Publications by authors named "Jihyun Je"

15 Publications

  • Page 1 of 1

P2Y2R Deficiency Ameliorates Hepatic Steatosis by Reducing Lipogenesis and Enhancing Fatty Acid β-Oxidation through AMPK and PGC-1α Induction in High-Fat Diet-Fed Mice.

Int J Mol Sci 2021 May 24;22(11). Epub 2021 May 24.

Department of Pharmacology, Institute of Health Sciences, Gyeongsang National University College of Medicine, Jinju 52727, Korea.

Non-alcoholic fatty liver disease (NAFLD) is a chronic metabolic liver disease associated with obesity and insulin resistance. Activation of the purinergic receptor P2Y2R has been reported to promote adipogenesis, inflammation and dyslipidemia in adipose tissues in obese mice. However, the role of P2Y2R and its mechanisms in NAFLD remain unknown. We hypothesized that P2Y2R deficiency may play a protective role in NAFLD by modulating lipid metabolism in the liver. In this study, we fed wild type and P2Y2R knockout mice with a high-fat diet (HFD) for 12 weeks and analyzed metabolic phenotypes. First, P2Y2R deficiency effectively improved insulin resistance with a reduction in body weight and plasma insulin. Second, P2Y2R deficiency attenuated hepatic lipid accumulation and injury with reduced alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. Third, P2Y2R deficiency decreased the expression of fatty acid synthesis mediators (cluster of differentiation (CD36), fatty acid synthase (FAS), and stearoyl-CoA desaturase 1 (SCD1)); and increased the expression of adipose triglyceride lipase (ATGL), a lipolytic enzyme. Mechanistically, P2Y2R deficiency increased the AMP-activated protein kinase (AMPK) activity to improve mitochondrial fatty acid β-oxidation (FAO) by regulating acetyl-CoA carboxylase (ACC) and carnitine palmitoyltransferase 1A (CPT1A)-mediated FAO pathway. In addition, P2Y2R deficiency increased peroxisome proliferator-activated gamma co-activator-1α (PGC-1α)-mediated mitochondrial biogenesis. Conclusively, P2Y2R deficiency ameliorated HFD-induced hepatic steatosis by enhancing FAO through AMPK signaling and PGC-1α pathway, suggesting P2Y2R as a promising therapeutic target for NAFLD.
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http://dx.doi.org/10.3390/ijms22115528DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8197197PMC
May 2021

Geniposide Improves Diabetic Nephropathy by Enhancing ULK1-Mediated Autophagy and Reducing Oxidative Stress through AMPK Activation.

Int J Mol Sci 2021 Feb 6;22(4). Epub 2021 Feb 6.

Department of Pharmacology, Institute of Health Sciences, Gyeongsang National University College of Medicine, Jinju 52727, Korea.

Diabetic nephropathy (DN) is a common pathological feature in patients with diabetes and the leading cause of end-stage renal disease. Although several pharmacological agents have been developed, the management of DN remains challenging. Geniposide, a natural compound has been reported for anti-inflammatory and anti-diabetic effects; however, its role in DN remains poorly understood. This study investigated the protective effects of geniposide on DN and its underlying mechanisms. We used a C57BL/6 mouse model of DN in combination with a high-fat diet and streptozotocin after unilateral nephrectomy and treated with geniposide by oral gavage for 5 weeks. Geniposide effectively improves DN-induced renal structural and functional abnormalities by reducing albuminuria, podocyte loss, glomerular and tubular injury, renal inflammation and interstitial fibrosis. These changes induced by geniposide were associated with an increase of AMPK activity to enhance ULK1-mediated autophagy response and a decrease of AKT activity to block oxidative stress, inflammation and fibrosis in diabetic kidney. In addition, geniposide increased the activities of PKA and GSK3β, possibly modulating AMPK and AKT pathways, efficiently improving renal dysfunction and ameliorating the progression of DN. Conclusively, geniposide enhances ULK1-mediated autophagy and reduces oxidative stress, inflammation and fibrosis, suggesting geniposide as a promising treatment for DN.
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http://dx.doi.org/10.3390/ijms22041651DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7915505PMC
February 2021

Fermentation of Sprouted Ginseng () Increases Flavonoid and Phenolic Contents to Attenuate Alcoholic Hangover and Acute Liver Injury in Mice.

Am J Chin Med 2021 26;49(1):131-146. Epub 2020 Dec 26.

Department of Pharmacology, Institute of Health Sciences, Gyeongsang National University College of Medicine, Jinju 52727, Republic of Korea.

Alcoholic liver damage is caused by ethanol and its oxidized intermediates, and endotoxin-induced acute liver failure is mediated by apoptosis and inflammation. We investigated whether extracts of sprouts of (SG) attenuate alcohol or endotoxin-induced acute liver injury in mice. Whole SG contains eight times more ginsenosides than the root and, because it grows quickly ([Formula: see text]30 days) without using pesticides, the whole-plant can be harvested. The extracts were enriched in phenolics and flavonoids and showed high radical scavenging activities. Mice received oral administration of SG or fermented SG (FSG) extracts 1 h before an injection of either ethanol or lipopolysaccharide and D-galactosamine (LPS/GalN). The latency of righting reflex was monitored to examine the effect of extracts on relieving hangover symptoms. The results indicate that FSG significantly reduced the latency of righting reflex, SG and FSG increased the activity and expression of ethanol-metabolizing enzymes, and FSG decreased hepatic necrosis and plasma levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). During the ethanol metabolism, cytochrome P450 2E1 expression was increased, but 4-hydroxynonenal levels were decreased by the extracts due to their anti-oxidant activity. LPS/GalN-induced liver injury was reduced by SG and FSG; plasma ALT and AST levels, hepatic necrosis, and apoptotic and inflammatory markers were all decreased. In conclusion, SG extracts attenuated ethanol-induced hangover and endotoxin-induced acute liver injury, and fermentation enhanced the efficacy with regard to relieving hangover.
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http://dx.doi.org/10.1142/S0192415X21500075DOI Listing
December 2020

P2Y2R contributes to the development of diabetic nephropathy by inhibiting autophagy response.

Mol Metab 2020 12 25;42:101089. Epub 2020 Sep 25.

Department of Pharmacology, Institute of Health Sciences, Gyeongsang National University School of Medicine, Jinju 52727, Republic of Korea; Department of Convergence Medical Sciences, Institute of Health Sciences, Gyeongsang National University Graduate School, Jinju 52727, Republic of Korea. Electronic address:

Objective: Diabetic nephropathy (DN) is one of the most common complications of diabetes and a critical risk factor for developing end-stage renal disease. Activation of purinergic receptors, including P2Y2R has been associated with the pathogenesis of renal diseases, such as polycystic kidney and glomerulonephritis. However, the role of P2Y2R and its precise mechanisms in DN remain unknown. We hypothesised that P2Y2R deficiency may play a protective role in DN by modulating the autophagy signalling pathway.

Methods: We used a mouse model of DN by combining a treatment of high-fat diet and streptozotocin after unilateral nephrectomy in wild-type or P2Y2R knockout mice. We measured renal functional parameter in plasma, examined renal histology, and analysed expression of autophagy regulatory proteins.

Results: Hyperglycaemia and ATP release were induced in wild type-DN mice and positively correlated with renal dysfunction. Conversely, P2Y2R knockout markedly attenuates albuminuria, podocyte loss, development of glomerulopathy, renal tubular injury, apoptosis and interstitial fibrosis induced by DN. These protective effects were associated with inhibition of AKT-mediated FOXO3a (forkhead box O3a) phosphorylation and induction of FOXO3a-induced autophagy gene transcription. Furthermore, inhibitory phosphorylation of ULK-1 was decreased, and the downstream Beclin-1 autophagy signalling was activated in P2Y2R deficiency. Increased SIRT-1 (sirtuin-1) and FOXO3a expression in P2Y2R deficiency also enhanced autophagy response, thereby ameliorating renal dysfunction in DN.

Conclusions: P2Y2R contributes to the pathogenesis of DN by impairing autophagy and serves as a therapeutic target for treating DN.
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http://dx.doi.org/10.1016/j.molmet.2020.101089DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7568185PMC
December 2020

Honokiol Protects the Kidney from Renal Ischemia and Reperfusion Injury by Upregulating the Glutathione Biosynthetic Enzymes.

Biomedicines 2020 Sep 15;8(9). Epub 2020 Sep 15.

Department of Pharmacology, Institute of Health Sciences, Gyeongsang National University College of Medicine, Jinju 52727, Korea.

Glutathione (GSH) is an endogenous antioxidant found in plants, animals, fungi, and some microorganisms that protects cells by neutralizing hydrogen peroxide. Honokiol, an active ingredient of , is known for antioxidant, anti-inflammatory, and anti-bacterial properties. We investigated the protective mechanism of honokiol through regulating cellular GSH in renal proximal tubules against acute kidney injury (AKI). First, we measured cellular GSH levels and correlated them with the expression of GSH biosynthetic enzymes after honokiol treatment in human kidney-2 (HK-2) cells. Second, we used pharmacological inhibitors or siRNA-mediated gene silencing approach to determine the signaling pathway induced by honokiol. Third, the protective effect of honokiol via GSH biosynthesis was investigated in renal ischemia-reperfusion (IR) mice. Honokiol significantly increased cellular GSH levels by upregulating the subunits of glutamate-cysteine ligase (Gcl)-Gclc and Gclm. These increases were mediated by activation of nuclear factor erythroid 2-related factor 2, via PI3K/Akt and protein kinase C signaling. Consistently, honokiol treatment reduced the plasma creatinine, tubular cell death, neutrophil infiltration and lipid peroxidation in IR mice and the effect was correlated with upregulation of Gclc and Gclm. Conclusively, honokiol may benefit to patients with AKI by increasing antioxidant GSH via transcriptional activation of the biosynthetic enzymes.
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http://dx.doi.org/10.3390/biomedicines8090352DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7555803PMC
September 2020

Fermented Extracts Attenuate Endotoxin-Induced Acute Liver Injury in Mice.

Nutrients 2020 Sep 13;12(9). Epub 2020 Sep 13.

Department of Pharmacology, Institute of Health Sciences, Gyeongsang National University College of Medicine, Jinju 52727, Korea.

Endotoxin-induced acute liver injury is mediated by an excessive inflammatory response, hepatocellular oxidative stress, and apoptosis. Traditional medicinal plants have been used to treat various disorders. (PG) has been shown to be beneficial in relieving cough and asthma and to have anti-tumor, anti-inflammatory, anti-diabetic activities. The pharmacological action of PG is mainly due to saponins, flavonoids, phenolic, and other compounds. However, raw PG exhibits some side effects at high doses. Here, we extracted raw PG with varying fermentation methods and examined its anti-inflammatory effect and associated signaling kinases in Raw264.7 cells. Then, we investigated the effect of fermented black PG (FBPG) on endotoxin-induced liver injury. Mice were administered FBPG orally at 1 h before the lipopolysaccharide and D-galactosamine (LPS/GalN) injection and sacrificed after 5 h. Black PG (BPG) and FBPG showed a significant reduction in pro-inflammatory cytokines and extracellular nitric oxide (NO); p-38 and ERK signaling was involved in reducing inducible NO synthase in Raw264.7 cells. Consistently, FBPG attenuates LPS/GalN-induced liver injury; plasma ALT and AST, hepatic necrosis, pro-inflammatory cytokines, apoptosis, and lipid peroxidation were all reduced. In conclusion, PG extracts, particularly FBPG, play anti-inflammatory, antioxidant, and anti-apoptotic roles, alleviating endotoxin-induced acute liver injury. Processing raw PG into FBPG extract may be clinically useful by improving the pharmacologically active ingredients and reducing the required dosage.
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http://dx.doi.org/10.3390/nu12092802DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7551015PMC
September 2020

Supplementation of Ameliorates Diabetic Nephropathy and Hepatic Steatosis by Activating Autophagy in Mice.

Nutrients 2018 Nov 7;10(11). Epub 2018 Nov 7.

Department of Pharmacology, Institute of Health Sciences, Gyeongsang National University School of Medicine, Jinju 52727, Korea.

Diabetic nephropathy (DN) is a diabetic complication marked by albuminuria and a decline of the glomerular filtration rate. Diabetic kidneys are defective in the autophagy process and mitochondrial function and their enhancement of activity alleviates the pathology. In this paper, we developed a mouse model of DN by a combined treatment of a high-fat diet and streptozotocin after unilateral nephrectomy and supplementation with flower or leaf extracts of (AM) were tested. The preventive effects of the extracts on DN pathology and changes on autophagy and mitochondrial proteins were investigated. DN mice showed a significant increase in fasting blood glucose, plasma creatinine, blood urea nitrogen, and urinary albumin levels. Periodic acid⁻Schiff and Sirius red staining of the diabetic kidney presented a significant change in glomerular and tubular structures that was associated with podocyte loss and fibrotic protein accumulation. These changes were attenuated by AM extract treatment in DN mice. In addition, hepatic injury, proinflammatory cytokines, and lipid accumulation were decreased by AM extracts in DN mice. As a protective mechanism, AM extracts significantly increased the expression of proteins by regulating autophagy and mitochondrial dynamics, which potentially prevented the kidney and liver from accumulating pathogenic proteins and dysfunctional mitochondria, which alleviated the progression of DN.
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http://dx.doi.org/10.3390/nu10111703DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6266484PMC
November 2018

Perilla Oil Decreases Aortic and Hepatic Lipid Accumulation by Modulating Lipogenesis and Lipolysis in High-Fat Diet-Fed Mice.

J Med Food 2019 Jan 12;22(1):14-21. Epub 2018 Sep 12.

1 Department of Pharmacology, Institute of Health Sciences, Gyeongsang National University School of Medicine, Jinju, Korea.

Perilla oil has been shown to be beneficial for ameliorating metabolic disorders, but its protective effect is still controversial. We investigated the effect of perilla oil on obesity-induced hepatic and vascular changes in high-fat diet (HFD)-fed mice and provided underlying mechanisms for potential therapeutic applications. Tomato and paprika extract was added to prevent the oxidation during storage of perilla oil. HFD-fed mice were orally administered palm or perilla oil for 90 days. Food intake, body and liver weight, and serum cholesterol levels were measured. Arterial and hepatic lipid accumulation was determined by histological staining. Hepatic triglyceride levels and the expression of proteins regulating lipid metabolism were analyzed. Food intake and body weight were not different between palm oil-treated and perilla oil-treated mice. Serum cholesterol level was significantly lower in perilla oil-treated mice compared with palm oil-treated mice. HFD-induced lipid accumulation was also lower in thoracic aorta and liver by perilla oil compared with palm oil. Perilla oil also decreased hepatic triglyceride level without changing the liver weight. Perilla oil treatment increased the AMP-activated protein kinase and acetyl-CoA carboxylase phosphorylation and the lipolytic protein levels, whereas it decreased the lipogenic protein levels in the liver. In conclusion, perilla oil reduced serum cholesterol and arterial and hepatic lipid accumulation in HFD-fed mice. The data suggest that perilla oil improves the balance of lipogenic and lipolytic protein expression, and ameliorates obesity-induced metabolic disorders and cardiovascular diseases.
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http://dx.doi.org/10.1089/jmf.2018.4226DOI Listing
January 2019

The proximal tubular α7 nicotinic acetylcholine receptor attenuates ischemic acute kidney injury through Akt/PKC signaling-mediated HO-1 induction.

Exp Mol Med 2018 04 20;50(4):1-17. Epub 2018 Apr 20.

Department of Pharmacology, Institute of Health Sciences, Gyeongsang National University School of Medicine, Jinju, Republic of Korea.

Activation of the α7 nicotinic acetylcholine receptor (α7nAChR) has been shown to attenuate excessive inflammation by inhibiting proinflammatory cytokines during ischemia-reperfusion (IR) injury; however, the underlying kidney-specific molecular mechanisms remain unclear. The protective action of α7nAChR against renal IR injury was investigated using a selective α7nAChR agonist and antagonist. α7nAChR activation reduced plasma creatinine levels and tubular cell damage, whereas α7nAChR inhibition aggravated the IR-induced phenotype. α7nAChR activation decreased neutrophil infiltration and proinflammatory cytokine expression, increased heme oxygenase-1 (HO-1) expression, and reduced proximal tubular apoptosis after IR as shown by terminal deoxynucleotidyl transferase dUTP nick-end labeling staining and caspase-3 cleavage. In this study, we first showed that α7nAChR activation in the proximal tubules induced HO-1 expression through the phosphoinositide 3-kinase (PI3K)/Akt and protein kinase C (PKC) signaling pathway in vivo in renal IR mice and in vitro in proximal tubular cells. Chemical inhibitors of PKC or PI3K/Akt and small interfering RNA-mediated PKC silencing confirmed the signal specificity of α7nAChR-mediated HO-1 induction in the proximal tubular cells. α7nAChR activation inhibited high-mobility group box 1 release by inducing HO-1 expression and reduced proinflammatory cytokine gene expression and apoptotic cell death in tumor necrosis factor α-stimulated proximal tubular cells. Taken together, we conclude that α7nAChR activation in proximal tubular cells directly protects cells against renal IR injury by inducing HO-1 expression through PI3K/Akt and PKC signaling.
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http://dx.doi.org/10.1038/s12276-018-0061-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5938048PMC
April 2018

Arabidopsis DREB2C modulates ABA biosynthesis during germination.

Biochem Biophys Res Commun 2014 Sep 19;452(1):91-8. Epub 2014 Aug 19.

Systems and Synthetic Agrobiotech Center and PMBBRC, Division of Applied Life Science, Graduate School of Gyeongsang National University, Jinju 660-701, Republic of Korea; Research Institute of Natural Science, Department of Biochemistry, Gyeongsang National University, Jinju 660-701, Republic of Korea. Electronic address:

Plant dehydration-responsive element binding factors (DREBs) are transcriptional regulators of the APETELA2/Ethylene Responsive element-binding Factor (AP2/ERF) family that control expression of abiotic stress-related genes. We show here that under conditions of mild heat stress, constitutive overexpression seeds of transgenic DREB2C overexpression Arabidopsis exhibit delayed germination and increased abscisic acid (ABA) content compared to untransformed wild-type (WT). Treatment with fluridone, an inhibitor of the ABA biosynthesis abrogated these effects. Expression of an ABA biosynthesis-related gene, 9-cis-epoxycarotenoid dioxygenase 9 (NCED9) was up-regulated in the DREB2C overexpression lines compared to WT. DREB2C was able to trans-activate expression of NCED9 in Arabidopsis leaf protoplasts in vitro. Direct and specific binding of DREB2C to a complete DRE on the NCED9 promoter was observed in electrophoretic mobility shift assays. Exogenous ABA treatment induced DREB2C expression in germinating seeds of WT. Vegetative growth of transgenic DREB2C overexpression lines was more strongly inhibited by exogenous ABA compared to WT. These results suggest that DREB2C is a stress- and ABA-inducible gene that acts as a positive regulator of ABA biosynthesis in germinating seeds through activating NCED9 expression.
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http://dx.doi.org/10.1016/j.bbrc.2014.08.052DOI Listing
September 2014

Ectopic expression of an Arabidopsis dehydration-responsive element-binding factor DREB2C improves salt stress tolerance in crucifers.

Plant Cell Rep 2014 Aug 16;33(8):1239-54. Epub 2014 Apr 16.

Division of Applied Life Science, Systems and Synthetic Agrobiotech Center and PMBBRC, Gyeongsang National University, Jinju, 660-701, Korea.

Key Message: DREB2C acts as a transcriptional activator of the salt tolerance-related COLD - REGULATED 15A gene. DEHYDRATION-RESPONSIVE ELEMENT BINDING FACTOR 2C (DREB2C) regulates plant responses to heat stress. We report here that DREB2C is induced by NaCl stress in Arabidopsis, based on quantitative RT-PCR analyses of transcript levels and DREB2C promoter-controlled GUS activity assays. Constitutive overexpression of DREB2C from the cauliflower mosaic virus (CaMV) 35S promoter led to enhanced salt tolerance in transgenic Arabidopsis and canola plants that was characterized by higher chlorophyll content, lower tissue Na(+) content, reduced rate of water loss, and tighter membrane integrity in plants grown in NaCl-containing medium. Basal expression of the stress-responsive genes COLD-REGULATED 15A (COR15A), RESPONSIVE TO DEHYDRATION (RD) 29A and RD29B, was higher in transgenic DREB2C-overexpressing Arabidopsis plants than in the wild-type. Promoter transactivation assays and electrophoretic mobility-shift assays showed that DREB2C interacts directly with the three DREs in the COR15A promoter, both in vivo and in vitro. Transgenic Arabidopsis constitutively overexpressing COR15A from the CaMV35S promoter exhibited greater NaCl tolerance than the untransformed wild-type. Taken together, the data suggest that DREB2C functions as transcriptional activator that promotes NaCl tolerance, in part through upregulation of the stress-responsive gene COR15A.
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http://dx.doi.org/10.1007/s00299-014-1612-9DOI Listing
August 2014

DREB2C acts as a transcriptional activator of the thermo tolerance-related phytocystatin 4 (AtCYS4) gene.

Transgenic Res 2014 Feb 19;23(1):109-23. Epub 2013 Jul 19.

Division of Applied Life Science, Systems and Synthetic Agrobiotech Center and PMBBRC, Gyeongsang National University, Jinju, 660-701, Korea.

Phytocystatins are proteinaceous inhibitors of cysteine proteases. They have been implicated in the regulation of plant protein turnover and in defense against pathogens and insects. Here, we have characterized an Arabidopsis phytocystatin family gene, Arabidopsis thaliana phytocystatin 4 (AtCYS4). AtCYS4 was induced by heat stress. The heat shock tolerance of AtCYS4-overexpressing transgenic plants was greater than that of wild-type and cys4 knock-down plants, as measured by fresh weight and root length. Although no heat shock elements were identified in the 5'-flanking region of the AtCYS4 gene, canonical ABA-responsive elements (ABREs) and dehydration-responsive elements (DREs) were found. Transient promoter activity measurements showed that AtCYS4 expression was up-regulated in unstressed protoplasts by co-expression of DRE-binding factor 2s (DREB2s), especially by DREB2C, but not by bZIP transcription factors that bind to ABREs (ABFs, ABI5 and AREBs). DREB2C bound to and activated transcription from the two DREs on the AtCYS4 promoter although some preference was observed for the GCCGAC DRE element over the ACCGAC element. AtCYS4 transcript and protein levels were elevated in transgenic DREB2C overexpression lines with corresponding decline of endogenous cysteine peptidase activity. We propose that AtCYS4 functions in thermotolerance under the control of the DREB2C cascade.
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http://dx.doi.org/10.1007/s11248-013-9735-2DOI Listing
February 2014

A proximal promoter region of Arabidopsis DREB2C confers tissue-specific expression under heat stress.

J Integr Plant Biol 2012 Sep 30;54(9):640-51. Epub 2012 Aug 30.

Systems and Synthetic Agrobiotech Center and PMBBRC, Division of Applied Life Science, Gyeongsang National University, Jinju 660-701, Korea.

The dehydration-responsive element-binding factor 2C (DREB2C) is a member of the CBF/DREB subfamily of proteins, which contains a single APETALA2/Ethylene responsive element-binding factor (AP2/ERF) domain. To identify the expression pattern of the DREB2C gene, which contains multiple transcription cis-regulatory elements in its promoter, an approximately 1.4 kb upstream DREB2C sequence was fused to the β-glucuronidase reporter gene (GUS) and the recombinant p1244 construct was transformed into Arabidopsis thaliana (L.) Heynh. The promoter of the gene directed prominent GUS activity in the vasculature in diverse young dividing tissues. Upon applying heat stress (HS), GUS staining was also enhanced in the vasculature of the growing tissues. Analysis of a series of 5'-deletions of the DREB2C promoter revealed that a proximal upstream sequence sufficient for the tissue-specific spatial and temporal induction of GUS expression by HS is localized in the promoter region between -204 and -34 bps relative to the transcriptional start site. Furthermore, electrophoretic mobility shift assay (EMSA) demonstrated that nuclear protein binding activities specific to a -120 to -32 bp promoter fragment increased after HS. These results indicate that the TATA-proximal region and some latent trans-acting factors may cooperate in HS-induced activation of the Arabidopsis DREB2C promoter.
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http://dx.doi.org/10.1111/j.1744-7909.2012.01137.xDOI Listing
September 2012

Overexpression of Arabidopsis dehydration- responsive element-binding protein 2C confers tolerance to oxidative stress.

Mol Cells 2012 Feb;33(2):135-40

Systems and Synthetic Agrobiotech Center and PMBBRC, Gyeongsang National University, Jinju 660-701, Korea.

Dehydration-responsive element-binding proteins (DREBs)regulate plant responses to environmental stresses. In the current study, transcription of DREB2C, a class 2 Arabidopsis DREB, was induced by a superoxide anion propagator, methyl viologen (MV). The oxidative stress tolerance of DREB2C-overexpressing transgenic plants was significantly greater than that of wild-type plants, as measured by ion leakage and chlorophyll fluorescence under light conditions. The transcriptional activity of several ascorbate peroxidase (APX) genes as well as APX protein activity was induced in DREB2C overexpressors. Additionally, the level of H2O2 in the overexpressors was lower than in wt plants under similar oxidative stress conditions. An electrophoretic mobility shift assay and transient activator reporter assay showed that APX2 expression was regulated by heat shock factor A3 (HsfA3) and that HsfA3 is regulated at the transcriptional level by DREB2C. These results suggest that DREB2C plays an important role in promoting oxidative stress tolerance in Arabidopsis.
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http://dx.doi.org/10.1007/s10059-012-2188-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3887724PMC
February 2012

Distinct expression patterns of two Arabidopsis phytocystatin genes, AtCYS1 and AtCYS2, during development and abiotic stresses.

Plant Cell Rep 2010 Aug 5;29(8):905-15. Epub 2010 Jun 5.

Division of Applied Life Science (BK21 Program), Environmental Biotechnology National Core Research Center and PMBBRC, Graduate School of Gyeongsang National University, Jinju 660-701, Korea.

The phytocystatins of plants are members of the cystatin superfamily of proteins, which are potent inhibitors of cysteine proteases. The Arabidopsis genome encodes seven phytocystatin isoforms (AtCYSs) in two distantly related AtCYS gene clusters. We selected AtCYS1 and AtCYS2 as representatives for each cluster and then generated transgenic plants expressing the GUS reporter gene under the control of each gene promoter. These plants were used to examine AtCYS expression at various stages of plant development and in response to abiotic stresses. Histochemical analysis of AtCYS1 promoter- and AtCYS2 promoter-GUS transgenic plants revealed that these genes have similar but distinct spatial and temporal expression patterns during normal development. In particular, AtCYS1 was preferentially expressed in the vascular tissue of all organs, whereas AtCYS2 was expressed in trichomes and guard cells in young leaves, caps of roots, and in connecting regions of the immature anthers and filaments and the style and stigma in flowers. In addition, each AtCYS gene has a unique expression profile during abiotic stresses. High temperature and wounding stress enhanced the expression of both AtCYS1 and AtCYS2, but the temporal and spatial patterns of induction differed. From these data, we propose that these two AtCYS genes play important, but distinct, roles in plant development and stress responses.
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http://dx.doi.org/10.1007/s00299-010-0876-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2903682PMC
August 2010