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iCell Bioscience Inc primary endothelial cell culture medium
Expression of SENP1 in liver sinusoidal <t>endothelial</t> cells following H-R. (A and B) Western blotting analysis. (C) Reverse transcription-quantitative polymerase chain reaction analysis. Data were presented as the mean ± SD (n=3); ***P<0.001, ****P<0.0001 vs. the control (normoxic) group. H-R, hypoxia-reoxygenation; SENP1, Sentrin/SUMO-specific protease 1.
Primary Endothelial Cell Culture Medium, supplied by iCell Bioscience Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "SENP1 attenuates hypoxia‑reoxygenation injury in liver sinusoid endothelial cells by relying on the HIF‑1α signaling pathway"

Article Title: SENP1 attenuates hypoxia‑reoxygenation injury in liver sinusoid endothelial cells by relying on the HIF‑1α signaling pathway

Journal: Molecular Medicine Reports

doi: 10.3892/mmr.2024.13188

Expression of SENP1 in liver sinusoidal endothelial cells following H-R. (A and B) Western blotting analysis. (C) Reverse transcription-quantitative polymerase chain reaction analysis. Data were presented as the mean ± SD (n=3); ***P<0.001, ****P<0.0001 vs. the control (normoxic) group. H-R, hypoxia-reoxygenation; SENP1, Sentrin/SUMO-specific protease 1.
Figure Legend Snippet: Expression of SENP1 in liver sinusoidal endothelial cells following H-R. (A and B) Western blotting analysis. (C) Reverse transcription-quantitative polymerase chain reaction analysis. Data were presented as the mean ± SD (n=3); ***P<0.001, ****P<0.0001 vs. the control (normoxic) group. H-R, hypoxia-reoxygenation; SENP1, Sentrin/SUMO-specific protease 1.

Techniques Used: Expressing, Western Blot, Reverse Transcription, Real-time Polymerase Chain Reaction, Control

Effects of SENP1 expression downregulation and reactivation on the extent of fenestration damage and the reduction in the viability of H-R injured LSECs. (A) Representative scanning electron microscopy images showing fenestrae in each treatment group. (B) Scanning electron microscopy images showing the number of fenestrae in LSECs. (C) Cell Counting Kit-8 assay results. Data were presented as the mean ± SD (n=3); *P<0.05 vs. the control (normoxic) group; ****P<0.0001 vs. the H-R + si-NC group; ***P<0.001, ****P<0.0001 vs. the H-R + si-SENP1 group. H-R, hypoxia-reoxygenation; LSECs, liver sinusoidal endothelial cells; NC, negative control; SENP1, Sentrin/SUMO-specific protease 1; si(RNA), short interfering RNA.
Figure Legend Snippet: Effects of SENP1 expression downregulation and reactivation on the extent of fenestration damage and the reduction in the viability of H-R injured LSECs. (A) Representative scanning electron microscopy images showing fenestrae in each treatment group. (B) Scanning electron microscopy images showing the number of fenestrae in LSECs. (C) Cell Counting Kit-8 assay results. Data were presented as the mean ± SD (n=3); *P<0.05 vs. the control (normoxic) group; ****P<0.0001 vs. the H-R + si-NC group; ***P<0.001, ****P<0.0001 vs. the H-R + si-SENP1 group. H-R, hypoxia-reoxygenation; LSECs, liver sinusoidal endothelial cells; NC, negative control; SENP1, Sentrin/SUMO-specific protease 1; si(RNA), short interfering RNA.

Techniques Used: Expressing, Electron Microscopy, Cell Counting, Control, Negative Control, Small Interfering RNA

Effects of SENP1 expression downregulation and reactivation on the apoptosis rate of H-R injured liver sinusoidal endothelial cells. (A and B) Flow cytometry plots. (C) Apoptosis rates of the normoxic and H-R groups. Data were presented as the mean ± SD (n=3); # P<0.05 vs. the normoxic group; ****P<0.0001 vs. the si-NC group; ***P<0.001 and *P<0.05 vs. the rescue group. H-R, hypoxia-reoxygenation; NC, negative control; SENP1, Sentrin/SUMO-specific protease 1; si(RNA), short interfering RNA.
Figure Legend Snippet: Effects of SENP1 expression downregulation and reactivation on the apoptosis rate of H-R injured liver sinusoidal endothelial cells. (A and B) Flow cytometry plots. (C) Apoptosis rates of the normoxic and H-R groups. Data were presented as the mean ± SD (n=3); # P<0.05 vs. the normoxic group; ****P<0.0001 vs. the si-NC group; ***P<0.001 and *P<0.05 vs. the rescue group. H-R, hypoxia-reoxygenation; NC, negative control; SENP1, Sentrin/SUMO-specific protease 1; si(RNA), short interfering RNA.

Techniques Used: Expressing, Flow Cytometry, Negative Control, Small Interfering RNA

SENP1, HIF-1α, HO-1, cleaved-caspase-3, Bax and Bcl-2 protein expression levels in SENP1-knockdown H-R-injured liver sinusoidal endothelial cells. (A) Representative western blots and ratio of SENP1, HIF-1α vs. GAPDH expression determined from the western blot images in the normoxia group. (B) Representative western blots and ratio of SENP1, HIF-1α in the H-R group. (C) Representative western blots and ratio of Bax and cleaved-caspase-3 in the normoxia group. (D) Representative western blots and ratio of Bax and cleaved-caspase-3 in the H-R group. (E) Representative western blots and ratio of Bcl-2 and HO-1 in the normoxia group. (F) Representative western blots and ratio of Bcl-2 and HO-1 in the H-R group. Date were shown as the mean ± SD (n=3); *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 vs. the si-NC or si-SENP1 group. HIF-1α, hypoxia-inducible transcription factor-1α; HO-1, heme oxygenase; NC, negative control; SENP1, Sentrin/SUMO-specific protease 1; si(RNA), short interfering RNA; H-R, hypoxia-reoxygenation.
Figure Legend Snippet: SENP1, HIF-1α, HO-1, cleaved-caspase-3, Bax and Bcl-2 protein expression levels in SENP1-knockdown H-R-injured liver sinusoidal endothelial cells. (A) Representative western blots and ratio of SENP1, HIF-1α vs. GAPDH expression determined from the western blot images in the normoxia group. (B) Representative western blots and ratio of SENP1, HIF-1α in the H-R group. (C) Representative western blots and ratio of Bax and cleaved-caspase-3 in the normoxia group. (D) Representative western blots and ratio of Bax and cleaved-caspase-3 in the H-R group. (E) Representative western blots and ratio of Bcl-2 and HO-1 in the normoxia group. (F) Representative western blots and ratio of Bcl-2 and HO-1 in the H-R group. Date were shown as the mean ± SD (n=3); *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 vs. the si-NC or si-SENP1 group. HIF-1α, hypoxia-inducible transcription factor-1α; HO-1, heme oxygenase; NC, negative control; SENP1, Sentrin/SUMO-specific protease 1; si(RNA), short interfering RNA; H-R, hypoxia-reoxygenation.

Techniques Used: Expressing, Knockdown, Western Blot, Negative Control, Small Interfering RNA

VEGF, IL-6 and TNF-α protein levels in SENP1-knockdown hypoxia-reoxygenation-injured LSECs. (A) ELISA of VEGF expression in all LSEC groups. (B and C) ELISAs of IL-6 and TNF-α expression in all LSEC groups. Data were presented as the mean ± SD (n=5); **P<0.01, ***P<0.001, ****P<0.0001 vs. the si-NC or si-SENP1 groups; ## P<0.01, ### P<0.001 vs. the normoxic group. ELISA, enzyme-linked immunosorbent assay; LSECs, liver sinusoidal endothelial cells; NC, negative control; VEGF, vascular endothelial growth factor; SENP1, Sentrin/SUMO-specific protease 1; si(RNA), short interfering RNA.
Figure Legend Snippet: VEGF, IL-6 and TNF-α protein levels in SENP1-knockdown hypoxia-reoxygenation-injured LSECs. (A) ELISA of VEGF expression in all LSEC groups. (B and C) ELISAs of IL-6 and TNF-α expression in all LSEC groups. Data were presented as the mean ± SD (n=5); **P<0.01, ***P<0.001, ****P<0.0001 vs. the si-NC or si-SENP1 groups; ## P<0.01, ### P<0.001 vs. the normoxic group. ELISA, enzyme-linked immunosorbent assay; LSECs, liver sinusoidal endothelial cells; NC, negative control; VEGF, vascular endothelial growth factor; SENP1, Sentrin/SUMO-specific protease 1; si(RNA), short interfering RNA.

Techniques Used: Knockdown, Enzyme-linked Immunosorbent Assay, Expressing, Negative Control, Small Interfering RNA



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Effects of anlotinib and SAR131675 on the structure and function of tumor blood vessels, tumor stroma and IFP. a – e During the time and dosing window of anlotinib used in this experiment, tumor vessel normalization did not occur. Immunohistochemistry staining for endothelial cells (CD31, brown) (Scale bar, 100 μm), immunofluorescence staining for endothelial cells (CD31, red) and pericytes (NG2, green) (Scale bar, 80 μm), fluorescence images of Dylight @ 488-lectin-perfused (green) tumor blood vessels (CD31, red) (Scale bar, 40 μm), and representative images of HIF-1α (brown) immunohistochemical staining (Scale bar, 40 μm) in 4T1 tumor sections from mice treated with saline or anlotinib are shown in ( a ). Quantitative analysis of tumor vascular density ( b ), pericyte coverage ( c ; NG2 + CD31 + area percentage of the total CD31 + area), perfused vessels ( d ; lectin + CD31 + area percentage of the total CD31 + area), and HIF-1α area ( e ) as shown in ( a ) ( n = 9 or n = 12; images were from three mice per group). f – h SAR131675 did not influence the density and function of tumor blood vessels. Immunohistochemistry staining for endothelial cells (CD31, brown) and HIF-1α (brown) in 4T1 tumor sections from mice treated with saline or SAR131675 are shown in ( f ). Scale bar, 100 μm in the upper panels and 20 μm in the lower panels. Quantification of tumor vascular density ( g ) and HIF-1α area ( h ) as shown in ( f ) ( n = 9; images were from three mice per group). i – k Anlotinib and SAR131675 did not modulate tumor stroma. Histological studies with trichrome staining of collagen and immunohistochemical staining of fibronectin in tumor ( i ). Scale bar, 50 μm. Quantitative analysis of collagen ( j ) and fibronectin ( k ) ( n = 9; images were from three mice per group). l Tumor IFP of tumor-bearing mice treated with saline, anlotinib, or SAR131675 for 10 consecutive days ( n = 9). The data are shown as the mean ± s.d. ns no significance, *** p < 0.001

Journal: Signal Transduction and Targeted Therapy

Article Title: Anti-lymphangiogenesis for boosting drug accumulation in tumors

doi: 10.1038/s41392-024-01794-4

Figure Lengend Snippet: Effects of anlotinib and SAR131675 on the structure and function of tumor blood vessels, tumor stroma and IFP. a – e During the time and dosing window of anlotinib used in this experiment, tumor vessel normalization did not occur. Immunohistochemistry staining for endothelial cells (CD31, brown) (Scale bar, 100 μm), immunofluorescence staining for endothelial cells (CD31, red) and pericytes (NG2, green) (Scale bar, 80 μm), fluorescence images of Dylight @ 488-lectin-perfused (green) tumor blood vessels (CD31, red) (Scale bar, 40 μm), and representative images of HIF-1α (brown) immunohistochemical staining (Scale bar, 40 μm) in 4T1 tumor sections from mice treated with saline or anlotinib are shown in ( a ). Quantitative analysis of tumor vascular density ( b ), pericyte coverage ( c ; NG2 + CD31 + area percentage of the total CD31 + area), perfused vessels ( d ; lectin + CD31 + area percentage of the total CD31 + area), and HIF-1α area ( e ) as shown in ( a ) ( n = 9 or n = 12; images were from three mice per group). f – h SAR131675 did not influence the density and function of tumor blood vessels. Immunohistochemistry staining for endothelial cells (CD31, brown) and HIF-1α (brown) in 4T1 tumor sections from mice treated with saline or SAR131675 are shown in ( f ). Scale bar, 100 μm in the upper panels and 20 μm in the lower panels. Quantification of tumor vascular density ( g ) and HIF-1α area ( h ) as shown in ( f ) ( n = 9; images were from three mice per group). i – k Anlotinib and SAR131675 did not modulate tumor stroma. Histological studies with trichrome staining of collagen and immunohistochemical staining of fibronectin in tumor ( i ). Scale bar, 50 μm. Quantitative analysis of collagen ( j ) and fibronectin ( k ) ( n = 9; images were from three mice per group). l Tumor IFP of tumor-bearing mice treated with saline, anlotinib, or SAR131675 for 10 consecutive days ( n = 9). The data are shown as the mean ± s.d. ns no significance, *** p < 0.001

Article Snippet: CT26 and 4T1 cell lines were cultured in RPMI 1640 supplemented with 10% FBS, penicillin (100 units ml −1 ), and streptomycin (100 μg ml −1 ) at 37 °C in a humidified incubator with 5% CO 2 . hLECs was cultured in primary endothelial cell culture medium purchased from ScienCell (USA).

Techniques: Immunohistochemistry, Staining, Immunofluorescence, Fluorescence, Immunohistochemical staining, Saline

Expression of SENP1 in liver sinusoidal endothelial cells following H-R. (A and B) Western blotting analysis. (C) Reverse transcription-quantitative polymerase chain reaction analysis. Data were presented as the mean ± SD (n=3); ***P<0.001, ****P<0.0001 vs. the control (normoxic) group. H-R, hypoxia-reoxygenation; SENP1, Sentrin/SUMO-specific protease 1.

Journal: Molecular Medicine Reports

Article Title: SENP1 attenuates hypoxia‑reoxygenation injury in liver sinusoid endothelial cells by relying on the HIF‑1α signaling pathway

doi: 10.3892/mmr.2024.13188

Figure Lengend Snippet: Expression of SENP1 in liver sinusoidal endothelial cells following H-R. (A and B) Western blotting analysis. (C) Reverse transcription-quantitative polymerase chain reaction analysis. Data were presented as the mean ± SD (n=3); ***P<0.001, ****P<0.0001 vs. the control (normoxic) group. H-R, hypoxia-reoxygenation; SENP1, Sentrin/SUMO-specific protease 1.

Article Snippet: This company obtained LSECs from male C57BL/6 mice by digesting dissected liver tissue with elastase and collagenase and then culturing the cells at 37°C with 5% CO 2 in primary endothelial cell culture medium (iCell Bioscience, Inc.).

Techniques: Expressing, Western Blot, Reverse Transcription, Real-time Polymerase Chain Reaction, Control

Effects of SENP1 expression downregulation and reactivation on the extent of fenestration damage and the reduction in the viability of H-R injured LSECs. (A) Representative scanning electron microscopy images showing fenestrae in each treatment group. (B) Scanning electron microscopy images showing the number of fenestrae in LSECs. (C) Cell Counting Kit-8 assay results. Data were presented as the mean ± SD (n=3); *P<0.05 vs. the control (normoxic) group; ****P<0.0001 vs. the H-R + si-NC group; ***P<0.001, ****P<0.0001 vs. the H-R + si-SENP1 group. H-R, hypoxia-reoxygenation; LSECs, liver sinusoidal endothelial cells; NC, negative control; SENP1, Sentrin/SUMO-specific protease 1; si(RNA), short interfering RNA.

Journal: Molecular Medicine Reports

Article Title: SENP1 attenuates hypoxia‑reoxygenation injury in liver sinusoid endothelial cells by relying on the HIF‑1α signaling pathway

doi: 10.3892/mmr.2024.13188

Figure Lengend Snippet: Effects of SENP1 expression downregulation and reactivation on the extent of fenestration damage and the reduction in the viability of H-R injured LSECs. (A) Representative scanning electron microscopy images showing fenestrae in each treatment group. (B) Scanning electron microscopy images showing the number of fenestrae in LSECs. (C) Cell Counting Kit-8 assay results. Data were presented as the mean ± SD (n=3); *P<0.05 vs. the control (normoxic) group; ****P<0.0001 vs. the H-R + si-NC group; ***P<0.001, ****P<0.0001 vs. the H-R + si-SENP1 group. H-R, hypoxia-reoxygenation; LSECs, liver sinusoidal endothelial cells; NC, negative control; SENP1, Sentrin/SUMO-specific protease 1; si(RNA), short interfering RNA.

Article Snippet: This company obtained LSECs from male C57BL/6 mice by digesting dissected liver tissue with elastase and collagenase and then culturing the cells at 37°C with 5% CO 2 in primary endothelial cell culture medium (iCell Bioscience, Inc.).

Techniques: Expressing, Electron Microscopy, Cell Counting, Control, Negative Control, Small Interfering RNA

Effects of SENP1 expression downregulation and reactivation on the apoptosis rate of H-R injured liver sinusoidal endothelial cells. (A and B) Flow cytometry plots. (C) Apoptosis rates of the normoxic and H-R groups. Data were presented as the mean ± SD (n=3); # P<0.05 vs. the normoxic group; ****P<0.0001 vs. the si-NC group; ***P<0.001 and *P<0.05 vs. the rescue group. H-R, hypoxia-reoxygenation; NC, negative control; SENP1, Sentrin/SUMO-specific protease 1; si(RNA), short interfering RNA.

Journal: Molecular Medicine Reports

Article Title: SENP1 attenuates hypoxia‑reoxygenation injury in liver sinusoid endothelial cells by relying on the HIF‑1α signaling pathway

doi: 10.3892/mmr.2024.13188

Figure Lengend Snippet: Effects of SENP1 expression downregulation and reactivation on the apoptosis rate of H-R injured liver sinusoidal endothelial cells. (A and B) Flow cytometry plots. (C) Apoptosis rates of the normoxic and H-R groups. Data were presented as the mean ± SD (n=3); # P<0.05 vs. the normoxic group; ****P<0.0001 vs. the si-NC group; ***P<0.001 and *P<0.05 vs. the rescue group. H-R, hypoxia-reoxygenation; NC, negative control; SENP1, Sentrin/SUMO-specific protease 1; si(RNA), short interfering RNA.

Article Snippet: This company obtained LSECs from male C57BL/6 mice by digesting dissected liver tissue with elastase and collagenase and then culturing the cells at 37°C with 5% CO 2 in primary endothelial cell culture medium (iCell Bioscience, Inc.).

Techniques: Expressing, Flow Cytometry, Negative Control, Small Interfering RNA

SENP1, HIF-1α, HO-1, cleaved-caspase-3, Bax and Bcl-2 protein expression levels in SENP1-knockdown H-R-injured liver sinusoidal endothelial cells. (A) Representative western blots and ratio of SENP1, HIF-1α vs. GAPDH expression determined from the western blot images in the normoxia group. (B) Representative western blots and ratio of SENP1, HIF-1α in the H-R group. (C) Representative western blots and ratio of Bax and cleaved-caspase-3 in the normoxia group. (D) Representative western blots and ratio of Bax and cleaved-caspase-3 in the H-R group. (E) Representative western blots and ratio of Bcl-2 and HO-1 in the normoxia group. (F) Representative western blots and ratio of Bcl-2 and HO-1 in the H-R group. Date were shown as the mean ± SD (n=3); *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 vs. the si-NC or si-SENP1 group. HIF-1α, hypoxia-inducible transcription factor-1α; HO-1, heme oxygenase; NC, negative control; SENP1, Sentrin/SUMO-specific protease 1; si(RNA), short interfering RNA; H-R, hypoxia-reoxygenation.

Journal: Molecular Medicine Reports

Article Title: SENP1 attenuates hypoxia‑reoxygenation injury in liver sinusoid endothelial cells by relying on the HIF‑1α signaling pathway

doi: 10.3892/mmr.2024.13188

Figure Lengend Snippet: SENP1, HIF-1α, HO-1, cleaved-caspase-3, Bax and Bcl-2 protein expression levels in SENP1-knockdown H-R-injured liver sinusoidal endothelial cells. (A) Representative western blots and ratio of SENP1, HIF-1α vs. GAPDH expression determined from the western blot images in the normoxia group. (B) Representative western blots and ratio of SENP1, HIF-1α in the H-R group. (C) Representative western blots and ratio of Bax and cleaved-caspase-3 in the normoxia group. (D) Representative western blots and ratio of Bax and cleaved-caspase-3 in the H-R group. (E) Representative western blots and ratio of Bcl-2 and HO-1 in the normoxia group. (F) Representative western blots and ratio of Bcl-2 and HO-1 in the H-R group. Date were shown as the mean ± SD (n=3); *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 vs. the si-NC or si-SENP1 group. HIF-1α, hypoxia-inducible transcription factor-1α; HO-1, heme oxygenase; NC, negative control; SENP1, Sentrin/SUMO-specific protease 1; si(RNA), short interfering RNA; H-R, hypoxia-reoxygenation.

Article Snippet: This company obtained LSECs from male C57BL/6 mice by digesting dissected liver tissue with elastase and collagenase and then culturing the cells at 37°C with 5% CO 2 in primary endothelial cell culture medium (iCell Bioscience, Inc.).

Techniques: Expressing, Knockdown, Western Blot, Negative Control, Small Interfering RNA

VEGF, IL-6 and TNF-α protein levels in SENP1-knockdown hypoxia-reoxygenation-injured LSECs. (A) ELISA of VEGF expression in all LSEC groups. (B and C) ELISAs of IL-6 and TNF-α expression in all LSEC groups. Data were presented as the mean ± SD (n=5); **P<0.01, ***P<0.001, ****P<0.0001 vs. the si-NC or si-SENP1 groups; ## P<0.01, ### P<0.001 vs. the normoxic group. ELISA, enzyme-linked immunosorbent assay; LSECs, liver sinusoidal endothelial cells; NC, negative control; VEGF, vascular endothelial growth factor; SENP1, Sentrin/SUMO-specific protease 1; si(RNA), short interfering RNA.

Journal: Molecular Medicine Reports

Article Title: SENP1 attenuates hypoxia‑reoxygenation injury in liver sinusoid endothelial cells by relying on the HIF‑1α signaling pathway

doi: 10.3892/mmr.2024.13188

Figure Lengend Snippet: VEGF, IL-6 and TNF-α protein levels in SENP1-knockdown hypoxia-reoxygenation-injured LSECs. (A) ELISA of VEGF expression in all LSEC groups. (B and C) ELISAs of IL-6 and TNF-α expression in all LSEC groups. Data were presented as the mean ± SD (n=5); **P<0.01, ***P<0.001, ****P<0.0001 vs. the si-NC or si-SENP1 groups; ## P<0.01, ### P<0.001 vs. the normoxic group. ELISA, enzyme-linked immunosorbent assay; LSECs, liver sinusoidal endothelial cells; NC, negative control; VEGF, vascular endothelial growth factor; SENP1, Sentrin/SUMO-specific protease 1; si(RNA), short interfering RNA.

Article Snippet: This company obtained LSECs from male C57BL/6 mice by digesting dissected liver tissue with elastase and collagenase and then culturing the cells at 37°C with 5% CO 2 in primary endothelial cell culture medium (iCell Bioscience, Inc.).

Techniques: Knockdown, Enzyme-linked Immunosorbent Assay, Expressing, Negative Control, Small Interfering RNA

TTR inhibits H 2 O 2 -induced endothelial cell injury in rat pulmonary arteries. ( A ) control group; ( B ) H 2 O 2 group; ( C ) TTR 20 µg; ( D ) TTR 40 µg; ( E ) TTR 80 µg; ( F ) results of the apoptosis analysis of PAECs

Journal: BMC Complementary Medicine and Therapies

Article Title: Protective effects of the Terminalia bellirica tannin-induced Nrf2/HO-1 signaling pathway in rats with high-altitude pulmonary hypertension

doi: 10.1186/s12906-023-03981-2

Figure Lengend Snippet: TTR inhibits H 2 O 2 -induced endothelial cell injury in rat pulmonary arteries. ( A ) control group; ( B ) H 2 O 2 group; ( C ) TTR 20 µg; ( D ) TTR 40 µg; ( E ) TTR 80 µg; ( F ) results of the apoptosis analysis of PAECs

Article Snippet: Primary endothelial cell basal culture medium, cell growth factor, and penicillin‒streptomycin double antibiotic were obtained from iCell Bioscience Inc. Pancreatin (0.25%) was purchased from HyClone, USA.

Techniques: Control