He T

References (10)

Title : The soluble epoxide hydrolase inhibitor TPPU improves comorbidity of chronic pain and depression via the AHR and TSPO signaling - Luo_2023_J.Transl.Med_21_71
Author(s) : Luo A , Wu Z , Li S , McReynolds CB , Wang D , Liu H , Huang C , He T , Zhang X , Wang Y , Liu C , Hammock BD , Hashimoto K , Yang C
Ref : J Transl Med , 21 :71 , 2023
Abstract : BACKGROUND: Patients suffering from chronic pain often also exhibit depression symptoms. Soluble epoxide hydrolase (sEH) inhibitors can decrease blood levels of inflammatory cytokines. However, whether inhibiting sEH signaling is beneficial for the comorbidity of pain and depression is unknown. METHODS: According to a sucrose preference test (SPT), spared nerve injury (SNI) mice were classified into pain with or without an anhedonia phenotype. Then, sEH protein expression and inflammatory cytokines were assessed in selected tissues. Furthermore, we used sEH inhibitor TPPU to determine the role of sEH in chronic pain and depression. Importantly, agonists and antagonists of aryl hydrocarbon receptor (AHR) and translocator protein (TSPO) were used to explore the pathogenesis of sEH signaling. RESULTS: In anhedonia-susceptible mice, the tissue levels of sEH were significantly increased in the medial prefrontal cortex (mPFC), hippocampus, spinal cord, liver, kidney, and gut. Importantly, serum CYP1A1 and inflammatory cytokines, such as interleukin 1beta (IL-1beta) and the tumor necrosis factor alpha (TNF-alpha), were increased simultaneously. TPPU improved the scores of mechanical withdrawal threshold (MWT) and SPT, and decreased the levels of serum CYP1A1 and inflammatory cytokines. AHR antagonist relieved the anhedonia behaviors but not the algesia behaviors in anhedonia-susceptible mice, whereas an AHR agonist abolished the antidepressant-like effect of TPPU. In addition, a TSPO agonist exerted a similar therapeutic effect to that of TPPU, whereas pretreatment with a TSPO antagonist abolished the antidepressant-like and analgesic effects of TPPU. CONCLUSIONS: sEH underlies the mechanisms of the comorbidity of chronic pain and depression and that TPPU exerts a beneficial effect on anhedonia behaviors in a pain model via AHR and TSPO signaling.
ESTHER : Luo_2023_J.Transl.Med_21_71
PubMedSearch : Luo_2023_J.Transl.Med_21_71
PubMedID: 36732752

Title : Medial septum tau accumulation induces spatial memory deficit via disrupting medial septum-hippocampus cholinergic pathway - Wu_2021_Clin.Transl.Med_11_e428
Author(s) : Wu D , Gao D , Yu H , Pi G , Xiong R , Lei H , Wang X , Liu E , Ye J , Gao Y , He T , Jiang T , Sun F , Su J , Song G , Peng W , Yang Y , Wang JZ
Ref : Clin Transl Med , 11 :e428 , 2021
Abstract : Tau accumulation and cholinergic impairment are characteristic pathologies in Alzheimer's disease (AD). However, the causal role of tau accumulation in cholinergic lesion is elusive. Here, we observed an aberrant tau accumulation in the medial septum (MS) of 3xTg and 5xFAD mice, especially in their cholinergic neurons. Overexpressing hTau in mouse MS (MS(hTau) ) for 6 months but not 3 months induced spatial memory impairment without changing object recognition and anxiety-like behavior, indicating a specific and time-dependent effect of MS-hTau accumulation on spatial cognitive functions. With increasing hTau accumulation, the MS(hTau) mice showed a time-dependent cholinergic neuron loss with reduced cholinergic projections to the hippocampus. Intraperitoneal administration of donepezil, a cholinesterase inhibitor, for 1 month ameliorated the MS-hTau-induced spatial memory deficits with preservation of MS-hippocampal cholinergic pathway and removal of tau load; and the beneficial effects of donepezil was more prominent at low dose. Proteomics revealed that MS-hTau accumulation deregulated multiple signaling pathways with numerous differentially expressed proteins (DEPs). Among them, the vacuolar protein sorting-associated protein 37D (VP37D), an autophagy-related protein, was significantly reduced in MS(hTau) mice; the reduction of VP37D was restored by donepezil, and the effect was more significant at low dose than high dose. These novel evidences reveal a causal role of tau accumulation in linking MS cholinergic lesion to hippocampus-dependent spatial cognitive damages as seen in the AD patients, and the new tau-removal and autophagy-promoting effects of donepezil may extend its application beyond simple symptom amelioration to potential disease modification.
ESTHER : Wu_2021_Clin.Transl.Med_11_e428
PubMedSearch : Wu_2021_Clin.Transl.Med_11_e428
PubMedID: 34185417

Title : A sensitive fluorescent assay for the determination of parathion-methyl using AHNSA probe with MnO(2) nanosheets - Liu_2020_Spectrochim.Acta.A.Mol.Biomol.Spectrosc_247_119146
Author(s) : Liu B , Peng Z , Wu S , He T , Qiu P
Ref : Spectrochim Acta A Mol Biomol Spectrosc , 247 :119146 , 2020
Abstract : In this paper, a novel fluorescence assay has been constructed for the determination of parathion-methyl (PM) by using 4-amino-3-hydroxy-1-naphthalenesulfonic acid (AHNSA) as probe. MnO(2) nanosheets (MnO(2) NS) could quench the fluorescence of AHNSA, while Mn(2+), the reduction product of MnO(2) NS, has no influence on it, resulting in fluorescence recovery. This is because that MnO(2) NS have oxidized characteristic, and they can react with choline (TCh), which is the product of acetylthiocholine (ATCh) catalyzed by acetylcholinesterase (AChE). In the presence of OPs, the activity of AChE was inhibited, accompanied by the restraint of the redox reaction of MnO(2) NS, therefore the fluorescence of AHNSA was quenched. Under the optimized experimental conditions, a linear range of PM was determined to be 0.4-40 ng/mL (R(2) = 0.997) by the proposed method with the limit of detection for 0.18 ng/mL (S/N = 3). The assay was successfully applied to the determination of PM in lake water, which average recoveries were between 86.5% and 114.4%.
ESTHER : Liu_2020_Spectrochim.Acta.A.Mol.Biomol.Spectrosc_247_119146
PubMedSearch : Liu_2020_Spectrochim.Acta.A.Mol.Biomol.Spectrosc_247_119146
PubMedID: 33186817

Title : A proteolytic fragment of histone deacetylase 4 protects the heart from failure by regulating the hexosamine biosynthetic pathway - Lehmann_2018_Nat.Med_24_62
Author(s) : Lehmann LH , Jebessa ZH , Kreusser MM , Horsch A , He T , Kronlage M , Dewenter M , Sramek V , Oehl U , Krebs-Haupenthal J , von der Lieth AH , Schmidt A , Sun Q , Ritterhoff J , Finke D , Volkers M , Jungmann A , Sauer SW , Thiel C , Nickel A , Kohlhaas M , Schafer M , Sticht C , Maack C , Gretz N , Wagner M , El-Armouche A , Maier LS , Londono JEC , Meder B , Freichel M , Grone HJ , Most P , Muller OJ , Herzig S , Furlong EEM , Katus HA , Backs J
Ref : Nat Med , 24 :62 , 2018
Abstract : The stress-responsive epigenetic repressor histone deacetylase 4 (HDAC4) regulates cardiac gene expression. Here we show that the levels of an N-terminal proteolytically derived fragment of HDAC4, termed HDAC4-NT, are lower in failing mouse hearts than in healthy control hearts. Virus-mediated transfer of the portion of the Hdac4 gene encoding HDAC4-NT into the mouse myocardium protected the heart from remodeling and failure; this was associated with decreased expression of Nr4a1, which encodes a nuclear orphan receptor, and decreased NR4A1-dependent activation of the hexosamine biosynthetic pathway (HBP). Conversely, exercise enhanced HDAC4-NT levels, and mice with a cardiomyocyte-specific deletion of Hdac4 show reduced exercise capacity, which was characterized by cardiac fatigue and increased expression of Nr4a1. Mechanistically, we found that NR4A1 negatively regulated contractile function in a manner that depended on the HBP and the calcium sensor STIM1. Our work describes a new regulatory axis in which epigenetic regulation of a metabolic pathway affects calcium handling. Activation of this axis during intermittent physiological stress promotes cardiac function, whereas its impairment in sustained pathological cardiac stress leads to heart failure.
ESTHER : Lehmann_2018_Nat.Med_24_62
PubMedSearch : Lehmann_2018_Nat.Med_24_62
PubMedID: 29227474

Title : Association between Lipoprotein Lipase Polymorphism and the Risk of Stroke: A Meta-analysis - He_2017_J.Stroke.Cerebrovasc.Dis_26_2570
Author(s) : He T , Wang J , Deng WS , Sun P
Ref : J Stroke Cerebrovasc Dis , 26 :2570 , 2017
Abstract : BACKGROUND: Several studies have studied the relationship between lipoprotein lipase (LPL) HindIII gene polymorphism and stroke susceptibility. However, the conclusions remain controversial. To clarify the association of LPL gene HindIII polymorphism and stroke susceptibility, we therefore conducted a comprehensive meta-analysis. MATERIALS AND
METHODS: The PubMed, Web of Science, EMBASE, and Google Scholar databases were systemically searched to indentify available studies. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated under the allelic, dominant, homozygous, heterozygous, and recessive models. The data were analyzed by using Stata 12.0 (StataCorp, College Station, TX).
RESULTS: Ten studies were enrolled, including a total of 2122 cases and 2235 controls. The overall results showed that LPL HindIII variants were associated with a decreased risk of stroke (G versus T: OR = .78, 95% CI = .70-.87, P < .001; GG + TG versus TT: OR = .76, 95% CI = .67-.87, P < .001; GG versus TT: OR = .69, 95% CI = .53-.90, P = .006; TG versus TT: OR = .78, 95% CI = .68-.90, P <.001; GG versus TG + TT: OR = .74, 95% CI = .57-.95, P = .02). Stratified analysis by ethnicity (Asian and non-Asian) indicated that LPL HindIII variants were associated with a decreased risk of stroke in the Asian population, but not in the non-Asian population. In the subgroup analysis by stroke subtype, the results suggested that LPL HindIII variants contributed to a decrease in both ischemic stroke and hemorrhagic stroke risks. CONCLUSION: Our meta-analysis suggested that LPL HindIII variants were associated with a decreased risk of stroke in the Asian population, but not in the non-Asian population.
ESTHER : He_2017_J.Stroke.Cerebrovasc.Dis_26_2570
PubMedSearch : He_2017_J.Stroke.Cerebrovasc.Dis_26_2570
PubMedID: 28687421

Title : Pigment epithelium-derived factor regulates microvascular permeability through adipose triglyceride lipase in sepsis - He_2015_Clin.Sci.(Lond)_129_49
Author(s) : He T , Hu J , Yan G , Li L , Zhang D , Zhang Q , Chen B , Huang Y
Ref : Clinical Science (Lond) , 129 :49 , 2015
Abstract : The integrity of the vascular barrier, which is essential to blood vessel homoeostasis, can be disrupted by a variety of soluble permeability factors during sepsis. Pigment epithelium-derived factor (PEDF), a potent endogenous anti-angiogenic molecule, is significantly increased in sepsis, but its role in endothelial dysfunction has not been defined. To assess the role of PEDF in the vasculature, we evaluated the effects of exogenous PEDF in vivo using a mouse model of cecal ligation and puncture (CLP)-induced sepsis and in vitro using human dermal microvascular endothelial cells (HDMECs). In addition, PEDF was inhibited using a PEDF-monoclonal antibody (PEDF-mAb) or recombinant lentivirus vectors targeting PEDF receptors, including adipose triglyceride lipase (ATGL) and laminin receptor (LR). Our results showed that exogenous PEDF induced vascular hyperpermeability, as measured by extravasation of Evan's Blue (EB), dextran and microspheres in the skin, blood, trachea and cremaster muscle, both in a normal state and under conditions of sepsis. In control and LR-shRNA-treated HDMECs, PEDF alone or in combination with inflammatory mediators resulted in activation of RhoA, which was accompanied by actin rearrangement and disassembly of intercellular junctions, impairing endothelial barrier function. But in ATGL-shRNA-treated HDMECs, PEDF failed to induce the aforementioned alterations, suggesting that PEDF-induced hyperpermeability was mediated through the ATGL receptor. These results reveal a novel role for PEDF as a potential vasoactive substance in septic vascular hyperpermeability. Furthermore, our results suggest that PEDF and ATGL may serve as therapeutic targets for managing vascular hyperpermeability in sepsis.
ESTHER : He_2015_Clin.Sci.(Lond)_129_49
PubMedSearch : He_2015_Clin.Sci.(Lond)_129_49
PubMedID: 25700221

Title : Selective blockade of the hydrolysis of the endocannabinoid 2-arachidonoylglycerol impairs learning and memory performance while producing antinociceptive activity in rodents - Griebel_2015_Sci.Rep_5_7642
Author(s) : Griebel G , Pichat P , Beeske S , Leroy T , Redon N , Jacquet A , Francon D , Bert L , Even L , Lopez-Grancha M , Tolstykh T , Sun F , Yu Q , Brittain S , Arlt H , He T , Zhang B , Wiederschain D , Bertrand T , Houtmann J , Rak A , Vallee F , Michot N , Auge F , Menet V , Bergis OE , George P , Avenet P , Mikol V , Didier M , Escoubet J
Ref : Sci Rep , 5 :7642 , 2015
Abstract : Monoacylglycerol lipase (MAGL) represents a primary degradation enzyme of the endogenous cannabinoid (eCB), 2-arachidonoyglycerol (2-AG). This study reports a potent covalent MAGL inhibitor, SAR127303. The compound behaves as a selective and competitive inhibitor of mouse and human MAGL, which potently elevates hippocampal levels of 2-AG in mice. In vivo, SAR127303 produces antinociceptive effects in assays of inflammatory and visceral pain. In addition, the drug alters learning performance in several assays related to episodic, working and spatial memory. Moreover, long term potentiation (LTP) of CA1 synaptic transmission and acetylcholine release in the hippocampus, two hallmarks of memory function, are both decreased by SAR127303. Although inactive in acute seizure tests, repeated administration of SAR127303 delays the acquisition and decreases kindled seizures in mice, indicating that the drug slows down epileptogenesis, a finding deserving further investigation to evaluate the potential of MAGL inhibitors as antiepileptics. However, the observation that 2-AG hydrolysis blockade alters learning and memory performance, suggests that such drugs may have limited value as therapeutic agents.
ESTHER : Griebel_2015_Sci.Rep_5_7642
PubMedSearch : Griebel_2015_Sci.Rep_5_7642
PubMedID: 25560837
Gene_locus related to this paper: mouse-ABHD6

Title : Whole-Genome Shotgun Assembly and Analysis of the Genome of Streptomyces mobaraensis DSM 40847, a Strain for Industrial Production of Microbial Transglutaminase - Yang_2013_Genome.Announc_1_e0014313
Author(s) : Yang H , He T , Wu W , Zhu W , Lu B , Sun W
Ref : Genome Announc , 1 :e0014313 , 2013
Abstract : Here, we report the draft annotated genome sequence of Streptomyces mobaraensis strain DSM 40847, which is used in industry to produce microbial transglutaminase. The genome sequence will allow for the characterization of the molecular mechanisms underlying the beneficial properties of this organism.
ESTHER : Yang_2013_Genome.Announc_1_e0014313
PubMedSearch : Yang_2013_Genome.Announc_1_e0014313
PubMedID: 23558536
Gene_locus related to this paper: strmb-m3c6n2 , strmb-m3c3t3 , strmb-m3a818 , strmb-m3ceh8 , strmb-m3cfp8 , strmb-m3bfl5 , strmb-m3c970 , 9actn-q9fb38 , strmb-m2zv71

Title : Small molecule activation of lecithin cholesterol acyltransferase modulates lipoprotein metabolism in mice and hamsters - Chen_2012_Metabolism_61_470
Author(s) : Chen Z , Wang SP , Krsmanovic ML , Castro-Perez J , Gagen K , Mendoza V , Rosa R , Shah V , He T , Stout SJ , Geoghagen NS , Lee SH , McLaren DG , Wang L , Roddy TP , Plump AS , Hubbard BK , Sinz CJ , Johns DG
Ref : Metabolism , 61 :470 , 2012
Abstract : The objective was to assess whether pharmacological activation of lecithin cholesterol acyltransferase (LCAT) could exert beneficial effects on lipoprotein metabolism. A putative small molecule activator (compound A) was used as a tool compound in in vitro and in vivo studies. Compound A increased LCAT activity in vitro in plasma from mouse, hamster, rhesus monkey, and human. To assess the acute pharmacodynamic effects of compound A, C57Bl/6 mice and hamsters received a single dose (20 mg/kg) of compound A. Both species displayed a significant increase in high-density lipoprotein cholesterol (HDLc) and a significant decrease in non-HDLc and triglycerides acutely after dosing; these changes tracked with ex vivo plasma LCAT activity. To examine compound A's chronic effect on lipoprotein metabolism, hamsters received a daily dosing of vehicle or of 20 or 60 mg/kg of compound A for 2 weeks. At study termination, compound treatment resulted in a significant increase in HDLc, HDL particle size, plasma apolipoprotein A-I level, and plasma cholesteryl ester (CE) to free cholesterol ratio, and a significant reduction in very low-density lipoprotein cholesterol. The increase in plasma CE mirrored the increase in HDL CE. Triglycerides trended toward a dose-dependent decrease in very low-density lipoprotein and HDL, with multiple triglyceride species reaching statistical significance. Gallbladder bile acids content displayed a significant and more than 2-fold increase with the 60 mg/kg treatment. We characterized pharmacological activation of LCAT by a small molecule extensively for the first time, and our findings support the potential of this approach in treating dyslipidemia and atherosclerosis; our analyses also provide mechanistic insight on LCAT's role in lipoprotein metabolism.
ESTHER : Chen_2012_Metabolism_61_470
PubMedSearch : Chen_2012_Metabolism_61_470
PubMedID: 22001333

Title : Complete genome sequence of the bacterium Methylovorus sp. strain MP688, a high-level producer of pyrroloquinolone quinone - Xiong_2011_J.Bacteriol_193_1012
Author(s) : Xiong XH , Zhi JJ , Yang L , Wang JH , Zhao Y , Wang X , Cui YJ , Dong F , Li MX , Yang YX , Wei N , An JJ , Du BH , Liang L , Zhang JS , Zhou W , Cheng SF , He T , Wang L , Chen HP , Liu DS , Zhang WC
Ref : Journal of Bacteriology , 193 :1012 , 2011
Abstract : Methylotrophic bacteria are widespread microbes which can use one carbon compound as their only carbon and energy sources. Here we report the finished, annotated genome sequence of the methylotrophic bacterium Methylovorus sp. strain MP688, which was isolated from soil for high-level production of pyrroloquinolone quinone (PQQ) in our lab.
ESTHER : Xiong_2011_J.Bacteriol_193_1012
PubMedSearch : Xiong_2011_J.Bacteriol_193_1012
PubMedID: 21148725
Gene_locus related to this paper: mets6-e4qna9 , mets6-e4qnd9 , metsd-c6xa50