Journal: Apoptosis

Article Title: Valproic acid upregulates the expression of the p75NTR/sortilin receptor complex to induce neuronal apoptosis

doi: 10.1007/s10495-020-01626-0

Figure Lengend Snippet: Effects of HDAC inhibitors on p75NTR and sortilin expression. SH-SY5Y ( a , b , e and f ) and LAN-1 ( c , d , g and h ) cells were incubated for 24 h with either vehicle, 1 mM VPA, 1 µM entinostat, 1 mM sodium butyrate (NaButyr), 300 nM trichostatin A (TSA), 10 µM MC1568, 30 nM romidepsin, 5 µM tubacin, or 5 µM PCI-34,051. Cell lysates were analysed for p75NTR and sortilin expression. Values are the mean ± SD of four ( a , b , e and f ) and six ( c , d , g and h ) independent experiments. * p < 0.05, ** p < 0.01 vs. control (vehicle-treated cells)

Article Snippet: Entinostat was obtained from Santa Cruz Biotechnology (Dallas, TX, USA).

Techniques: Expressing, Incubation, Control

Journal: Apoptosis

Article Title: Valproic acid upregulates the expression of the p75NTR/sortilin receptor complex to induce neuronal apoptosis

doi: 10.1007/s10495-020-01626-0

Figure Lengend Snippet: VPA upregulates p75NTR and sortilin expression and promotes proNGF-induced apoptosis in mouse cerebellar granule cells. a cells were incubated for 24 h with either vehicle, 1 mM VPA or 1 µM entinostat and cell lysates were analysed for p75NTR and sortilin expression. Values are the mean ± SD of four independent experiments. b cells were incubated for 24 h with either vehicle or 1 mM VPA and then exposed for additional 24 h to either vehicle or 5 ng/ml proNGF. Cells were analysed for cleaved caspase 3 (green color) and neurofilament 160/200 (red color) by immunofluorescence microscopy. Nuclei were stained with DAPI (blue color). Bar = 50 µm. Values are the mean ± SD of four experiments. * p < 0.05 vs. vehicle. # p < 0.05 (Color figure online)

Article Snippet: Entinostat was obtained from Santa Cruz Biotechnology (Dallas, TX, USA).

Techniques: Expressing, Incubation, Immunofluorescence, Microscopy, Staining

Journal: Neuropharmacology

Article Title: Differential effects of HDAC inhibitors on PPN oscillatory activity in vivo

doi: 10.1016/j.neuropharm.2019.107922

Figure Lengend Snippet: A. Ramp-induced oscillations in the presence of SB+TTX (3 μM) and 15 min after SB+TTX (10 μM). B. Power spectrum corresponding to the same cell shown in A. C. Bar graph representing mean oscillation frequency for all PPN neurons recorded from Vehicle (black bar; n=19 cells), MS275 low dose (dashed blue bar; 4 mg/Kg, i.p.; n=12 cells), and MS275 middle dose (solid blue bar; 20 mg/Kg, i.p.; n=16 cells) treatments. No significant differences were observed (One Way ANOVA, F(2,46)=1.1, p=0.3). D. Bar graph representing mean oscillation amplitude for PPN neurons from Vehicle (black bar; n=17 cells), MS275 middle dose (dashed blue bar; 20 mg/Kg, i.p.; n= 10 cells), and MS275 high dose (solid blue bar; 100 mg/Kg, i.p.; n=17 cells) treatments. Significantly higher oscillation amplitudes were observed for TSA high dose (100 mg/Kg) treatment. One-way ANOVA, F(2,43)=4.4, p=0.02. * P<0.05, post hoc Tukey’s test, MS275 (100 mg/Kg) vs Vehicle, q=3.9, p=0.02. E. Bar graph representing mean input resistance (Rm) for PPN neurons from Vehicle (black bar; n=19 cells), MS175 low dose (dashed blue bar; 4 mg/Kg, i.p.; n=12 cells), and MS275 middle dose (solid blue bar; 20 mg/Kg, i.p.; n=16 cells) treatments. No significant differences were observed (One Way ANOVA F(2,46)=0.008, p=0.9).

Article Snippet: HDACi in vivo administration (acute, single dose) was performed with the following agents: the selective HDAC class IIa inhibitor, MC1568 (4 or 20 mg/Kg, i.p. ; Catalog #M1824; Sigma Aldrich, St. Louis, MO, USA or Catalog #4077; TOCRIS, MN, USA) [3-[5-(3-(3-Fluorophenyl)-3-oxopropen-1-yl)-1-methyl-1H-pyrrol-2-yl]-N-hydroxy-2-propenamide]; the HDAC class I & II inhibitor Trichostatin-A (4 or 20 mg/Kg, i.p. ; Catalog #T8552; Sigma Aldrich, St. Louis, MO, USA or Catalog #1406; TOCRIS, MN, USA) [(2E,4E,6R)-7-(4-(Dimethylamino)phenyl)-N-hydroxy-4,6-dimethyl-7-oxo-2,4-heptadienamide]; and a HDAC class I inhibitor MS275 (20 or 100 mg/Kg, i.p. ; Catalog #EPS002; Sigma Aldrich, St. Louis, MO, USA or Catalog #6208; TOCRIS, MN, USA) [Pyridin-3-yl)methyl 4-(2-aminophenylcarbamoyl) benzylcarbamate].

Techniques:

Journal: Neuropharmacology

Article Title: Differential effects of HDAC inhibitors on PPN oscillatory activity in vivo

doi: 10.1016/j.neuropharm.2019.107922

Figure Lengend Snippet: A. Representative ICa (current density values, pA/pF) recordings in PPN neurons elicited by a 50 msec long depolarizing square step from a holding potential of −50 mV to 0 mV after Vehicle (black record), MC1568 (red record), TSA (brown record), and MS275 (blue record) treatments. B. Percent change of ICa amplitude after Vehicle (black bar; n=39 cells), 20 mg/Kg MC1568 (red bar; n=17 cells), 20 mg/Kg TSA (brown bar; n=12 cells), and 20 mg/Kg MS275 treatments (blue bar; n=11 cells). One Way ANOVA, F(3,77)=24.3, p<0.001. * p<0.05; ICa comparing all treatments; post hoc Tukey’s test, 20mg/Kg MC1568 vs Vehicle, q=8.1, p<0.001; 20 mg/Kg TSA vs Vehicle, q=6.8, p<0.001; 20 mg/Kg MS275 vs Vehicle, q=4.3, p=0.016. # P<0.05 post hoc Tukey’s test, 20 mg/Kg MS275 vs 20 mg/Kg MC1568, q=9.9, p<0.001; 20 mg/Kg MS275 vs 20 mg/Kg TSA, q=8.9, p<0.001. C. Percent change of ICa amplitude after Vehicle (black bar; n=16 cells), 4 mg/Kg MC1568 (red bar; n=9 cells), 4 mg/Kg TSA (brown bar; n=11 cells), and 100 mg/Kg MS275 treatments (blue bar; n=15 cells). One Way ANOVA, F(3,50)=8.0, p<0.001. * p<0.05; ICa comparing all treatments; post hoc Tukey’s test, 100 mg/Kg MS275 vs Vehicle, q=4.3, p<0.01; MC1568 4 mg/Kg vs Vehicle, q=4.1, p=0.03. No statistically significant differences were observed comparing 4 mg/Kg TSA vs Vehicle, q=1.4, p=0.7. # p<0.05 post hoc Tukey’s test, 100 mg/Kg MS275 vs 4 mg/Kg MC1568, q=6.8, p<0.001; 4 mg/Kg TSA vs 4 mg/Kg MC1568, q=5.0, P=0.005; 100 mg/Kg MS275 vs Vehicle, q=4.3, p<0.005. No statistically significant differences were observed comparing 20mg/Kg vs 100 mg/Kg MS275, one way ANOVA, F(1,25)=0.02, p=0.9.

Article Snippet: HDACi in vivo administration (acute, single dose) was performed with the following agents: the selective HDAC class IIa inhibitor, MC1568 (4 or 20 mg/Kg, i.p. ; Catalog #M1824; Sigma Aldrich, St. Louis, MO, USA or Catalog #4077; TOCRIS, MN, USA) [3-[5-(3-(3-Fluorophenyl)-3-oxopropen-1-yl)-1-methyl-1H-pyrrol-2-yl]-N-hydroxy-2-propenamide]; the HDAC class I & II inhibitor Trichostatin-A (4 or 20 mg/Kg, i.p. ; Catalog #T8552; Sigma Aldrich, St. Louis, MO, USA or Catalog #1406; TOCRIS, MN, USA) [(2E,4E,6R)-7-(4-(Dimethylamino)phenyl)-N-hydroxy-4,6-dimethyl-7-oxo-2,4-heptadienamide]; and a HDAC class I inhibitor MS275 (20 or 100 mg/Kg, i.p. ; Catalog #EPS002; Sigma Aldrich, St. Louis, MO, USA or Catalog #6208; TOCRIS, MN, USA) [Pyridin-3-yl)methyl 4-(2-aminophenylcarbamoyl) benzylcarbamate].

Techniques:

Journal: Neuropharmacology

Article Title: Differential effects of HDAC inhibitors on PPN oscillatory activity in vivo

doi: 10.1016/j.neuropharm.2019.107922

Figure Lengend Snippet: A. Representative ramp-induced oscillations of PPN neurons from a rat treated systemically with MS275 (100 mg/Kg, i.p.; left panel) or MS275+MC1568 (100 mg/Kg+20 mg/Kg; right panel) in the presence of SB+TTX. B. Bar graph representing mean amplitude of oscillations in PPN neurons from a MS275 (black bar; 100 mg/Kg; n=17 cells) or a MS275+MC1568 (100 mg/Kg+20 mg/Kg; grey bar; n=6 cells) treated rat. Significantly lower amplitudes were observed for the combination MS275+MC1568 treatment. * P<0.05, One-way ANOVA, F(1,22)=7.3, p=0.01, post hoc Tukey’s test, MS275+MC1568 vs MS275, q=3.8, p=0.01. C. Bar graph representing mean frequency of oscillations for PPN neurons from a MS275 (black bar; 100 mg/Kg; n=16 cells) or a MS275+MC1568 (100 mg/Kg+20 mg/Kg; grey bar; n=6 cells) treated rat. No significant differences were observed (One Way ANOVA, F(2,21)=0.2, p=0.7). D. Bar graph representing mean input resistance (Rm) for PPN neurons from a MS275 (black bar; 100 mg/Kg; n=16 cells) or a MS275+MC1568 (100 mg/Kg+20 mg/Kg; grey bar; n=6 cells) treated rat. No significant differences were observed (One Way ANOVA, F(2,21)=1.0, p=0.3).

Article Snippet: HDACi in vivo administration (acute, single dose) was performed with the following agents: the selective HDAC class IIa inhibitor, MC1568 (4 or 20 mg/Kg, i.p. ; Catalog #M1824; Sigma Aldrich, St. Louis, MO, USA or Catalog #4077; TOCRIS, MN, USA) [3-[5-(3-(3-Fluorophenyl)-3-oxopropen-1-yl)-1-methyl-1H-pyrrol-2-yl]-N-hydroxy-2-propenamide]; the HDAC class I & II inhibitor Trichostatin-A (4 or 20 mg/Kg, i.p. ; Catalog #T8552; Sigma Aldrich, St. Louis, MO, USA or Catalog #1406; TOCRIS, MN, USA) [(2E,4E,6R)-7-(4-(Dimethylamino)phenyl)-N-hydroxy-4,6-dimethyl-7-oxo-2,4-heptadienamide]; and a HDAC class I inhibitor MS275 (20 or 100 mg/Kg, i.p. ; Catalog #EPS002; Sigma Aldrich, St. Louis, MO, USA or Catalog #6208; TOCRIS, MN, USA) [Pyridin-3-yl)methyl 4-(2-aminophenylcarbamoyl) benzylcarbamate].

Techniques:

Journal: International Journal of Molecular Sciences

Article Title: Class I-Histone Deacetylase (HDAC) Inhibition is Superior to pan-HDAC Inhibition in Modulating Cisplatin Potency in High Grade Serous Ovarian Cancer Cell Lines

doi: 10.3390/ijms20123052

Figure Lengend Snippet: Cytotoxic activity of entinostat, panobinostat, and nexturastat A.

Article Snippet: Cells were treated with indicated concentrations of entinostat, panobinostat, or nexturastat A for 48h prior to cisplatin (24 h) or 72 h entinostat, panobinostat, or nexturastat A without cisplatin, or vehicle for 72 h. Cell pellets were dissolved with RIPA buffer (50 mM Tris-HCl pH8.0, 1% Triton X-100, 0.5% sodium deoxycholate, 0.1% SDS, 150 mM sodium chloride, 2 mM EDTA, supplemented with protease and phosphatase inhibitors (PierceTM protease and phosphatase inhibitor mini tablets, Thermo Scientific, Wesel, Germany)) and clarified by centrifugation.

Techniques: Activity Assay

Journal: International Journal of Molecular Sciences

Article Title: Class I-Histone Deacetylase (HDAC) Inhibition is Superior to pan-HDAC Inhibition in Modulating Cisplatin Potency in High Grade Serous Ovarian Cancer Cell Lines

doi: 10.3390/ijms20123052

Figure Lengend Snippet: HDAC inhibitory activity of entinostat, panobinostat, and nexturastat A.

Article Snippet: Cells were treated with indicated concentrations of entinostat, panobinostat, or nexturastat A for 48h prior to cisplatin (24 h) or 72 h entinostat, panobinostat, or nexturastat A without cisplatin, or vehicle for 72 h. Cell pellets were dissolved with RIPA buffer (50 mM Tris-HCl pH8.0, 1% Triton X-100, 0.5% sodium deoxycholate, 0.1% SDS, 150 mM sodium chloride, 2 mM EDTA, supplemented with protease and phosphatase inhibitors (PierceTM protease and phosphatase inhibitor mini tablets, Thermo Scientific, Wesel, Germany)) and clarified by centrifugation.

Techniques: Activity Assay

Journal: International Journal of Molecular Sciences

Article Title: Class I-Histone Deacetylase (HDAC) Inhibition is Superior to pan-HDAC Inhibition in Modulating Cisplatin Potency in High Grade Serous Ovarian Cancer Cell Lines

doi: 10.3390/ijms20123052

Figure Lengend Snippet: HDACi concentrations used for combination treatment.

Article Snippet: Cells were treated with indicated concentrations of entinostat, panobinostat, or nexturastat A for 48h prior to cisplatin (24 h) or 72 h entinostat, panobinostat, or nexturastat A without cisplatin, or vehicle for 72 h. Cell pellets were dissolved with RIPA buffer (50 mM Tris-HCl pH8.0, 1% Triton X-100, 0.5% sodium deoxycholate, 0.1% SDS, 150 mM sodium chloride, 2 mM EDTA, supplemented with protease and phosphatase inhibitors (PierceTM protease and phosphatase inhibitor mini tablets, Thermo Scientific, Wesel, Germany)) and clarified by centrifugation.

Techniques:

Journal: International Journal of Molecular Sciences

Article Title: Class I-Histone Deacetylase (HDAC) Inhibition is Superior to pan-HDAC Inhibition in Modulating Cisplatin Potency in High Grade Serous Ovarian Cancer Cell Lines

doi: 10.3390/ijms20123052

Figure Lengend Snippet: Effect of HDACi pretreatment on cisplatin-induced cytotoxicity (MTT assay).

Article Snippet: Cells were treated with indicated concentrations of entinostat, panobinostat, or nexturastat A for 48h prior to cisplatin (24 h) or 72 h entinostat, panobinostat, or nexturastat A without cisplatin, or vehicle for 72 h. Cell pellets were dissolved with RIPA buffer (50 mM Tris-HCl pH8.0, 1% Triton X-100, 0.5% sodium deoxycholate, 0.1% SDS, 150 mM sodium chloride, 2 mM EDTA, supplemented with protease and phosphatase inhibitors (PierceTM protease and phosphatase inhibitor mini tablets, Thermo Scientific, Wesel, Germany)) and clarified by centrifugation.

Techniques:

Journal: International Journal of Molecular Sciences

Article Title: Class I-Histone Deacetylase (HDAC) Inhibition is Superior to pan-HDAC Inhibition in Modulating Cisplatin Potency in High Grade Serous Ovarian Cancer Cell Lines

doi: 10.3390/ijms20123052

Figure Lengend Snippet: Synergism studies (CI-values) between HDACi entinostat, panobinostat, or nexturastat A and cisplatin.

Article Snippet: Cells were treated with indicated concentrations of entinostat, panobinostat, or nexturastat A for 48h prior to cisplatin (24 h) or 72 h entinostat, panobinostat, or nexturastat A without cisplatin, or vehicle for 72 h. Cell pellets were dissolved with RIPA buffer (50 mM Tris-HCl pH8.0, 1% Triton X-100, 0.5% sodium deoxycholate, 0.1% SDS, 150 mM sodium chloride, 2 mM EDTA, supplemented with protease and phosphatase inhibitors (PierceTM protease and phosphatase inhibitor mini tablets, Thermo Scientific, Wesel, Germany)) and clarified by centrifugation.

Techniques:

Journal: International Journal of Molecular Sciences

Article Title: Class I-Histone Deacetylase (HDAC) Inhibition is Superior to pan-HDAC Inhibition in Modulating Cisplatin Potency in High Grade Serous Ovarian Cancer Cell Lines

doi: 10.3390/ijms20123052

Figure Lengend Snippet: Representative fluorescent imaging pictures (10× magnification) are shown for each cell line for the treatment of cisplatin (IC 50 concentration), entinostat, and the combination of cisplatin and entinostat. Cell nuclei were stained by Hoechst 33342 and appear blue while cells with activated caspases3/7 showed green fluorescence. Scale bar in upper left image is 100 µm and applies to all images.

Article Snippet: Cells were treated with indicated concentrations of entinostat, panobinostat, or nexturastat A for 48h prior to cisplatin (24 h) or 72 h entinostat, panobinostat, or nexturastat A without cisplatin, or vehicle for 72 h. Cell pellets were dissolved with RIPA buffer (50 mM Tris-HCl pH8.0, 1% Triton X-100, 0.5% sodium deoxycholate, 0.1% SDS, 150 mM sodium chloride, 2 mM EDTA, supplemented with protease and phosphatase inhibitors (PierceTM protease and phosphatase inhibitor mini tablets, Thermo Scientific, Wesel, Germany)) and clarified by centrifugation.

Techniques: Imaging, Concentration Assay, Staining, Fluorescence

Journal: Neurotoxicity research

Article Title: The MT1G Gene in LUHMES Neurons Is a Sensitive Biomarker of Neurotoxicity

doi: 10.1007/s12640-020-00272-3

Figure Lengend Snippet: Chemicals used and abbreviations

Article Snippet: Chemicals Chemicals included Ferbam from TCI America, Portland, OR; ML385 and MS275 from Toris Biosciences, Minneapolis, MN; APTO235 (MedChemExpress, Princeton, NJ); and sankel (Muse Chem, Fairfield, NJ).

Techniques:

Journal: Neurotoxicity research

Article Title: The MT1G Gene in LUHMES Neurons Is a Sensitive Biomarker of Neurotoxicity

doi: 10.1007/s12640-020-00272-3

Figure Lengend Snippet: RNA sequencing responses of LUHMES neurons to neurotoxicants. dLUHMES neurons were treated with parkinsonian toxicants 6HD, 6-hydroxydopamine 1 μM; MPP, 1-methyl-4-phenylpyridinium 5 μM, ROT, rotenone 1 μM; and additional neurotoxicants PQ 5 μM, ziram (ZIR) 2 μM, MHG 0.5 μM, and possible neurotoxicant MS275 5 μM (Vashishta and Hetman 2014). a Heatmap shows genes as rows and chemical treatments as columns. Colors indicate increased (red) or decreased (green) mRNA relative to vehicle control with color saturation at 32-fold. No cytotoxicity was observed after 24 h at these concentrations. b Bar graph shows mRNA reads counted per 100 million normalized mRNA transcripts for three metallothionein genes. Among 83 million mRNA reads for three replicate vehicle-treated samples, MT1G, MT1E, and MT2A reads numbered 2, 8, and 42 reads, respectively. ***Ziram-treated dLUHMES neurons yielded 53,000, 31,000 and 31,000 transcripts per 100 million for MT1G, MT1E, and MT2A, respectively. c Dot plot comparing RNA-Seq and qRT-PCR quantitation of responses by six biomarker genes using the samples from “a” above

Article Snippet: Chemicals Chemicals included Ferbam from TCI America, Portland, OR; ML385 and MS275 from Toris Biosciences, Minneapolis, MN; APTO235 (MedChemExpress, Princeton, NJ); and sankel (Muse Chem, Fairfield, NJ).

Techniques: RNA Sequencing, Control, Quantitative RT-PCR, Quantitation Assay, Biomarker Discovery

Journal: Neurotoxicity research

Article Title: The MT1G Gene in LUHMES Neurons Is a Sensitive Biomarker of Neurotoxicity

doi: 10.1007/s12640-020-00272-3

Figure Lengend Snippet: Transcriptional responses of three biomarker genes to 15 toxicants in six cell lines. The six cell lines indicated at left were treated with vehicle or one of 15 toxicants. Transcriptional responses by DDIT3, MT1G, PDK4, and GAPDH were quantified by qRT-PCR at 6 h, and cell viability was assessed at 24 h as intracellular [ATP]. Below the four genes for each cell line is a row of cells that indicate cell viability. White indicates no detectable loss of viability whereas blue color saturation indicates the % of cell death 24 h post-treatment. Toxicant treatments were HCP, Hexachlorophene 10 μM; CAP, captan 10 μM; 6HD, 6-hydroxydopamine 3 μM; MAP, 4-(methylamino)phenol hemisulfate salt 5 μM; CR2, sodium dichromate 5 μM; CLM, chlorambucil 10 μM; MPP, 1-methyl-4-phenylpyridinium 10 μM; MNC, manganese chloride 10 μM; PQ, paraquat 10 μM; STA, staurosporine 2 μM; ROT, rotenone 3 μM; MS5, MS275 10 μM; TER, terfenadine 10 μM; MHG, methylmercury chloride 2 μM; ZIR, ziram, 6 μM

Article Snippet: Chemicals Chemicals included Ferbam from TCI America, Portland, OR; ML385 and MS275 from Toris Biosciences, Minneapolis, MN; APTO235 (MedChemExpress, Princeton, NJ); and sankel (Muse Chem, Fairfield, NJ).

Techniques: Biomarker Discovery, Quantitative RT-PCR

Journal: PLoS ONE

Article Title: Class I histone deacetylase inhibitor MS-275 attenuates vasoconstriction and inflammation in angiotensin II-induced hypertension

doi: 10.1371/journal.pone.0213186

Figure Lengend Snippet: (A) After angiotensin II infusion (1.3 mg·kg -1 ·day -1 ) to mice for 1 week, we injected MS-275 or RGFP966 (both 3 mg·kg -1 ·day -1 ) daily to mice for additional 7 days. Systolic blood pressures were measured in awake mice. (B and C) Transcript levels of aortic AT1 and ACE1 were quantified using quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR). GAPDH was used to normalize the values. Data are presented as the means ± SE (n = 8 per group). ***p < 0.001 versus sham group; # p < 0.05 and ### p < 0.001 versus angiotensin II group; NS, not significant.

Article Snippet: To evaluate the HDAC enzyme inhibitory activity of MS-275 and RGFP966, we determined enzyme activities of HDAC1, HDAC2, HDAC3, and HDAC8 using enzyme assay kits (BPS Bioscience, San Diego, CA, USA) according to the manufacturer’s protocols.

Techniques: Injection, Reverse Transcription Polymerase Chain Reaction, Quantitative RT-PCR

Journal: PLoS ONE

Article Title: Class I histone deacetylase inhibitor MS-275 attenuates vasoconstriction and inflammation in angiotensin II-induced hypertension

doi: 10.1371/journal.pone.0213186

Figure Lengend Snippet: (A) Representative images of H&E stained aortas from sham, angiotensin II group (Ang II), MS-275-treated angiotensin II group (Ang II + MS-275), and RGFP966-treated angiotensin II group (Ang II + RGFP966). Scale bar = 100 μm. (B) Arterial wall thickness was quantified. Data are means ± SE (n = 7/group). ***p < 0.001 versus sham group; ## p < 0.01 and ### p < 0.001 versus angiotensin II group. (C‒D) Masson’s trichrome and orcein staining of representative aorta sections. Scale bar = 100 μm. Collagen deposition in aorta is shown as blue staining. (E‒H) The transcript levels of cyclin D1, cyclin E1, E2F3, and GATA6 were quantified using quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR). * p < 0.05 versus sham group; # p < 0.05 versus angiotensin II group; NS, not significant.

Article Snippet: To evaluate the HDAC enzyme inhibitory activity of MS-275 and RGFP966, we determined enzyme activities of HDAC1, HDAC2, HDAC3, and HDAC8 using enzyme assay kits (BPS Bioscience, San Diego, CA, USA) according to the manufacturer’s protocols.

Techniques: Staining, Reverse Transcription Polymerase Chain Reaction, Quantitative RT-PCR

Journal: PLoS ONE

Article Title: Class I histone deacetylase inhibitor MS-275 attenuates vasoconstriction and inflammation in angiotensin II-induced hypertension

doi: 10.1371/journal.pone.0213186

Figure Lengend Snippet: (A) U46619-precontracted endothelium-intact and -denuded aortic rings were relaxed by cumulative concentrations of MS-275. (B) Concentration-response curves of endothelium-intact aortic rings were precontracted with U46619 and incubated with MS-275 in the absence or presence of the NO synthase inhibitor L -NAME (10 and 100 μM). (C) VSMCs were treated with MS-275 (10 and 100 μM) or vehicle in the presence or absence of angiotensin II (1 μM) for 24 h. NO production in VSMC medium was evaluated using Griess reagent. The values are the means ± SE of three independent experiments. ** p < 0.01 versus vehicle-treated group; ### p < 0.001 versus angiotensin II group. NO production in serum (D) or aortic tissues (E) from sham, angiotensin II group (Ang II), and MS-275-treated angiotensin II group (Ang II + MS-275).

Article Snippet: To evaluate the HDAC enzyme inhibitory activity of MS-275 and RGFP966, we determined enzyme activities of HDAC1, HDAC2, HDAC3, and HDAC8 using enzyme assay kits (BPS Bioscience, San Diego, CA, USA) according to the manufacturer’s protocols.

Techniques: Concentration Assay, Incubation

Journal: PLoS ONE

Article Title: Class I histone deacetylase inhibitor MS-275 attenuates vasoconstriction and inflammation in angiotensin II-induced hypertension

doi: 10.1371/journal.pone.0213186

Figure Lengend Snippet: The transcript levels for arginase 1 (A), arginase 2 (B), GTPCH1 (C), PRMT1 (D), DDAH1 (E), and DDAH2 (F) were determined using quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) in aortas of sham and angiotensin II treated with vehicle, MS-275, or RGFP966. Data are presented as the means ± SE (n = 8 per group). *p < 0.05 and ***p < 0.001 versus sham group; # p < 0.05 versus angiotensin II group; NS, not significant.

Article Snippet: To evaluate the HDAC enzyme inhibitory activity of MS-275 and RGFP966, we determined enzyme activities of HDAC1, HDAC2, HDAC3, and HDAC8 using enzyme assay kits (BPS Bioscience, San Diego, CA, USA) according to the manufacturer’s protocols.

Techniques: Reverse Transcription Polymerase Chain Reaction, Quantitative RT-PCR

Journal: PLoS ONE

Article Title: Class I histone deacetylase inhibitor MS-275 attenuates vasoconstriction and inflammation in angiotensin II-induced hypertension

doi: 10.1371/journal.pone.0213186

Figure Lengend Snippet: The transcript levels of Nox1 (A), Nox2 (B), Nox4 (C), p22phox (D), p47phox (E), Cox-2 (F), and SOD3 (G) were determined using qRT-PCR in aortas of sham and Ang II-induced mice treated with vehicle, MS-275, or RGFP966. Results are ± SE (n = 8 per group). * p < 0.05 and ** p < 0.01 versus sham group; NS, not significant.

Article Snippet: To evaluate the HDAC enzyme inhibitory activity of MS-275 and RGFP966, we determined enzyme activities of HDAC1, HDAC2, HDAC3, and HDAC8 using enzyme assay kits (BPS Bioscience, San Diego, CA, USA) according to the manufacturer’s protocols.

Techniques: Quantitative RT-PCR

Journal: PLoS ONE

Article Title: Class I histone deacetylase inhibitor MS-275 attenuates vasoconstriction and inflammation in angiotensin II-induced hypertension

doi: 10.1371/journal.pone.0213186

Figure Lengend Snippet: The transcript levels of iNOS (A), TNF-α (B), IL-1β (C), MCP-1 (D), VCAM-1 (E), and ICAM-1 (F) were determined using quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) in aortas of sham and Ang II-induced mice treated with vehicle, MS-275, or RGFP966. Results are means ± SE (n = 8 per group). * p < 0.05, ** p < 0.01, and *** p < 0.001 versus sham group; # p < 0.05 and ## p < 0.01 versus angiotensin II group; NS, not significant. (G) Representative aortic images for macrophage infiltration are shown. Scale bar = 50 μm.

Article Snippet: To evaluate the HDAC enzyme inhibitory activity of MS-275 and RGFP966, we determined enzyme activities of HDAC1, HDAC2, HDAC3, and HDAC8 using enzyme assay kits (BPS Bioscience, San Diego, CA, USA) according to the manufacturer’s protocols.

Techniques: Reverse Transcription Polymerase Chain Reaction, Quantitative RT-PCR

Journal: International Journal of Molecular Sciences

Article Title: Chronic Cardiotoxicity Assays Using Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes (hiPSC-CMs)

doi: 10.3390/ijms23063199

Figure Lengend Snippet: Summary of drugs/compounds, dosage and timepoints tested on hiPSC-CMs along with key findings.

Article Snippet: This study subjected Cor.4U CMs from Axiogenesis to HDAC inhibitors, such as dacinostat, panobinostat, vorinostat, entinostat and tubastatin A in a chronic setting to follow the long-term effects of HDAC inhibitors on the beating properties of Cor.4U-CMs using an impedance-based functional assay.

Techniques: Histone Deacetylase Assay, Phospho-proteomics, Activation Assay, Functional Assay, Activity Assay, RNA Sequencing, Microscopy, Plasmid Preparation, Expressing, Inhibition, Chromatography, Mass Spectrometry, Gene Expression