Short-term environmental enrichment, in the absence of exercise, improves memory, and increases NGF concentration, early neuronal survival, and synaptogenesis in the dentate gyrus in a time-dependent manner

Hippocampus ◽  
2013 ◽  
Vol 23 (6) ◽  
pp. 437-450 ◽  
Author(s):  
Amy M. Birch ◽  
Niamh B. McGarry ◽  
Áine M. Kelly
Keyword(s):  
Dentate Gyrus ◽  
Environmental Enrichment ◽  
Neuronal Survival ◽  
Time Dependent ◽  
Dependent Manner ◽  
Short Term

Presynaptic Group II mGluR Inhibition of Short-Term Depression in the Medial Perforant Path of the Dentate Gyrus In Vitro

2001 ◽  
Vol 85 (6) ◽  
pp. 2509-2515 ◽  
Author(s):  
John Kilbride ◽  
Anthony M. Rush ◽  
Michael J. Rowan ◽  
Roger Anwyl
Keyword(s):  
Dentate Gyrus ◽  
Metabotropic Glutamate Receptors ◽  
State Level ◽  
Perforant Path ◽  
Dependent Manner ◽  
Short Term ◽  
Concentration Dependent Manner ◽  
Postsynaptic Response ◽  
Group Ii

Inhibition of short-term plasticity by activation of presynaptic group II metabotropic glutamate receptors (group II mGluR) was investigated in the medial perforant path of the dentate gyrus in the hippocampus in vitro. Brief trains of stimulation (10 stimuli at 1–200 Hz) evoked short-term depression of field excitatory postsynaptic potentials (EPSPs). The steady-state level of depression, measured after 10 stimuli, was frequency dependent, increasing between 1 and 200 Hz. Activation of group II mGluR by the selective agonist LY354740 did not alter short-term depression evoked by frequencies up to 10 Hz, but did inhibit short-term depression evoked at higher frequencies in a frequency- and concentration-dependent manner. The time-averaged postsynaptic response (EPSP per unit time) was found to increase linearly with frequency up to ∼20 Hz. At higher frequencies, the response plateaued, thereby becoming independent of frequency. Frequencies above this were differentiated only during the transient postsynaptic response that accompanies changes in firing rates. Activation of presynaptically located group II mGluR increased the frequency at which the EPSP per unit time plateaued up to 30–50 Hz.

scholarly journals Short-term cortisol exposure alters cardiac hypertrophic and non-hypertrophic signalling in a time-dependent manner in rainbow trout

Biology Open ◽  
2018 ◽  
Vol 7 (12) ◽  
pp. bio037853 ◽  
Author(s):  
Karoline S. Nørstrud ◽  
Marco A. Vindas ◽  
Göran E. Nilsson ◽  
Ida B. Johansen
Keyword(s):  
Rainbow Trout ◽  
Time Dependent ◽  
Dependent Manner ◽  
Short Term

Mesenchymal Stem Cells Can Be Mobilized Into Peripheral Blood by Short-Term Hypoxia: a Possible Role of HIF-1α.

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 1450-1450
Author(s):  
Lizhen Liu ◽  
Qin Yu ◽  
Jie Lin ◽  
Weijie Cao ◽  
Xiaoyu Lai ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Peripheral Blood ◽  
Time Dependent ◽  
Haematopoietic Stem Cell ◽  
Hypoxic Exposure ◽  
Dependent Manner ◽  
Short Term ◽  
Lower Oxygen

Abstract Abstract 1450 Background: Mesenchymal stem cells (MSCs) constitute a population of multipotential cells giving rise to adipocytes, osteoblasts and chondrocytes. Combining with their engraftment promoting capacity and immunosuppressive property, MSCs may be therapeutically useful for haematopoietic stem cell transplantation. There is growing evidence that these cells can, under the right circumstances, enter peripheral circulation. Previous study revealed that MSCs are mobilized into peripheral blood (PB) by 3 weeks of chronic hypoxia, but the mobilization effect of short-term hypoxia and the underlying mechanisms are currently unknown. In this study, we used rat model to determine whether short-term hypoxia can mobilize MSCs into PB and investigated the related factors which may regulate the mobilization process. Design and Methods: Rats were housed in a hypoxic chamber (FiO2=10%) for 1, 2, 3, 5, 7 and 14 days, respectively, while control ones were housed in normoxic environment for equal periods. To quantify the number of MSCs and evaluate mobilization efficiency, PB and bone barrow (BM) samples of each group were collected and colony-forming unit fibroblast (CFU-F) assays were performed. Mobilized PB derived MSCs were identified by immunophenotype and trilineage differentiation. Since BM is the main reservoir and typical microenvironment of MSCs, we investigated the response of BM environment exposed to hypoxia which may potentially facilitate MSCs mobilization. Hypoxia-inducible factor 1α (HIF-1α) expression of BM cells was detected by Western blot; vascular endothelial growth factor (VEGF) in BM was qualified by ELISA and Immunohistochemistry (IHC). To evaluate the change of BM sinusoid vessels (BMSVs), VEGFR3 was stained by IHC and positive vessels were counted. The levels of stromal cell-derived factor-1α (SDF-1α) and VEGF in PB were tested by ELISA. Moreover, we compared migration capacity of MSCs in hypoxic condition (PO2=1% or 8%) with normal condition (PO2=21%) in vitro using Transwell assay. Results: We found that MSCs were mobilized into PB by exposing to short-term hypoxia (2d) and the CFU-F frequency was 5.80±0.58 vs. 1.40±0.24 CFU-Fs per 3×106 cells (p<0.05, n=5). From 2d to 14d of hypoxic exposure, the number of CFU-Fs mobilized in PB of hypoxic group was gradually increased in a time dependent manner. However, no significant differences were observed in bone marrow CFU-Fs among varies groups (P>0.05). Mobilized PB derived adherent cells were positive for CD90, CD29 and CD44, but negative for CD34 and CD45 and they could differentiate into adipocyte, osteoblast, and chondrocyte, which indicated that mobilized PB-derived cells are bona fide MSCs. What's more, we showed here that during hypoxic exposure, HIF-1α was stabilized and expressed continuously in BM of rats which is a main niche of MSCs. Stabilization and up-regulation of HIF-1α suggested that BM is hypoxia-sensitive and during hypoxic exposure it became a lower oxygen environment (PO2<1%). Previous studies have proved that VEGF and SDF-1α are directly regulated by the transcription factor HIF-1α. Our results showed that, induced by HIF-1α, VEGF was elevated from 2d to 7d in the BM of hypoxic rats which may increase BM vascular permeability and induce vasodilatation; VEGFR3(+) BMSVs increased in 7d and 14d hypoxic BM which may further facilitate the egress of MSCs. SDF-1α in PB increased from 2d to 14d, especially 7d of hypoxia (1976.7±148.1 vs. 663.6±56.7pg/ml, P<0.01). In addition, exposure of MSCs to low oxygen (8% PO2) significantly promoted their in vitro migration and a further increase was observed under lower oxygen condition (1% PO2). MSCs migrated more rapidly in response to SDF-1α exposed to hypoxia. Conclusion: Taken together, we show here that MSCs can be mobilized into PB by short-term hypoxia and the mobilization efficacy increased in a time dependent manner. Our results suggest the mechanisms of hypoxia inducing MSCs mobilization relate to the lower oxygen milieu of BM and stabilization of HIF-1α may play a pivotal role in MSCs mobilization. Our data provide meaningful clues to clarify the mechanisms of MSCs mobilization and important evidence for further exploring the exact agents that of clinical use. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Modulation of Astrocytic Glutamine Synthetase by Endocannabinoid 2-Arachidonoylglycerol in JNK-Independent Pathway

2021 ◽  
Vol 2 ◽  
Author(s):  
Jing Wang ◽  
Shenghong Wang ◽  
Hua Zhang
Keyword(s):  
Glutamine Synthetase ◽  
Time Dependent ◽  
Dependent Manner ◽  
Specific Enzyme ◽  
Short Term ◽  
Jnk Signaling ◽  
Extracellular Signal ◽  
Short Term Exposure ◽  
Jnk Signaling Pathway

Background and Objective: The glutamine synthetase (GS), an astrocyte-specific enzyme, plays an important role in neuroprotection through the glutamate/glutamine shuttle and can be modulated by endocannabinoid (eCB) 2-arachidonoylglycerol (2-AG) through extracellular signal-regulated protein kinase ½ (ERK1/2) and p38 signaling pathways. However, the role of c-Jun N-terminal kinase (JNK) signaling pathway in the modulation of GS in astrocytes by 2-AG is not clear.Materials and Methods: The expression of GS and JNK in astrocytes following the exposure to lipopolysaccharide (LPS) was examined with Western blotting and immunochemistry.Results: The results revealed that short-term exposure to LPS activated GS and increased phosphorylation of JNK in astrocytes in a time-dependent manner. Treatment with 2-AG reversed the changes in GS but had no effect on the activation of JNK.Conclusions: These findings suggest that the activation of JNK induced by LPS is not involved in the modulation of astrocytic GS by 2-AG.

The Natural Flavonoid Naringenin Inhibits the Cell Growth of WilmsTumorinChildren by Suppressing TLR4/NF-κB Signaling

2020 ◽  
Vol 20 ◽  
Author(s):  
Hongtao Li ◽  
Peng Chen ◽  
Lei Chen ◽  
Xinning Wang
Keyword(s):  
Cell Growth ◽  
Western Blot ◽  
Wilms Tumor ◽  
Critical Role ◽  
Time Dependent ◽  
Luciferase Assay ◽  
Dependent Manner ◽  
Tlr4 Expression ◽  
Protein Levels

Background: Nuclear factor kappa B (NF-κB) is usually activated in Wilms tumor (WT) cells and plays a critical role in WT development. Objective: The study purpose was to screen a NF-κB inhibitor from natural product library and explore its effects on WT development. Methods: Luciferase assay was employed to assess the effects of natural chemical son NF-κB activity. CCK-8 assay was conducted to assess cell growth in response to naringenin. WT xenograft model was established to analyze the effect of naringenin in vivo. Quantitative real-time PCR and Western blot were performed to examine the mRNA and protein levels of relative genes, respectively. Results: Naringenin displayed significant inhibitory effect on NF-κB activation in SK-NEP-1 cells. In SK-NEP-1 and G-401 cells, naringenin inhibited p65 phosphorylation. Moreover, naringenin suppressed TNF-α-induced p65 phosphorylation in WT cells. Naringenin inhibited TLR4 expression at both mRNA and protein levels in WT cells. CCK-8 staining showed that naringenin inhibited cell growth of the two above WT cells in dose-and time-dependent manner, whereas Toll-like receptor 4 (TLR4) over expression partially reversed the above phenomena. Besides, naringenin suppressed WT tumor growth in dose-and time-dependent manner in vivo. Western blot found that naringenin inhibited TLR4 expression and p65 phosphorylation in WT xenograft tumors. Conclusion: Naringenin inhibits WT development viasuppressing TLR4/NF-κB signaling

scholarly journals Synthesis and Evaluation of the Antitumor Activity of Novel 1-(4-Substituted phenyl)-2-ethyl Imidazole Apoptosis Inducers In Vitro

Molecules ◽  
2020 ◽  
Vol 25 (18) ◽  
pp. 4293
Author(s):  
Zhen-Wang Li ◽  
Chun-Yan Zhong ◽  
Xiao-Ran Wang ◽  
Shi-Nian Li ◽  
Chun-Yuan Pan ◽  
...  
Keyword(s):  
Antitumor Activity ◽  
Tumor Cells ◽  
Antiproliferative Activity ◽  
Antitumor Agent ◽  
Positive Control ◽  
Selectivity Index ◽  
Time Dependent ◽  
Potential Candidate ◽  
Dependent Manner

Novel imidazole derivatives were designed, prepared, and evaluated in vitro for antitumor activity. The majority of the tested derivatives showed improved antiproliferative activity compared to the positive control drugs 5-FU and MTX. Among them, compound 4f exhibited outstanding antiproliferative activity against three cancer cell lines and was considerably more potent than both 5-FU and MTX. In particular, the selectivity index indicated that the tolerance of normal L-02 cells to 4f was 23–46-fold higher than that of tumor cells. This selectivity was significantly higher than that exhibited by the positive control drugs. Furthermore, compound 4f induced cell apoptosis by increasing the protein expression levels of Bax and decreasing those of Bcl-2 in a time-dependent manner. Therefore, 4f could be a potential candidate for the development of a novel antitumor agent.

scholarly journals Moxifloxacin Activates the SOS Response in Mycobacterium tuberculosis in a Dose- and Time-Dependent Manner

2021 ◽  
Vol 9 (2) ◽  
pp. 255
Author(s):  
Angelo Iacobino ◽  
Giovanni Piccaro ◽  
Manuela Pardini ◽  
Lanfranco Fattorini ◽  
Federico Giannoni
Keyword(s):  
Gene Expression ◽  
Mycobacterium Tuberculosis ◽  
Physiological State ◽  
Transcriptional Response ◽  
Sos Response ◽  
Resistant Mutant ◽  
Time Dependent ◽  
Dependent Manner ◽  
Gyra Gene ◽  
Drug Concentrations

Previous studies on Escherichia coli demonstrated that sub-minimum inhibitory concentration (MIC) of fluoroquinolones induced the SOS response, increasing drug tolerance. We characterized the transcriptional response to moxifloxacin in Mycobacterium tuberculosis. Reference strain H37Rv was treated with moxifloxacin and gene expression studied by qRT-PCR. Five SOS regulon genes, recA, lexA, dnaE2, Rv3074 and Rv3776, were induced in a dose- and time-dependent manner. A range of moxifloxacin concentrations induced recA, with a peak observed at 2 × MIC (0.25 μg/mL) after 16 h. Another seven SOS responses and three DNA repair genes were significantly induced by moxifloxacin. Induction of recA by moxifloxacin was higher in log-phase than in early- and stationary-phase cells, and absent in dormant bacilli. Furthermore, in an H37Rv fluoroquinolone-resistant mutant carrying the D94G mutation in the gyrA gene, the SOS response was induced at drug concentrations higher than the mutant MIC value. The 2 × MIC of moxifloxacin determined no significant changes in gene expression in a panel of 32 genes, except for up-regulation of the relK toxin and of Rv3290c and Rv2517c, two persistence-related genes. Overall, our data show that activation of the SOS response by moxifloxacin, a likely link to increased mutation rate and persister formation, is time, dose, physiological state and, possibly, MIC dependent.

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