Jiang G

References (12)

Title : Neurotoxicities induced by micro\/nanoplastics: A review focusing on the risks of neurological diseases - Liu_2024_J.Hazard.Mater_469_134054
Author(s) : Liu S , He Y , Yin J , Zhu Q , Liao C , Jiang G
Ref : J Hazard Mater , 469 :134054 , 2024
Abstract : Pollution of micro/nano-plastics (MPs/NPs) is ubiquitously prevalent in the environment, leading to an unavoidable exposure of the human body. Despite the protection of the blood-brain barrier, MPs/NPs can be transferred and accumulated in the brain, which subsequently exert negative effects on the brain. Nevertheless, the potential neurodevelopmental and/or neurodegenerative risks of MPs/NPs remain largely unexplored. In this review, we provide a systematic overview of recent studies related to the neurotoxicity of MPs/NPs. It covers the environmental hazards and human exposure pathways, translocation and distribution into the brain, the neurotoxic effects, and the possible mechanisms of environmental MPs/NPs. MPs/NPs are widely found in different environment matrices, including air, water, soil, and human food. Ambient MPs/NPs can enter the human body by ingestion, inhalation and dermal contact, then be transferred into the brain via the blood circulation and nerve pathways. When MPs/NPs are present in the brain, they can initiate a series of molecular or cellular reactions that may harm the blood-brain barrier, cause oxidative stress, trigger inflammatory responses, affect acetylcholinesterase activity, lead to mitochondrial dysfunction, and impair autophagy. This can result in abnormal protein folding, loss of neurons, disruptions in neurotransmitters, and unusual behaviours, ultimately contributing to the initiation and progression of neurodegenerative changes and neurodevelopmental abnormalities. Key challenges and further research directions are also proposed in this review as more studies are needed to focus on the potential neurotoxicity of MPs/NPs under realistic conditions.
ESTHER : Liu_2024_J.Hazard.Mater_469_134054
PubMedSearch : Liu_2024_J.Hazard.Mater_469_134054
PubMedID: 38503214

Title : Aporphines: A privileged scaffold in CNS drug discovery - Zhu_2023_Eur.J.Med.Chem_256_115414
Author(s) : Zhu R , Jiang G , Tang W , Zhao X , Chen F , Zhang X , Ye N
Ref : Eur Journal of Medicinal Chemistry , 256 :115414 , 2023
Abstract : Aporphine alkaloids embedded in 4H-dibenzo[de,g]quinoline four-ring structures belong to one of the largest subclasses of isoquinoline alkaloids. Aporphine is a privileged scaffold in the field of organic synthesis and medicinal chemistry for the discovery of new therapeutic agents for central nervous system (CNS) diseases, cancer, metabolic syndrome, and other diseases. In the past few decades, aporphine has attracted continuing interest to be widely used to develop selective or multitarget directed ligands (MTDLs) targeting the CNS (e.g., dopamine D(1/2/5), serotonin 5-HT(1A/2A/2C) and 5-HT(7), adrenergic alpha/beta receptors, and cholinesterase enzymes), thereby serving as valuable pharmacological probes for mechanism studies or as potential leads for CNS drug discovery. The aims of the present review are to highlight the diverse CNS activities of aporphines, discuss their SAR, and briefly summarize general synthetic routes, which will pave the way for the design and development of new aporphine derivatives as promising CNS active drugs in the future.
ESTHER : Zhu_2023_Eur.J.Med.Chem_256_115414
PubMedSearch : Zhu_2023_Eur.J.Med.Chem_256_115414
PubMedID: 37172474

Title : A Fast-Response AIE-Active Ratiometric Fluorescent Probe for the Detection of Carboxylesterase - Xia_2022_Biosensors.(Basel)_12_
Author(s) : Xia M , Li C , Liu L , He Y , Li Y , Jiang G , Wang J
Ref : Biosensors (Basel) , 12 : , 2022
Abstract : Hepatocellular carcinoma (HCC) is associated with a high mortality rate worldwide. The therapeutic outcomes can be significantly improved if diagnosis and treatment are initiated earlier in the disease process. Recently, the carboxylesterase (CaE) activity/level in human plasma was reported to be a novel serological biomarker candidate for HCC. In this article, we fabricated a new fluorescent probe with AIE characteristics for the rapid detection of CaE with a more reliable ratiometric response mode. The TCFISE probe showed high sensitivity (LOD: 93.0 microU/mL) and selectivity toward CaE. Furthermore, the good pH stability, superior resistance against photobleaching, and low cytotoxicity highlight the high potential of the TCFISE probe for application in the monitoring of CaE activity in complex biological samples and in live cells, tissues, and animals.
ESTHER : Xia_2022_Biosensors.(Basel)_12_
PubMedSearch : Xia_2022_Biosensors.(Basel)_12_
PubMedID: 35884287

Title : Proteomic and metabolomic responses in hepatopancreas of whiteleg shrimp Litopenaeus vannamei infected by microsporidian Enterocytozoon hepatopenaei - Ning_2019_Fish.Shellfish.Immunol_87_534
Author(s) : Ning M , Wei P , Shen H , Wan X , Jin M , Li X , Shi H , Qiao Y , Jiang G , Gu W , Wang W , Wang L , Meng Q
Ref : Fish Shellfish Immunol , 87 :534 , 2019
Abstract : Enterocytozoon hepatopenaei (EHP) causes hepatopancreatic microsporidiosis (HPM) in shrimp. HPM is not normally associated with shrimp mortality, but is associated with significant growth retardation. In this study, the responses induced by EHP were investigated in hepatopancreas of shrimp Litopenaeus vannamei using proteomics and metabolomics. Among differential proteins identified, several (e.g., peritrophin-44-like protein, alpha2 macroglobulin isoform 2, prophenoloxidase-activating enzymes, ferritin, Rab11A and cathepsin C) were related to pathogen infection and host immunity. Other proteomic biomarkers (i.e., farnesoic acid o-methyltransferase, juvenile hormone esterase-like carboxylesterase 1 and ecdysteroid-regulated protein) resulted in a growth hormone disorder that prevented the shrimp from molting. Both proteomic KEGG pathway (e.g., "Glycolysis/gluconeogenesis" and "Glyoxylate and dicarboxylate metabolism") and metabolomic KEGG pathway (e.g., "Galactose metabolism" and "Biosynthesis of unsaturated fatty acids") data indicated that energy metabolism pathway was down-regulated in the hepatopancreas when infected by EHP. More importantly, the changes of hormone regulation and energy metabolism could provide much-needed insight into the underlying mechanisms of stunted growth in shrimp after EHP infection. Altogether, this study demonstrated that proteomics and metabolomics could provide an insightful view into the effects of microsporidial infection in the shrimp L. vannamei.
ESTHER : Ning_2019_Fish.Shellfish.Immunol_87_534
PubMedSearch : Ning_2019_Fish.Shellfish.Immunol_87_534
PubMedID: 30721776

Title : The potential neurotoxicity of emerging tetrabromobisphenol A derivatives based on rat pheochromocytoma cells - Liu_2016_Chemosphere_154_194
Author(s) : Liu Q , Ren X , Long Y , Hu L , Qu G , Zhou Q , Jiang G
Ref : Chemosphere , 154 :194 , 2016
Abstract : Tetrabromobisphenol A (TBBPA) can cause diverse adverse effects including neurotoxicity. Emerging TBBPA derivatives, with high structure similarity to the parent compound, are now being concerned. In this study, the potential neurotoxicities of four TBBPA derivatives and their parent compound were studied by cell viability inhibition in rat pheochromocytoma cells (PC12) and the corresponding molecular mechanisms were investigated. The cellular toxicity was correlated with the chemical hydrophobicity. Tetrabromobisphenol A bis(2-hydroxyethyl ether) (TBBPA-BHEE) exhibited the highest cellular toxicity to PC12 due to its lowest hydrophobicity among these 5 tested compounds. Further experiments showed that TBBPA-BHEE disturbed dopamine (DA) secretion and altered acetylcholinesterase (AChE) enzymatic activity in PC12 cells. The molecular mechanism study indicated that TBBPA-BHEE induced cellular toxicity to PC12 cells through ROS-mediated caspase activation to a large extent, which was partially attenuated by the anti-oxidation of Vitamin E. Moreover, in contrast to TBBPA, the occurrence of TBBPA-BHEE toxicity to PC12 was not attributed to activation of mitogen-activated protein kinases (MAPKs) or thyroid hormone (TH) signaling pathway. These findings suggest TBBPA derivatives, especially TBBPA-BHEE, as potential neurotoxins need urgent attention.
ESTHER : Liu_2016_Chemosphere_154_194
PubMedSearch : Liu_2016_Chemosphere_154_194
PubMedID: 27055180

Title : Anticancer drugs induce hypomethylation of the acetylcholinesterase promoter via a phosphorylated-p38-DNMT1-AChE pathway in apoptotic hepatocellular carcinoma cells - Xi_2015_Int.J.Biochem.Cell.Biol_68_21
Author(s) : Xi Q , Gao N , Yang Y , Ye W , Zhang B , Wu J , Jiang G , Zhang X
Ref : International Journal of Biochemistryistry & Cell Biology , 68 :21 , 2015
Abstract : Apoptosis, also known as programmed cell death, plays an essential role in eliminating excessive, damaged or harmful cells. Previous work has demonstrated that anticancer drugs induce cell apoptosis by inducing cytotoxicity. In recent years, several reports demonstrated modulated expression of DNA methyltransferases 1 (DNMT1) and acetylcholinesterase (AChE) in a variety of tumors. In this study, we showed that the expression of DNMT1 was decreased and the methylation of CpGs in the promoter of AChE was reduced in anticancer drugs-induced apoptotic hepatocellular carcinoma cells. Silencing of DNMT1 expression by AZA or RNA interference (RNAi) restored AChE production and inhibition of AChE expression by RNAi protected HCC cells from anticancer drugs-induced apoptosis. Furthermore, we demonstrated that the regulation of AChE by DNMT1 was involved in the phosphorylated p38 pathway in anticancer drugs-induced apoptosis. In addition, immunohistochemical staining showed that P-p38, DNMT1 and AChE were aberrantly expressed in a subset of HCC tumors. Taken together, we demonstrated the regulation of AChE by DNMT1 and further, we found that this regulation was involved in the phosphorylated p38 pathway in anticancer drugs-induced apoptosis.
ESTHER : Xi_2015_Int.J.Biochem.Cell.Biol_68_21
PubMedSearch : Xi_2015_Int.J.Biochem.Cell.Biol_68_21
PubMedID: 26299326

Title : Bis (monoacylglycero) phosphate interfacial properties and lipolysis by pancreatic lipase-related protein 2, an enzyme present in THP-1 human monocytes - Record_2011_Biochim.Biophys.Acta_1811_419
Author(s) : Record M , Amara S , Subra C , Jiang G , Prestwich GD , Ferrato F , Carriere F
Ref : Biochimica & Biophysica Acta , 1811 :419 , 2011
Abstract : The interfacial physical properties of bis(monoacylglycero)phosphate (BMP) and its derivatives with three oleoyl chains (hemi-BDP) and four oleoyl chains (bis(diacylglycero)phosphate, BDP) were investigated using Langmuir monomolecular films. The mean molecular area of BMP at the collapse surface pressure (45mN m(-1)) was similar to those measured with other phospholipids bearing two acyl chains (66 and 59.6A(2) molecule(-1) at pH 5.5 and 8.0, respectively). In Hemi-BDP and BDP, the mean molecular area increased by 26 and 35A(2) molecule(-1) per additional acyl chain at pH 5.5 and 8.0, respectively. When BMP was added to a phospholipid mixture mimicking late endosome membrane composition at pH 8.0, the mean phospholipid molecular area increased by 7% regardless of the surface pressure. In contrast, the variation in molecular area was surface pressure-dependent at pH 5.5, a pH value close to that of intra-endosomal content. BMP and hemi-BDP, but not BDP, were hydrolyzed by pancreatic lipase-related protein 2 (PLRP2), which exhibits phospholipase A(1) activity. At pH 5.5, the maximum activities of PLRP2 on BMP were recorded at high surface pressures (25-35mN/m). At pH 8.0, the PLRP2 activity vs. surface pressure showed a bell-shaped curve with maximum activities at 15mN/m for both BMP and hemi-BDP. This is a new activity for this enzyme which could degrade cellular BMP since both human PLRP2 (HPLRP2) and BMP were localized in human monocytic THP-1 cells. This is the first report on the cellular localization of HPLRP2 in human monocytes.
ESTHER : Record_2011_Biochim.Biophys.Acta_1811_419
PubMedSearch : Record_2011_Biochim.Biophys.Acta_1811_419
PubMedID: 21554982

Title : Dipeptidyl peptidase-4 inhibitors administered in combination with metformin result in an additive increase in the plasma concentration of active GLP-1 - Migoya_2010_Clin.Pharmacol.Ther_88_801
Author(s) : Migoya EM , Bergeron R , Miller JL , Snyder RN , Tanen M , Hilliard D , Weiss B , Larson P , Gutierrez M , Jiang G , Liu F , Pryor KA , Yao J , Zhu L , Holst JJ , Deacon C , Herman G , Thornberry N , Amatruda J , Williams-Herman D , Wagner JA , SinhaRoy R
Ref : Clinical Pharmacology & Therapeutics , 88 :801 , 2010
Abstract : The aim of the study was to investigate the effects of a dipeptidyl peptidase-4 (DPP-4) inhibitor, of metformin, and of the combination of the two agents, on incretin hormone concentrations. Active and inactive (or total) incretin plasma concentrations, plasma DPP-4 activity, and preproglucagon (GCG) gene expression were determined after administration of each agent alone or in combination to mice with diet-induced obesity (DIO) and to healthy human subjects. In mice, metformin increased Gcg expression in the large intestine and elevated the plasma concentrations of inactive glucagon-like peptide 1 (GLP-1) (9-36) and glucagon. In healthy subjects, a DPP-4 inhibitor elevated both active GLP-1 and glucose dependent insulinotropic polypeptide (GIP), metformin increased total GLP-1 (but not GIP), and the combination resulted in additive increases in active GLP-1 plasma concentrations. Metformin did not inhibit plasma DPP-4 activity either in vitro or in vivo. The study results show that metformin is not a DPP-4 inhibitor but rather enhances precursor GCG expression in the large intestine, resulting in increased total GLP-1 concentrations. DPP-4 inhibitors and metformin have complementary mechanisms of action and additive effects with respect to increasing the concentrations of active GLP-1 in plasma.
ESTHER : Migoya_2010_Clin.Pharmacol.Ther_88_801
PubMedSearch : Migoya_2010_Clin.Pharmacol.Ther_88_801
PubMedID: 21048706

Title : Mating factor linkage and genome evolution in basidiomycetous pathogens of cereals - Bakkeren_2006_Fungal.Genet.Biol_43_655
Author(s) : Bakkeren G , Jiang G , Warren RL , Butterfield Y , Shin H , Chiu R , Linning R , Schein J , Lee N , Hu G , Kupfer DM , Tang Y , Roe BA , Jones S , Marra M , Kronstad JW
Ref : Fungal Genet Biol , 43 :655 , 2006
Abstract : Sex in basidiomycete fungi is controlled by tetrapolar mating systems in which two unlinked gene complexes determine up to thousands of mating specificities, or by bipolar systems in which a single locus (MAT) specifies different sexes. The genus Ustilago contains bipolar (Ustilago hordei) and tetrapolar (Ustilago maydis) species and sexual development is associated with infection of cereal hosts. The U. hordei MAT-1 locus is unusually large (approximately 500 kb) and recombination is suppressed in this region. We mapped the genome of U. hordei and sequenced the MAT-1 region to allow a comparison with mating-type regions in U. maydis. Additionally the rDNA cluster in the U. hordei genome was identified and characterized. At MAT-1, we found 47 genes along with a striking accumulation of retrotransposons and repetitive DNA; the latter features were notably absent from the corresponding U. maydis regions. The tetrapolar mating system may be ancestral and differences in pathogenic life style and potential for inbreeding may have contributed to genome evolution.
ESTHER : Bakkeren_2006_Fungal.Genet.Biol_43_655
PubMedSearch : Bakkeren_2006_Fungal.Genet.Biol_43_655
PubMedID: 16793293
Gene_locus related to this paper: ustho-q2a721

Title : Monitoring enzyme reaction and screening enzyme inhibitor based on MALDI-TOF-MS platform with a matrix of oxidized carbon nanotubes - Hu_2006_J.Am.Soc.Mass.Spectrom_17_1616
Author(s) : Hu L , Jiang G , Xu S , Pan C , Zou H
Ref : J Am Soc Mass Spectrom , 17 :1616 , 2006
Abstract : A matrix assisted laser desorption/ionization time-of-flight mass spectrometry platform for quantitatively monitoring enzyme activity and screening enzyme inhibitors has been demonstrated. The described method employs a new matrix of oxidized carbon nanotubes. Compared with the traditional fluorescence approach, this label-free method has the advantage of directly identifying the substrates and products in enzymatic reactions. Moreover, the method could be conveniently carried out with any commercial mass spectrometer without modification. We quantitatively monitored the acetylcholinesterase activity and screened acetylcholinesterase inhibitors with a detection rate of about 3.3 s per sample.
ESTHER : Hu_2006_J.Am.Soc.Mass.Spectrom_17_1616
PubMedSearch : Hu_2006_J.Am.Soc.Mass.Spectrom_17_1616
PubMedID: 16905330

Title : Mice lacking dipeptidyl peptidase IV are protected against obesity and insulin resistance - Conarello_2003_Proc.Natl.Acad.Sci.U.S.A_100_6825
Author(s) : Conarello SL , Li Z , Ronan J , Roy RS , Zhu L , Jiang G , Liu F , Woods J , Zycband E , Moller DE , Thornberry NA , Zhang BB
Ref : Proc Natl Acad Sci U S A , 100 :6825 , 2003
Abstract : Dipeptidyl peptidase IV (DP-IV), a member of the prolyl oligopeptidase family of peptidases, is involved in the metabolic inactivation of a glucose-dependent insulinotropic hormone, glucagon-like peptide 1 (GLP-1), and other incretin hormones. Here, we investigated the impact of DP-IV deficiency on body weight control and insulin sensitivity in mice. Whereas WT mice displayed accelerated weight gain and hyperinsulinemia when fed a high-fat diet (HFD), mice lacking the gene encoding DP-IV (DP-IV-/-) are refractory to the development of obesity and hyperinsulinemia. Pair-feeding and indirect calorimetry studies indicate that reduced food intake and increased energy expenditure accounted for the resistance to HFD-induced obesity in the DP-IV-/- mice. Ablation of DP-IV also is associated with elevated GLP-1 levels and improved metabolic control in these animals, resulting in improved insulin sensitivity, reduced pancreatic islet hypertrophy, and protection against streptozotocin-induced loss of beta cell mass and hyperglycemia. Together, these observations suggest that chronic deletion of DP-IV gene has significant impact on body weight control and energy homeostasis, providing validation of DP-IV inhibition as a viable therapeutic option for the treatment of metabolic disorders related to diabetes and obesity.
ESTHER : Conarello_2003_Proc.Natl.Acad.Sci.U.S.A_100_6825
PubMedSearch : Conarello_2003_Proc.Natl.Acad.Sci.U.S.A_100_6825
PubMedID: 12748388
Gene_locus related to this paper: mouse-dpp4

Title : Five unique compounds: xyloketals from mangrove fungus Xylaria sp. from the South China Sea coast - Lin_2001_J.Org.Chem_66_6252
Author(s) : Lin Y , Wu X , Feng S , Jiang G , Luo J , Zhou S , Vrijmoed LL , Jones EB , Krohn K , Steingrover K , Zsila F
Ref : J Org Chem , 66 :6252 , 2001
Abstract : Five unique metabolites, xyloketals A (1), B (2), C (3), D (4), and E (5), and the known 6 were isolated from mangrove fungus Xylaria sp. (no. 2508), obtained from the South China Sea. The structures of these compounds were elucidated by spectroscopic and X-ray diffraction experiments. Xyloketal A is a ketal compound with a C(3) symmetry and xyloketals B-E are its analogues. It was found that xytoketal C slowly rearranged to xytoketal B in DMSO-d(6)() solution at room temperature. Xyloketal A exhibited the activity of inhibiting acetylcholine esterase.
ESTHER : Lin_2001_J.Org.Chem_66_6252
PubMedSearch : Lin_2001_J.Org.Chem_66_6252
PubMedID: 11559170