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( Amit Subedi ),( Mi Jin Kim ),( Saroj Nepal ),( Eung Seok Lee ),( Jung Ae Kim ),( Dong Hwan Sohn ),( Kyung Song ),( Sung Hee Lee ),( Won Sang Park ),( Byeong Seon Jeong ),( Pil Hoon Park ) 영남대학교 약품개발연구소 2013 영남대학교 약품개발연구소 연구업적집 Vol.23 No.0
MicroRNA-21 and programmed cell death 4 (PDCD4), a downstream target of miR-21, mediate diverse physiological responses. Here we demonstrate that globular adiponectin (gAcrp) modulates expressionof miR-21 and PDCD4 in RAW 264.7 macrophages. These effects were abrogated by inhibitors of ERK1/2, JNK or NF-κB. Conditioned media collected from gAcrp-stimulated RAW 264.7 macrophages caused similar effects as direct gAcrp treatment, showing the paracrine effect of gAcrp. These data indicate that gAcrp modulates the miR-21/PDCD4 axis through the ERK and JNK/NF-κB pathways in RAW 264.7 macrophages and further suggest that the miR-21/PDCD4 axis may be a novel target mediating adiponectin-induced biological responses.ⓒ2013 Federation of European Biochemical Societies. Published by Elsevier B.B. All rights reserved.
( Amit Subedi ),( Pil Hoon Park ) 영남대학교 약품개발연구소 2014 영남대학교 약품개발연구소 연구업적집 Vol.24 No.0
Adiponectin, a hormone produced from adipose tissue, regulates various biological responses, including inflammation and many metabolic processes. MicroRNAs control expression of diverse target genes and various physiological responses. Many of these responses are commonly regulated by adiponectin. However, effects of adiponectin on microRNAs regulation are largely unknown. Herein we demonstrated that globular adiponectin induces increase in miR-155 expression, which plays an important role in inflammatory response, in RAW 264.7 macrophages. We further showed that this effect was modulated by and MAPK/NF-κB dependent mechanisms. These results suggest that miR-155 would be a novel promising target mediating adiponectin-induced various biological responses.ⓒ2013 Elsevier Ltd. All rights reserved.
( Nirmala Tilija Pun ),( Amit Subedi ),( Mi Jin Kim ),( Pil Hoon Park ) 영남대학교 약품개발연구소 2015 영남대학교 약품개발연구소 연구업적집 Vol.25 No.-
Adiponectin,an adipokine predominantly produced from adipose tissue,exhibited potent anti-inflammatory properties.in particular,it inhibits production df pro-inflammatory cyto-kines,including tumor necrosis factor-a(TNF-a),in macrophages.Autophagy,an intracellu-lar self-digestion process,has been recently shown to rengulate inflammatory responses.in the present study,we investigated the role of autophagy induction in the suppression of-Li-popolysaccharide(LPS)-induced TNF-a expression by giobular adiponectin(gAcrp)and its potential mechanisms.Herein,we found that gAcrp treatment increased espressin of genes related with autophagy,including Atg5 and microtubule-associated protein light chain(LC3B),induced autophagosome formation and autophagy flux in RAW264.7macro-phages.Similar results were observed in primary macrophages isolated peritoneum of mice.interestingly,inhibition of autophagy by pretreatment with Bafilomycin A1 or knocking down of LC3B gene restored suppression of TNF-a espression,tumor necrosis factor re-ceptor-associated factor 6(TRAF6)espression and p38MAPK phosphorylation by gAcrp.implying a critical role of autophagy induction in the debelopment of tolerance to LPS-in-duced TNF-a expression bygAcrp.Wealso found that knocking-down of FoxO3A,a fork-head box O member of transcription factor,biocked gAcrp-induced espression of LC3ll and Atg5.Moreover,gene silencing of Silent information regulator 1(SIRT1)blocked both gAcrp-induced nuclear translocation of FoxO3A and LC3ll expression.Finally,pretreatment with ROS inhibitors,prevented gAcrp-induced SIRT1 espression and further generated in-hibitory effects on gAcrp-induced autophagy,indicating role of ROS production in gAcrp-induced SIRT1 espression and subsequent autophagy induction.Taken together,these findings indicate that globular adiponectin suppresses LPS-induced TNF-a expression,at least in part,via autophagy activation,Furthermore,SIRT1-FoxO3A axis plays a crucial role in gAcro-induced autophagy in macerophages.
( Saroj Nepal ),( Mi Jin Kim ),( Amit Subedi ),( Eung Seok Lee ),( Chul Soon Yong ),( Jung Ae Kim ),( Wonku Kang ),( Mi Kyung Kwak ),( Dharamvie Singh Arya ),( Pil Hoon Park ) 영남대학교 약품개발연구소 2013 영남대학교 약품개발연구소 연구업적집 Vol.23 No.0
Hepatocellular apoptosis is an essential pathological feature of alcoholic liver disease. Adiponectin, an adipokine predominantly secreted from adipose tissue, has been shown to play beneficial roles in alcoholic liver disease against various inflammatory and pro-apoptotic molecules. However, the effects of adiponectin on ethanol-induced apoptosis in liver cells are largely unknown. Herein, we investigated the role of globularadiponectin (gAcrp) in the prevention of ethanol-induced apoptosis and further tried to decipher the potential mechanisms involved. In the present study, we demonstrated that gAcrp significantly inhibits both ethanol-induced increase in Fas ligand expression and activation of caspase-3 in human hepatoma cell lines (HepG2 cells), suggesting that gAcrp plays a protective role against ethanol-induced apoptosis in liver cells. This protective effect of gAcrp was mediated through adiponectin receptor R1 (adipoR1). Further, globular adiponectin treatment caused induction of heme oxygenase-1 (HO-1) through, at least in part, nuclear factor (erythroid-derived 2)-like 2, (Nrf2) signaling. Treatment with SnPP, a pharmacological inhibitor of HO-1, and knockdown of HO-1 with small interfering RNA (siRNA) restored caspase-3 activity suppressed by gAcrp, indicating a critical role of HO-1 in mediating the protective role of gAcrp in ethanol-induced apoptosis in liver cells. In addition, carbon monoxide, a byproduct obtained from the catabolism of free heme was found to contribute to the anti-apoptotic effect of adiponectin. In conclusion, these data demonstrated that globular adiponectin prevents ethanol-induced apoptosis in HepG2 cells via HO-1 induction and revealed a novel biological response of globular adiponectin in the protection of liver injury from alcohol consumption. ⓒ2012 Elsevier lnc. All rights reserved.