced VSMC phenotypic alteration and vasodilatory dysfunction were blocked by NF-kappa B inhibition. These results suggest that TNF alpha impairs NO/cGMP-mediated maintenance of the VSMC contractile phenotype and vascular relaxation by down-regulating PKG1 through NF-kappa B-dependent biogenesis of miR-155-5p. Thus, the NF-kappa B/miR-155-5p/PKG1 axis may be crucial in the pathogenesis of inflammatory vascular diseases, such as atherosclerotic intimal hyperplasia and preeclamptic hypertension.</P>
Choi, Kyung-Chul,Lee, Youn Sook,Lim, Seunghwan,Choi, Hyo Kyoung,Lee, Chang-Hun,Lee, Eun-Kyung,Hong, Suntaek,Kim, In-Hoo,Kim, Seong-Jin,Park, Seok Hee Nature Publishing Group 2006 Nature immunology Vol.7 No.10
Transforming growth factor-β1 (TGF-β1) is a potent cytokine with pleiotropic effects, including anti-inflammatory activity. Here we show that the signaling protein Smad6 bound to Pellino-1, an adaptor protein of mammalian interleukin 1 receptor (IL-1R)–associated kinase 1 (IRAK1), and thereby promoted TGF-β-mediated anti-inflammatory effects. Smad6–Pellino-1 interaction abrogated signaling mediated by a complex of IRAK1, Pellino-1 and adaptor protein TRAF6 that formed after stimulation by IL-1β treatment. Blockade of IRAK1–Pellino-1–TRAF6 signaling prevented degradation of the inhibitor IκBα and subsequent nuclear translocation of transcription factor NF-κB and thus expression of proinflammatory genes. 'Knockdown' of endogenous Smad6 expression by RNA interference reduced anti-inflammatory activity mediated by TGF-β1 or the TGF-β family member BMP-4. Thus Smad6 is a critical mediator of the TGF-β–BMP pathway that mediates anti-inflammatory activity and negatively regulates IL-1R–Toll-like receptor signals.
Choi, Seunghwan,Yamada, Akihiro,Kim, Woojin,Kim, Sun Kwang,Furue, Hidemasa Springer-Verlag 2017 JOURNAL OF PHYSIOLOGICAL SCIENCES Vol.67 No.3
<P>We investigated the spinal action of noradrenaline on cold-elicited hyperexcitation detected in dorsal horn neurons of rats with allodynia induced by an oxaliplatin (6 mg/kg, i.p.) injection. In vivo extracellular recordings from the spinal dorsal horn showed that wide dynamic range neurons responded to cutaneous acetone (10 mu l) stimulation in normal rats, and cold-elicited firings in oxaliplatin-administered rats were increased with a longer duration, correlated with behavioral responses. These responses were significantly attenuated by spinal administration (50 mu M) of noradrenaline or its agonists, clonidine (alpha(2)), phenylephrine (alpha(1)) and isoprenaline (beta), in descending order of efficacy. Thus, the inhibitory effect of noradrenaline on spinal oxaliplatin-induced cold hyperexcitation is mediated mainly by activation of alpha(2)- and/or alpha(1)-adrenoceptors.</P>
최승환(Seunghwan Choi),곽진호(Jinho Kwak),김명일(Myungil Kim),노명현(Myunghyun Roh),권해붕(Haeboung Kwon),최선모(Sunmo Choi) 한국자동차공학회 2006 한국자동차공학회 춘 추계 학술대회 논문집 Vol.- No.-
In case of conventional speed humps, there are problems of grounding because of the induced heavy pitching motion for the buses especially. Therefore it is strongly needed to new vehicle speed reduction schemes. It will be thought that speed cushions do not generally cause excessive discomfort to passengers of large buses, or excessive discomfort to emergency vehicles such as fire service vehicles or ambulances. To optimize the shape of speed cushion which is replaced with the conventional speed humps, the specifications of the domestic vehicles are surveyed. Based on these survey results, several types of speed cushions are designed and the vertical acceleration data are acquired through the 3D-accelerometers. Two-types of design with heights of 75 or 100 ㎜, plateau width of 1400 ㎜, plateau length of 2400 ㎜, ramp slope of 1-in-8 and side slope of 1-in-4 would give the least effect on buses while still causing discomfort for car occupants.