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김석,노구섭,정태식,김화진,허록원,이진옥,이정은,전병탁,김원호,함종렬 대한약리학회 2014 The Korean Journal of Physiology & Pharmacology Vol.18 No.4
Exendin-4 (Ex-4), a glucagon-like peptide-1 receptor (GLP-1R) agonist, has been known to reversehepatic steatosis in ob/ob mice. Although many studies have evaluated molecular targets of Ex-4, itsmechanism of action on hepatic steatosis and fibrosis has not fully been determined. In the liver,glucose transporter 4 (GLUT4) is mainly expressed in hepatocytes, endothelial cells and hepatic stellatecells (HSCs). In the present study, the effects of Ex-4 on GLUT4 expression were determined in theliver of ob/ob mice. Ob/ob mice were treated with Ex-4 for 10 weeks. Serum metabolic parameters,hepatic triglyceride levels, and liver tissues were evaluated for hepatic steatosis. The weights of thewhole body and liver in ob/ob mice were reduced by long-term Ex-4 treatment. Serum metabolicparameters, hepatic steatosis, and hepatic fibrosis in ob/ob mice were reduced by Ex-4. Particularly,Ex-4 improved hepatic steatosis by enhancing GLUT4 via GLP-1R activation in ob/ob mice. Ex-4treatment also inhibited hepatic fibrosis by decreasing expression of connective tissue growth factorin HSCs of ob/ob mice. Our data suggest that GLP-1 agonists exert a protective effect on hepaticsteatosis and fibrosis in obesity and type 2 diabetes.
GyeongJaeCho,노구섭,HyunJoonKim,YoonSookKim,SooHyunCho,WonJunChoi,WonYoungPaik,SangSooKang,WanSungChoi 대한의학회 2003 Journal of Korean medical science Vol.18 No.3
Placental development requires extensive angiogenesis and the invasion of the maternal decidua by the trophoblasts. Adequate and organized interaction of vascular endothelial growth factors (VEGF), placenta growth factors (PlGF), and their receptors are essential for a normal development and function of the placenta. In this study, we evaluated the expressions of PlGFs and their receptors, mRNAs by Northern blotting, in situ hybridization and RT-PCR in the normal and pregnancy-induced hypertensive (PIH) placentas. The expression level of PlGF-2 mRNA was lower in the PIH placentas compared to control as assessed by Northern blotting and in situ hybridization. PlGF mRNA was mainly localized to the vasculosyncytial membrane of placental villi and villous stroma. The expression of PlGF receptor-1 (PlGFR-1) was significantly increased in the PIH placentas compared to the normal ones. These results suggest that the alteration of PlGF-2 and PlGFR-1 mRNA expressions in the placenta are related to the pathogenesis of PIH.
손은영,이동훈,노구섭,김현준,강상수,조경제,최완성 대한해부학회 2008 Anatomy & Cell Biology Vol.41 No.3
Reactive oxygen species (ROS) are important signaling molecules or mediators in many cellular responses, including the oxidative-burst defense response. Certain hormones are neuroprotective because they are modulators of neuronal activity or ROS scavengers. We have examined the effect of a hormone-free condition on ROS levels following glutamate-induced excitotoxicity in the mouse hippocampal HT22 cell line. We show that hormone starvation slightly elevates ROS and that continuous low concentrations of ROS induce expression of antioxidant enzymes, such as heme oxygenase-1 (HO-1). In addition, N-acetyl-L-cysteine (NAC) restores the expression of ERK1/2 protein in hormone-starved HT22 cells. These findings suggest that whereas high-dose ROS are cytotoxic and lead to tissue damage in the brain low-dose ROS may act in neuroprotective signaling.
CD137 induces adhesion and cytokine production in human monocytic THP-1cells
최정원,이현우,노구섭,김홍희,KyuBum Kwack 생화학분자생물학회 2005 Experimental and molecular medicine Vol.37 No.2
CD137, which is expressed on activated T cells, plays a critical role in inflammatory responses. However, the exact role that CD137 plays in monocytes is not fully known. Here we studied the expression and function of CD137 in human monocytic THP-1 cells, which we found constitutively expresses CD137 at the mRNA and protein level. Cross-linking of CD137 increased the secretion of IL-8 and TNF-a, promoted the expression of CD54 and CD11b, and increased adhesion to ECM proteins. In particular CD137-induced adhesion of THP-cells was inhibited by an inhibitor of MEK, but not by a p38 kinase inhibitor. Taken together, these results show that the adhesion and cytokine production of THP-1 cells induced by CD137 occurs via activation of MEK, which results in the activation of ERK-1/2 signaling pathways. Therefore, this study suggests that CD137 induces an activating and migrating signal during inflammatory processes.
Metformin inhibits cervical cancer cell proliferation via decreased AMPK O-GlcNAcylation
김민영,김윤숙,김민준,최미영,노구섭,이동훈,김현준,강상수,조경제,신정규,최완성 한국통합생물학회 2019 Animal cells and systems Vol.23 No.4
Metformin is a widely used drug for the treatment of type 2 diabetes. Antidiabetic drugs are also known to influence cancer progression, as high glucose levels affect both cancer and diabetes. Metformin induces cell cycle arrest in cancer cells, but the underlying mechanism remains unclear in cervical cancer system. Here, we examined how metformin affects cell cycle arrest and apoptosis in cervical cancer cells. Western blot analysis showed that levels of O-linked Nacetylglucosamine (O-GlcNAc) and O-GlcNAc transferase (OGT) were increased in cervical cancer cells; these effects were reversed by metformin treatment. Immunoprecipitation analysis was used to examine the interplay between O-GlcNAcylation and phosphorylation in HeLa cells, revealing that metformin decreased O-GlcNAcylated AMP-activated protein kinase (AMPK) and increased levels of phospho-AMPK compared to untreated cells. These results were associated with decreased cell cycle arrest and apoptotic cell death in HeLa cells, as shown by flow cytometry. Moreover, 6-diazo-5-oxo-L-norleucine (a glutamine fructose-6-phosphate aminotransferase inhibitor) or thiamet G (an O-GlcNAcase inhibitor) decreased or increased levels of O-GlcNAcylated AMPK, and increased or decreased levels of phosphorylated AMPK, respectively, suggesting that OGlcNAc modification affects AMPK activation. Of note, we found that metformin treatment of HeLa cells increased the levels of p21 and p27 (which are AMPK-dependent cell cycle inhibitors), leading to increased cell cycle arrest and apoptosis in HeLa cells compared to untreated cells. These findings suggest that metformin may serve as a useful antiproliferative drug in cervical cancer cells, with potential therapeutic benefit.
김윤숙,김민준,최미영,이동훈,노구섭,김현준,강상수,조경제,박기훈,김성재,유지명,최완성 한국식품영양과학회 2017 Journal of medicinal food Vol.20 No.10
Aralia elata (Miq) Seem (AES) is a medicinal plant used in traditional Chinese and Korean medicine for the treatment of several diseases, including diabetes. This study aimed to investigate the neuroprotective effect of AES extract against high glucose-induced retinal injury in diabetic mice. AES extract (20 and 100 mg/kg body weight) was orally administered to control mice or mice with streptozotocin-induced diabetes. Protein levels of O-linked β-N-acetylglucosamine (O-GlcNAc) transferase (OGT), carbohydrate-responsive element-binding protein (ChREBP), sterol regulatory elementbinding protein (SREBP)-1, thioredoxin-interacting protein (TXNIP), fatty acid synthase (FAS), and acetyl CoA carboxylase (ACC) were analyzed by western blotting. Colocalization of terminal deoxynucleotide transferase-mediated dUTP nicked-end labeling (TUNEL)-positive ganglion cells and OGT, ChREBP, or TXNIP were monitored using double immunofluorescence analysis. Interaction between ChREBP and OGT was assessed using coimmunoprecipitation analysis. AES extract protected the retinas from neuronal injury and decreased levels of OGT, ChREBP, TXNIP, SREBP-1, FAS, and ACC in the diabetic retinas. AES extract reduced colocalization of TUNEL-positive ganglion cells and OGT, ChREBP, or TXNIP in the diabetic retinas. Coimmunoprecipitation analysis indicated that AES extract reduced interaction between ChREBP and OGT and attenuated ganglion cell death in diabetic retinas. Moreover, the ChREBP that colocalized with OGT or the TUNEL signal was significantly decreased in diabetic mice treated with AES extract. These findings show that AES extract can alleviate OGT-, ChREBP-, TXNIP-, or SREBP-1-related retinal injury in diabetic retinopathy.