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김상훈,Doh-Hyung Kim,Paul Lavender,Ji-Hee Seo,Yun-Seop Kim,Jae-Suk Park,Sahng-June Kwak,Young-Koo Jee 생화학분자생물학회 2009 Experimental and molecular medicine Vol.41 No.5
Increased expression of a number of proinflammatory genes, including IL-8, is associated with inflammatory conditions such as asthma. Glucocorticoid receptor (GR)β, one of the GR isoforms, has been suggested to be upregulated in asthma associated with glucocorticoid insensitivity and to work as a dominant negative inhibitor of wild type GRα. However, recent data suggest that GRβ is not a dominant negative inhibitor of GRα in the transrepressive process and has its own functional role. We investigated the functional role of GRβ expression in the suppressive effect of glucocorticoids on tumor necrosis factor (TNF)-α-induced IL-8 release in an airway epithelial cell line. GRβ expression was induced by treatment of epithelial cells with either dexamethasone or TNF-α. GRβ was able to inhibit glucocorticoid-induced transcriptional activation mediated by binding to glucocorticoid response elements (GREs). The suppressive effect of dexamethasone on TNF-α-induced IL-8 transcription was not affected by GRβ overexpression, rather GRβ had its own weak suppressive activity on TNF-α-induced IL-8 expression. Overall histone deacetylase activity and histone acetyltransferase activity were not changed by GRβ overexpression, but TNF-α-induced histone H4 acetylation at the IL-8 promoter was decreased with GRβ overexpression. This study suggests that GRβ overexpression does not affect glucocorticoid- induced suppression of IL-8 expression in airway epithelial cells and GRβ induces its own histone deacetylase activity around IL-8 promoter site. Increased expression of a number of proinflammatory genes, including IL-8, is associated with inflammatory conditions such as asthma. Glucocorticoid receptor (GR)β, one of the GR isoforms, has been suggested to be upregulated in asthma associated with glucocorticoid insensitivity and to work as a dominant negative inhibitor of wild type GRα. However, recent data suggest that GRβ is not a dominant negative inhibitor of GRα in the transrepressive process and has its own functional role. We investigated the functional role of GRβ expression in the suppressive effect of glucocorticoids on tumor necrosis factor (TNF)-α-induced IL-8 release in an airway epithelial cell line. GRβ expression was induced by treatment of epithelial cells with either dexamethasone or TNF-α. GRβ was able to inhibit glucocorticoid-induced transcriptional activation mediated by binding to glucocorticoid response elements (GREs). The suppressive effect of dexamethasone on TNF-α-induced IL-8 transcription was not affected by GRβ overexpression, rather GRβ had its own weak suppressive activity on TNF-α-induced IL-8 expression. Overall histone deacetylase activity and histone acetyltransferase activity were not changed by GRβ overexpression, but TNF-α-induced histone H4 acetylation at the IL-8 promoter was decreased with GRβ overexpression. This study suggests that GRβ overexpression does not affect glucocorticoid- induced suppression of IL-8 expression in airway epithelial cells and GRβ induces its own histone deacetylase activity around IL-8 promoter site.
Eun Jung Cho,Myoung Soo Park,Sahng Seop Kim,Gun Kang,Sunga Choi,이유란,장석종,Kwon Ho Lee,이상도,박진봉,전병화 대한약리학회 2011 The Korean Journal of Physiology & Pharmacology Vol.15 No.6
Ulmus davidiana var. japonica Rehder (Urticales: Ulmaceae) (UD) is a tree widespread in northeast Asia. It is traditionally used for anticancer and anti-inflammatory therapy. The present study investigated the effect of an ethanol extract of UD on vascular tension and its underlying mechanism in rats. The dried root bark of UD was ground and extracted with 80% ethanol. The prepared UD extract was used in further analysis. The effect of UD on the cell viability, vasoreactivity and hemodynamics were investigated using propidium iodide staining in cultured cells, isometric tension recording and blood pressure analysis, respectively. Low dose of UD (10∼100μg/ml) did not affect endothelial cell viability, but high dose of UD reduced cell viability. UD induced vasorelaxation in the range of 0.1∼10μg/ml with an ED50 value of 2μg/ml. UD-induced vasorelaxation was completely abolished by removal of the endothelium or by pre-treatment with L-NAME, an inhibitor of nitric oxide synthase. UD inhibited calcium influx induced by phenylephrine and high K+ and also completely abolished the effect of L-NAME. Intravenous injection of UD extracts (10∼100 mg/kg) decreased arterial and ventricular pressure in a dose-dependent manner. Moreover, UD extracts reduced the ventricular contractility (+dP/dt) in anesthetized rats. However, UD-induced hypotensive actions were minimized in L-NAME-treated rats. Taken together, out results showed that UD induced vasorelaxation and has antihypertensive properties, which may be due the activation of nitric oxide synthase in endothelium.
박문권(Moon Kweon Bang),김상섭(Sahng Seop Kim),주봉덕(Bong Deok Ju),송문식(Moon Sik Song),박미자(Mee Ja Park),한균인(Kyun In Han),김주옥(Ju Ock Kim),김선영(Sun Young Kim) 대한내과학회 1989 대한내과학회지 Vol.37 No.5
N/A In 1904, Albrecht first used the term hamartoma to refer to a congenital abnormal mixing of the normal components of an organ. Hamartomas can occur in any organ. The pulmonary hamartoma is an uncommon benign tumor, which is mainly located parenchymally and rarely located Intrabronchially. Fifty eight Case of intrabronchial hamartoma and 4 cases of multiple hamartoma were reported worldwide by 1972 and 1973, respectively. Intrabronchial hamartomas, 6 cases of which were presented by Cho and 1 case of which was presented by Lee, were reported domestically, in which, however, no intrabronchial multiple hamartoma was found. Recently we experienced a case of endobronchial multiple chondroid hamartoma identified with flexible bronchoscopic biopsies, and we herein report it with a review of the literature.
전병화(Jeon, Byeong-Hwa),김상섭(Kim, Sahng-Seop),김세훈(Kim, Se-Hoon),장석종(Chang, Seok-Jong) 대한생리학회 1990 대한생리학회지 Vol.24 No.2
The contractile action of barium (Ba<sup>2+</sup>) was investigated in the arterial strip of rabbit renal artery. The helical strip of isolated renal artery was immersed in the Tris-buffered Tyrode s solution equilibrated with 100% O<sup>2</sup> at 37℃ and its isometric tension was measured. Ba<sup>2+</sup>-induced contraction of arterial strip was dose-dependent and its maximal tension corresponded to 92.1±4.5% of tension by K<sup>+</sup>(100 mM). Ba<sup>2+</sup>-induced contraction did not show the tachyphylactic phenomenon in the normal Tyrode s solution. Ba<sup>+2</sup> induced the tonic contraction in the Ca<sup>2+</sup>-free tyrode s solution and that was increased by the extracellula addition of Ca<sup>2+</sup>. During the repeated exposure of the same dose of Ba<sup>2+</sup> (10 mM) in the Ca<sup>2+</sup>-free Tyrode s solution, Ba<sup>2+</sup>-induced contraction was progressively decreased. Even though the intracellular NE-and caffeine-sensitive Ca<sup>2+</sup> was depleted, Ba<sup>+2</sup> induced the tonic contraction. After the pretreatment of lanthnum or verapamil, Ba<sup>+2</sup> did not induce contraction. Ba<sup>2+</sup>-inducedcontraction was suppressed by extracellular K<sup>+</sup> in the normal Tyrode s solution and that was dependent on K<sup>+</sup> concentration. Suppressive effect of K<sup>+</sup> (14 mM) on the Ba<sup>2+</sup>-induced contraction was also dependent on the intracellular Ca<sup>2+</sup> concentration. From the above resuts, it is suggested that Ba<sup>+2</sup> activate indirectly the contractile process by promoting the mobilization of intracellular Ca<sup>2+</sup> and the influx of extracellular Ca<sup>2+</sup>. It is also suggested that action of Ba<sup>+2</sup> on the Ca<sup>2+</sup>-activated K<sup>+</sup> channel can result in the depolarization of cell membrane in the rabbit renal artery.
Cho, Eun-Jung,Park, Myoung-Soo,Kim, Sahng-Seop,Kang, Gun,Choi, Sung-A,Lee, Yoo-Rhan,Chang, Seok-Jong,Lee, Kwon-Ho,Lee, Sang-Do,Park, Jin-Bong,Jeon, Byeong-Hwa The Korean Society of Pharmacology 2011 The Korean Journal of Physiology & Pharmacology Vol.15 No.6
Ulmus davidiana var. japonica Rehder (Urticales: Ulmaceae) (UD) is a tree widespread in northeast Asia. It is traditionally used for anticancer and anti-inflammatory therapy. The present study investigated the effect of an ethanol extract of UD on vascular tension and its underlying mechanism in rats. The dried root bark of UD was ground and extracted with 80% ethanol. The prepared UD extract was used in further analysis. The effect of UD on the cell viability, vasoreactivity and hemodynamics were investigated using propidium iodide staining in cultured cells, isometric tension recording and blood pressure analysis, respectively. Low dose of UD ($10{\sim}100{\mu}g/ml)$ did not affect endothelial cell viability, but high dose of UD reduced cell viability. UD induced vasorelaxation in the range of $0.1{\sim}10{\mu}g/ml$ with an $ED_{50}$ value of $2{\mu}g/ml$. UD-induced vasorelaxation was completely abolished by removal of the endothelium or by pre-treatment with L-NAME, an inhibitor of nitric oxide synthase. UD inhibited calcium influx induced by phenylephrine and high $K^+$ and also completely abolished the effect of L-NAME. Intravenous injection of UD extracts (10~100 mg/kg) decreased arterial and ventricular pressure in a dose-dependent manner. Moreover, UD extracts reduced the ventricular contractility (+dP/dt) in anesthetized rats. However, UD-induced hypotensive actions were minimized in L-NAME-treated rats. Taken together, out results showed that UD induced vasorelaxation and has antihypertensive properties, which may be due the activation of nitric oxide synthase in endothelium.
폐상피세포에서 Dexamethasone에 의한 NF-${\kappa}B$ Transactivation 억제기전에 관한 연구
이계영,김윤섭,고미혜,박재석,지영구,김건열,곽상준,Lee, Kye-Young,Kim, Yoon-Seop,Ko, Mi-Hye,Park, Jae-Seok,Jee, Young-Koo,Kim, Keun-Youl,Kwak, Sahng-June 대한결핵및호흡기학회 2000 Tuberculosis and Respiratory Diseases Vol.48 No.5
Glucocorticoid receptor (GR) functions as a suppressor of inflammation by inhibiting the expression of many cytokine genes activated by NF-${\kappa}B$. The goal of this study is to investigate the mechanism by which GR repress NF-${\kappa}B$ activation in lung epithelial cells. We used A549 and BEAS-2B lung epithelia! cell lines. Using Ig$G{\kappa}$-NF-${\kappa}B$ luciferase reporter gene construct, we found that dexamethasone significantly suppressed TNF-$\alpha$-induced NF-${\kappa}B$ activation and the overexpression of GR showed dose-dependent reduction of TNF-$\alpha$-induced NF-${\kappa}B$ activity in both cell lines. However, DNA binding of NF-${\kappa}B$ induced by TNF-$\alpha$ in electromobility shift assay was not inhibited by dexamethasone. Super shift assay with anti-p65 antibody demonstrated the existence of p65 in NF-${\kappa}B$ complex induced by $\alpha$ Western blot showed that $I{\kappa}B{\alpha}$ degradation induced by TNF-$\alpha$ was not affected by dexamethasone and $I{\kappa}B{\kappa}$ was not induced by dexamethasone, neither. To evaluate p65 specific transactivation, we adopted co-transfection study of Gal4-p65TA1 or TA2 fusion protein expression system together with 5xGal4-luciferase vector. Co-transfection of GR with Gal4-p65TA1 or TA2 repressed luciferase activity profoundly to the level of 10-20% of p65TA1- or TA2-induced transcriptional activity. And this transrepressional effect was abolished by co-transfection of CBP of SRC-1 expression vectors. These results suggest that GR-mediated transrepression of NF-${\kappa}B$ in lung epithelial cells is through competing for binding to limiting amounts of transcriptional coactivators, CBP or SRC-1.