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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.
이종호,이세영,김명진,이은진,안강민,김성민,최원재,명훈,황순정,서병무,최진영,정필훈 大韓顎顔面成形再建外科學會 2003 Maxillofacial Plastic Reconstructive Surgery Vol.25 No.2
The surgery of oral and maxillofacial area poses the risk of cranial nerve damage such as trigeminal nerve or facial nerve. Inferior alveolar nerve is prone to damage in the third molar extraction, implant installation, orthognathic surgery, open reduction and rigid fixation, and tumor ablation surgery. On the other hands,facial nerve is likely to be damaged or sacrificed with trauma or parotidectomy. In case of inferior alveolar nerve injury, the incidence is reported to be about 1.3%. The nerve function will almost recover in minimal damage, but it won't recover at last in total damage of a part of nerve unit. In latter cases, nerve regeneration in intended by allograft as nerve substitute or various route of merve condit. But the recovery with autograft is believed to be most relialbe mrthod in the rapair of long-span(longer than 15㎜)nerve defect. We have performed autologous sural nerve graft in the repair of nerve defect, which is caused by resection of benign or malignant tumor. Hereby we report the method of nerve harvesting, recovery of defected peripheral nerve and the complications of donor site with the discussion of sural nerve anatomy.
신부전이 동반된 당뇨병 환자에서 발생된 침습성 모균증 : 수술과 Liposomal amphotericin B 및 GM-CSF 병합 요법에 의한 성공적인 치험 1예
이원영,오기원,임국희,장재혁,이동건,최정현,강무일,신완식,차봉연,이광우,손호영,강성구 대한화학요법학회 1999 대한화학요법학회지 Vol.17 No.4
저자들은 신부전이 동반된 당뇨병 환자에서 발생된 부비동형 모균증에 대하여 수술과 함께 liposomal amphotericin B 및 GM-CSF의 복합치료를 하여 성공적으로 치료한 1예를 경험하였기에 문헌 고찰과 함께 보고하는 바이다. Mucormycosis (zygomycosis) primarily affects diabetic or immunocompromised patients and typically progresses rapidly, necessitating surgical excision and antifungal therapy with amphotericin B. Large doses of amphotericin B are needed for cure, but it has the risk of causing significant renal toxicity. The recent development of liposomal amphotericin B allows antifungal therapy to be administered with potentially improved efficacy and reduced nephrotoxicity. We have experienced a case of paranasal mucormycosis successfully treated with surgery, liposomal amphotericin B and GM-CSF. A 59-year-old male suffering from diabetes mellitus for 6 years was admitted with pain at left maxillary area. He was diagnosed as mucormycosis after cytologic exam on the necrotic nasal mucosa, which showed typical hyphae. He have had diabetic nephropathy with macroproteinuria and had rapidly rising serum creatinine levels with the amphotericin B treatment: creatinine levels reverted to basal level with the use of liposomal amphotericin B. Despite surgical excision and continued antifungal therapy, his infection was not effectively controlled. Therefore, GM-CSF was administered additionally to improve phagocytic activity of leukocytes. He was finally cured after receiving a combination of aggressive surgery, liposomal amphotericin B and GM-CSF. To our knowledge, this is the first detailed clinical description of the treatment of mucormycosis with liposomal amphotericin B in Korea.