• Title/Summary/Keyword: C-Jun expression

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Molecular cloning and characterization of novel human JNK2 (MAPK9) transcript variants that show different stimulation activities on AP-1

  • Wang, Pingzhang;Xiong, Ying;Ma, Chuan;Shi, Taiping;Ma, Dalong
    • BMB Reports
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    • v.43 no.11
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    • pp.738-743
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    • 2010
  • The c-Jun $NH_2$-terminal kinase (JNK) signaling pathway participates in many physiological functions. In the current study we reported the cloning and characterization of five novel JNK2 transcript variants, which were designated as $JNK2\alpha3$, $JNK2\alpha4$, $JNK2\beta3$, $JNK2\gamma1$ and $JNK2\gamma2$, respectively. Among them, $JNK2\alpha4$ and $JNK2\gamma2$ are potential non-coding RNA because they contain pre-mature stop codons. Both $JNK2\alpha3$ and $JNK2\beta3$ contain an intact kinase domain, and both encode a protein product of 46 kDa, the same as those of $JNK2\alpha1$ and $JNK2\beta1$. $JNK2\gamma1$ contains a disrupted kinase domain and it showed a disable function. When over-expressed in mammalian cells, $JNK2\alpha3$ showed higher activity on AP-1 than that of $JNK2\beta3$ and $JNK2\gamma1$. Furthermore, $JNK2\alpha3$ and $JNK2\beta3$ showed different levels of substrate phosphorylation, although they both could promote the proliferation of 293T cells. Our results further demonstrate that JNK2 isoforms preferentially target different substrates and may regulate the expression of various target genes.

Molecular Cloning of Vps26a, Vps26b, Vps29, and Vps35 and Expression Analysis of Retromer Complex in Micro Pig

  • Kim, Ek-Yune;Kim, Young-Hyun;Ryu, Chung-Hun;Lee, Jae-Woong;Kim, Sang-Hyun;Lee, Sang-Rae;Kim, Myeong-Su;Kim, Wan-Jun;Lim, Jeong-Mook;Chang, Kyu-Tae
    • Reproductive and Developmental Biology
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    • v.32 no.1
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    • pp.65-70
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    • 2008
  • Members of the Vps (Vacuolar protein sorting) protein family involved in the formation of the retromer complex have been discovered in a variety of species such as yeast, mouse, and human. A mammalian retromer complex is composed of Vps26, Vps29, and Vps35 proteins and plays and important role in cation-independent mannose-6-phosphate receptor retrieval from the endosome to the trans-Golgi network. In this study, we have identified the full-length sequences of the retromer components of Vps26, Vps29, and Vps35 in micro pigs. The cDNA sequences of these retromer components have been determined and the result showed there is 99% homology among the component counterparts from mouse, micro pigs, and humans. In addition, the retromer complexes formed with hetero-components were found in the brain of micro pigs. Based on above results, we suggest mammalian Vps components are well conserved in micro pigs.

Effect of Melissa officinalis L. leaf extract on lipid accumulation by modulating specific adipogenic gene transcription factors in 3T3-L1 adipocytes

  • Lee, Hyun Jeong;Lim, Jonghak;Peak, Junoh;Ki, Mun-sang;Lee, Sang-bong;Choe, Gayong;Jung, Jaeyun;Jung, Hansang;Jeon, Suwon;Park, Tae-Sik;Shim, Soon-Mi
    • Journal of Applied Biological Chemistry
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    • v.63 no.2
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    • pp.169-174
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    • 2020
  • The objective of this study was to investigate the effects of a hypodermic injectable solution comprised of an LPM LB meso solution containing Melissa officinalis L. leaf extract (LPM) on the lipogenesis in the 3T3-L1 cells line. The lipid accumulation measured by oil red o staining in the 3T3-L1 adipocytes treated with LPM, which was reduced in a dose dependent manner and showed 91.7 to 62.9% compared to control group. Its effectiveness with a 50% solution was significantly higher than the hydroxycitric acid (positive control) treatment without showing cell cytotoxicity. In a quantitative real-time PCR, it was demonstrated that the LPM treatment appeared to upregulate the mRNA expression of the adipogenesis-related genes, which included the peroxisome proliferator-activated receptor gamma (50% concentration) while down-regulating the CCAAT-enhancer binding protein alpha (50% concentration) and the sterol regulatory element-binding protein 1c (10, 25, and 50% concentrations). The results from the current study suggest that the LPM could be useful biomaterials that can inhibit obesity in the 3T3-L1 cells, which could possibly be by regulating the specific adipogenic gene transcription factors.

Immunohistochemical Study of Wild Ginseng on Benzopyrene Induced $TNF-{\alpha}$ and COX-2 Expression in Rats (장뇌산삼이 Benzopyrene으로 유도된 간조직의 $TNF-{\alpha}$와 COX-2의 면역조직학적 분포에 미치는 영향)

  • Ahn Sang-Hyun;Jo Sung-Jun;Yoon Chang-Hwan;Cho Min-Kyung;Kim Jin-Taek;Shin Heung-Muk
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.19 no.6
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    • pp.1568-1572
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    • 2005
  • Polycyclic aromatic hydrocarbon (PAH), such as benzo(a)pyrene (B(a)P), are toxic environmental contaminants known to enhance oxidative stress, production of pro-inflammatory and inflammatory cytokines. The present study was designed in order to determine whether wild ginseng (Panax ginseng C. A. Meyer) protect PAH-induced oxidative stress and inflammation. B(a)P (0.5 mg/kg, i.p.) treatment increased the distribution of immunoreactive cells for tumor necrosis factor $(TNF)-\alpha$ and cyclooxygenase (COX)-2 in peri-portal triad region and immunoreaction was shown in the cytoplasm of macrophage. Pre-treatment with wild ginseng significantly decreased immune responses in the rats treated with B(a)p. The rats given 50 mg/kg/day for 4 weeks before B(a)P treatment had 1.39-fold and 1.5-fold inhibition of $TNF-\alpha$ and COX-2 positive reaction, respectively. Wild ginseng extract alone had no effect on the distributional changes. The SOD activity as scavenger enzymes after wild ginseng administration dose-dependantly increased compared with butylated hydroxytoluene, a general radical scavenger. These data likely indicate that wild ginseng extract may act as inflammatory regulator in conjunction with inhibition of oxidant dependent metabolic activation in environmental contaminants-induced hepatic inflammation.

Taurine supplementation in diet for olive flounder at low water temperature

  • Kim, Joo-Min;Malintha, G.H.T.;Gunathilaka, G.L.B.E.;Lee, Chorong;Kim, Min-Gi;Lee, Bong-Joo;Kim, Jeong-Dae;Lee, Kyeong-Jun
    • Fisheries and Aquatic Sciences
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    • v.20 no.9
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    • pp.20.1-20.8
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    • 2017
  • The objective of this study was to examine the effect of dietary supplementation of taurine for juvenile olive flounder (Paralichthys olivaceus) at low water temperature ($16.4{\pm}0.36^{\circ}C$). Fish meal (FM)-based diet was used as the control diet. Four other experimental diets were prepared by adding taurine to FM-based diet at 0.25, 0.50, 1.00, and 1. 50% (T1, T2, T3, and T4, respectively). Each experimental diet was fed to triplicate groups of fish (initial mean body weight, 19.5 g) for 10 weeks. At the end of the feeding trial, growth performance and feed utilization, hematological parameters, non-specific immune responses, whole-body proximate composition, and liver mRNA expression of insulin-like growth factor-1 (IGF-1) were investigated. Feed conversion ratio was significantly reduced while protein efficiency ratio was significantly increased in taurine-supplemented groups. Hematocrit and hemoglobin were also significantly increased while plasma cholesterol levels were decreased in taurine-supplemented groups than those in the control group. Nitroblue-tetrazolium, myeloperoxidase and lysozyme activities, and plasma immunoglobulin level were significantly increased by taurine supplementation. These results suggest that dietary taurine supplementation is effective in improving growth performances, feed utilization, and innate immunity of olive flounder in low water temperature season.

Anti-Inflammatory Effect of Aqueous Extract of Scolopendrae Corpus in RAW 264.7 Cells (마우스 대식세포주인 RAW 264.7 세포에서 오공(蜈蚣)의 항염증 효과)

  • Jo, Il-Joo;Choi, Mee-Ok;Park, Min-Cheol;Song, Ho-Joon;Park, Sung-Joo
    • The Korea Journal of Herbology
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    • v.26 no.3
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    • pp.23-29
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    • 2011
  • Objective : The purpose of this study was to investigate the anti-inflammatory effects of aqueous extract from Scolopendrae Corpus (SC) on lipopolysaccharide (LPS)-induced inflammatory response. Methods : To evaluate the anti-inflammatory effects of SC, we examined the inflammatory mediators such as nitric oxide (NO) and pro-inflammatory cytokines (TNF-a, inteleukin (IL)-$1{\beta}$ and IL-6) on RAW 264.7 cells. We also examined molecular mechanisms such as mitogen-activated protein kinases (MAPKs) and inhibitory kappa B a ($I{\kappa}$-Ba) using western blot. Furthermore, we also investigated the effect of SC on LPS-induced endotoxin shock. Results : Extract from SC itself had not any cytotoxic effect in RAW 264.7 cells. Aqueous extract from SC inhibited LPS-induced NO production and iNOS expression. SC pre-treatment also inhibited IL-$1{\beta}$, IL-6 production in RAW 264.7 cells. To investigate inhibitory effects of SC on inflammatory mediators, activation of MAPKs was examined. SC inhibited the phosphorylation of p38 kinases (p38), c-Jun $NH_2$-terminal kinase (JNK) and also the degradation of $I{\kappa}$-$B{\alpha}$ in RAW 264.7 cells stimulated with LPS. Furthermore, SC administration reduced LPS-induced endotoxin shock. Conclusion : SC down-regulated LPS-induced production of inflammatory mediators through inhibition of activation of p38, JNK and degradation of $I{\kappa}$-$B{\alpha}$. Taken together, our results suggest that SC may be a beneficial drug against inflammatory diseases such as sepsis.

Lisophosphatidic Acid Inhibits Melanocyte Proliferation via Cell Cycle Arrest

  • Kim, Dong-Seok;Park, Seo-Hyoung;Kim, Sung-Eun;Kwon, Sun-Bang;Park, Eun-Sang;Youn, Sang-Woong;Park, Kyoung-Chan
    • Archives of Pharmacal Research
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    • v.26 no.12
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    • pp.1055-1060
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    • 2003
  • Lysophosphatidic acid (LPA) is a well-known mitogen in various cell types. However, we found that LPA inhibits melanocyte proliferation. Thus, we further investigated the possible signaling pathways involved in melanocyte growth inhibition. We first examined the regulation of the three major subfamilies of mitogen-activated protein (MAP) kinases and of the Akt pathway by LPA. The activations of extracellular signal-regulated protein kinase (ERK) and c-Jun N-terminal kinase (JNK) were observed in concert with the inhibition of melanocyte proliferation by LPA, whereas p38 MAP kinase and Akt were not influenced by LPA. However, the specific inhibition of the ERK or JNK pathways by PD98059 or D-JNKI1, respectively, did not restore the antiproliferative effect. We next examined changes in the expression of cell cycle related proteins. LPA decreased cyclin $D_1 and cyclin D_2$ levels but increased $p21^{WAF1/CIP1}$ (p21) and $p27^{KIP1}$ (p27) levels, which are known inhibitors of cyclin-dependent kinase. Flow cytometric analysis showed the inhibition of DNA synthesis by a reduction in the S phase and an increase in the $G_0/G_1$ phase of the cell cycle. Our results suggest that LPA induces cell cycle arrest by regulating the expressions of cell cycle related proteins.

Total ginsenosides suppress monocrotaline-induced pulmonary hypertension in rats: involvement of nitric oxide and mitogen-activated protein kinase pathways

  • Qin, Na;Yang, Wei;Feng, Dongxu;Wang, Xinwen;Qi, Muyao;Du, Tianxin;Sun, Hongzhi;Wu, Shufang
    • Journal of Ginseng Research
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    • v.40 no.3
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    • pp.285-291
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    • 2016
  • Background: Ginsenosides have been shown to exert beneficial pharmacological effects on the central nervous, cardiovascular, and endocrine systems. We sought to determine whether total ginsenosides (TG) inhibit monocrotaline (MCT)-induced pulmonary hypertension and to elucidate the underlying mechanism. Methods: MCT-intoxicated rats were treated with gradient doses of TG, with or without $N^G$-nitro-$\small{L}$-arginine methyl ester. The levels of molecules involving the regulation of nitric oxide and mitogen-activated protein kinase pathways were determined. Results: TG ameliorated MCT-induced pulmonary hypertension in a dose-dependent manner, as assessed by the right ventricular systolic pressure, the right ventricular hypertrophy index, and pulmonary arterial remodeling. Furthermore, TG increased the levels of pulmonary nitric oxide, endothelial nitric oxide synthase, and cyclic guanosine monophosphate. Lastly, TG increased mitogen-activated protein kinase phosphatase-1 expression and promoted the dephosphorylation of extracellular signal-regulated protein kinases 1/2, p38 mitogen-activated protein kinase, and c-Jun NH2-terminal kinase 1/2. Conclusion: TG attenuates MCT-induced pulmonary hypertension, which may involve in part the regulation of nitric oxide and mitogen-activated protein kinase pathways.

Propyl Gallate Inhibits Adipogenesis by Stimulating Extracellular Signal-Related Kinases in Human Adipose Tissue-Derived Mesenchymal Stem Cells

  • Lee, Jeung-Eun;Kim, Jung-Min;Jang, Hyun-Jun;Lim, Se-Young;Choi, Seon-Jeong;Lee, Nan-Hee;Suh, Pann-Ghill;Choi, Ung-Kyu
    • Molecules and Cells
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    • v.38 no.4
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    • pp.336-342
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    • 2015
  • Propyl gallate (PG) used as an additive in various foods has antioxidant and anti-inflammatory effects. Although the functional roles of PG in various cell types are well characterized, it is unknown whether PG has effect on stem cell differentiation. In this study, we demonstrated that PG could inhibit adipogenic differentiation in human adipose tissue-derived mesenchymal stem cells (hAMSCs) by decreasing the accumulation of intracellular lipid droplets. In addition, PG significantly reduced the expression of adipocyte-specific markers including peroxisome proliferator-activated receptor-${\gamma}$ (PPAR-${\gamma}$), CCAAT enhancer binding protein-${\alpha}$ (C/EBP-${\alpha}$), lipoprotein lipase (LPL), and adipocyte fatty acid-binding protein 2 (aP2). PG inhibited adipogenesis in hAMSCs through extracellular regulated kinase (ERK) pathway. Decreased adipogenesis following PG treatment was recovered in response to ERK blocking. Taken together, these results suggest a novel effect of PG on adipocyte differentiation in hAMSCs, supporting a negative role of ERK1/2 pathway in adipogenic differentiation.

Effects of Noradrenaline on the Membrane Potential of Prostatic Neuroendocrine Cells of Rat

  • Kim, Jun-Hee;Shin, Sun-Young;Uhm, Dae-Yong;Kim, Sung-Joon
    • The Korean Journal of Physiology and Pharmacology
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    • v.7 no.1
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    • pp.47-52
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    • 2003
  • The prostate gland contains numerous neuroendocrine cells that are believed to influence the function of the prostate gland. Our recent study demonstrated the expression of both ${\alpha}1$- and ${\alpha}2$-ARs, signaling the release of stored $Ca^{2+}$ and the inhibition of N-type $Ca^{2+}$ channels, respectively, in rat prostate neuroendocrine cells (RPNECs). In this study, the effects of NA on the resting membrane potential (RMP) of RPNECs were investigated using a whole-cell patch clamp method. Fresh RPNECs were dissociated from the ventral lobe of rat prostate and identified from its characteristic shape; round or oval shape with dark cytoplasm. Under zero-current clamp conditions with KCl pipette solution, the resting membrane potential (RMP) of RPNECs was between -35 mV and -85 mV. In those RPNECs with relatively hyperpolarized RMP (<-60 mV), the application of noradrenaline (NA, $1{\mu}M$) depolarized the membrane to around -40 mV. In contrast, the RPNECs with relatively depolarized RMP (>-45 mV) showed a transient hyperpolarization and subsequent fluctuation at around -40 mV on application of NA. Under voltage clamp conditions (holding voltage, -40 mV) with CsCl pipette solution, NA evoked a slight inward current (<-20 pA). NA induced a sharp increase of cytosolic $Ca^{2+}$ concentration ($[Ca^{2+}]_c$), measured by the fura-2 fluorescence, and the voltage clamp study showed the presence of charybdotoxin-sensitive $Ca^{2+}$-activated $K^+$ currents. In summary, adrenergic stimulation induced either depolarization or hyperpolarization of RPNECs, depending on the initial level of RMP. The inward current evoked by NA and the $Ca^{2+}$-activated $K^+$ current might partly explain the depolarization and hyperpolarization, respectively.