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( Sun-uk Bak ),( Suji Kim ),( Hae-jun Hwang ),( Jung-a Yun ),( Wan-sung Kim ),( Moo-ho Won ),( Ji-yoon Kim ),( Kwon-soo Ha ),( Young-guen Kwon ),( Young-myeong Kim ) 생화학분자생물학회(구 한국생화학분자생물학회) 2017 BMB Reports Vol.50 No.2
Heme oxygenase (HO-1) catalyzes heme to carbon monoxide (CO), biliverdin/bilirubin, and iron and is known to prevent the pathogenesis of several human diseases. We assessed the beneficial effect of heme degradation products on osteoclastogenesis induced by receptor activator of NF-κB ligand (RANKL). Treatment of RAW264.7 cells with CORM-2 (a CO donor) and bilirubin, but not with iron, decreased RANKLinduced osteoclastogenesis, with CORM-2 having a more potent anti-osteogenic effect. CORM-2 also inhibited RANKLinduced osteoclastogenesis and osteoclastic resorption activity in marrow-derived macrophages. Treatment with hemin, a HO-1 inducer, strongly inhibited RANKL-induced osteoclastogenesis in wild-type macrophages, but was ineffective in HO-1<sup>+/- </sup>cells. CORM-2 reduced RANKL-induced NFATc1 expression by inhibiting IKK-dependent NF-κB activation and reactive oxygen species production. These results suggest that CO potently inhibits RANKL-induced osteoclastogenesis by inhibiting redox-sensitive NF-κB-mediated NFATc1 expression. Our findings indicate that HO-1/CO can act as an antiresorption agent and reduce bone loss by blocking osteoclast differentiation. [BMB Reports 2017; 50(2): 103-108]
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>
Kim, Ji-Hee,Lee, Kwang-Soon,Lee, Dong-Keon,Kim, Joohwan,Kwak, Su-Nam,Ha, Kwon-Soo,Choe, Jongseon,Won, Moo-Ho,Cho, Byung-Ryul,Jeoung, Dooil,Lee, Hansoo,Kwon, Young-Guen,Kim, Young-Myeong Mary Ann Liebert 2014 Antioxidants & redox signaling Vol.21 No.18
<P>Aims: Hypoxia induces expression of various genes and microRNAs (miRs) that regulate angiogenesis and vascular function. In this study, we investigated a new functional role of new hypoxia-responsive miR-101 in angiogenesis and its underlying mechanism for regulating heme oxygenase-1 (HO-1) and vascular endothelial growth factor (VEGF) expression. Results: We found that hypoxia induced miR-101, which binds to the 3 ' untranslated region of cullin 3 (Cul3) and stabilizes nuclear factor erythroid-derived 2-related factor 2 (Nrf2) via inhibition of the proteasomal degradation pathway. miR-101 overexpression promoted Nrf2 nuclear accumulation, which was accompanied with increases in HO-1 induction, VEGF expression, and endothelial nitric oxide synthase (eNOS)-derived nitric oxide (NO) production. The elevated NO-induced S-nitrosylation of Kelch-like ECH-associated protein 1 and subsequent induction of Nrf2-dependent HO-1 lead to further elevation of VEGF production via a positive feedback loop between the Nrf2/HO-1 and VEGF/eNOS axes. Moreover, miR-101 promoted angiogenic signals and angiogenesis both in vitro and in vivo, and these events were attenuated by inhibiting the biological activity of HO-1, VEGF, or eNOS. Moreover, these effects were also observed in aortic rings from HO-1(+/-) and eNOS(-/-) mice. Local overexpression of miR-101 improved therapeutic angiogenesis and perfusion recovery in the ischemic mouse hindlimb, whereas antagomiR-101 diminished regional blood flow. Innovation: Hypoxia-responsive miR-101 stimulates angiogenesis by activating the HO-1/VEGF/eNOS axis via Cul3 targeting. Thus, miR-101 is a novel angiomir. Conclusion: Our results provide new mechanistic insights into a functional role of miR-101 as a potential therapeutic target in angiogenesis and vascular remodeling. Antioxid. Redox Signal. 21, 2469-2482.</P>
원무호 동국대학교 의학연구소 2000 東國醫學 Vol.7 No.-
This study was carried out to the effect of neuronal degeneration in the anterior horn after spinal cord ischemia. White rabbits (2.5-3 kg) were used in this study as control and experimental groups. Spinal cord ischemia was induced by occlusion of the abdominal aorta located underneath the left renal artery for 15 minutes. Subsequently, the animal were sacrified at 0.5, 1, 3, 6, 12 and 24 hours after the ischemic injury. Spinal cord sections at the level of L7 were stained with Cresyl violet and Acid fuchsin. The results obtained from the studies are as follows. The number of Cresyl violet-positive neurons began to be reduced in the laminae IX 3 hours after ischemia. In contrast, the Cresyl violet-positive neurons in the laminae Ⅶ and Ⅷ began to be decreased 6 hours after ischemia. Finally, no neurons could be detectable with Cresyl violet 24 hr after the ischemic injury. These result suggest that the neuronal degeneration in the anterior horn may occur rapidly after ischemic insults at normothermic condition.
內耳組織의 Na^+, K^+ ATPase 分布와 알부민輸送에 關한 超微形態學的 硏究
손진호,박경란,이영호,노승무,김원식 충남대학교 의과대학 지역사회의학연구소 1991 충남의대잡지 Vol.18 No.2
This study was carried out to investigate distribution of Na^+, K^+ -ATPase in the cochlear tissues by means of electron microscopic immunocytochemistry and transcytosis of albumin in the cochlear tissues. Ten cochleas obtained from guinea pigs were stained by avidin-biotin-peroxidase with anti-human Na^+, K^+ -ATPase rabbit IgG as primary antibody. Three guinea pigs were perfused with colloidal gold binding bovine serum albumin. Four were injected into the endolymphatic and perilymphatic spaces via oval and round windows. The cochlear tissues were observed with electron microscope. The results obtained were were as follows. Na^+, K^+ -ATPase was predominently distributed in basolateral infoldings and mitochondrial membranes and cristae, and moderately in the cytoplasmicn membrane and interdental cells. Albumin was distributed on the endothelial cells of the strial capillaries and surrounding interstitium. There were no albumins in marginal cells, intermediate cells, basal cells, Reissner' s membrane, and cells of the organ of Corti. According to the above results. it is suspected that transport of Na^+ and K^+ is performed in basolateral infoldings of marginal cells by active transport mechanism, and that immuncoytochemical method is more excellent to demonstrate Na^+, K^+ -ATPase than that of enzyme histochemistry. Transcytosis of albumin into the endolymphatics may be restricted by stria vascularis, Reissner' s membrane, and the cells of the organ of Corti.