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Proteintech plau
Plau, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 46 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/plau/pm41687403-54-6-19?v=Proteintech
Average 94 stars, based on 46 article reviews

plau - by Bioz Stars, 2026-07

94/100 stars

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Image Search Results

Identification and annotation analysis of hub differentially expressed genes in baicalein-treated KTC-1 cells. (A) Protein-protein interaction network of hub differentially expressed genes all BA-treated groups (50, 100, 150 μM) versus the control group. (B) Hierarchical clustering of hub differentially expressed genes using the RobustRankAggreg method. (C) Boxplot illustrates the significant differences in PLAU and F3 mRNA levels between thyroid carcinoma and matched normal thyroid samples. (D) Boxplot showing the mRNA levels of EGR1, CCN2, TRIB3, H2AC6, and VCAM1 in thyroid carcinoma compared to matched normal thyroid samples, with no significant differences observed. (E) PLAU expression correlates with tumor stage, but it is not linked to overall survival and disease-free survival. (F) F3 expression correlates with tumor stage, overall survival, and disease-free survival. (G) Immunohistochemical analysis of PLAU expression in papillary thyroid carcinoma versus normal thyroid tissues from the HPA database. * p < 0.05.

Journal: Frontiers in Endocrinology

Article Title: Baicalein inhibits the progression of thyroid cancer by suppressing the TPL2/MEK2/ERK2 pathway

doi: 10.3389/fendo.2026.1739944

Figure Lengend Snippet: Identification and annotation analysis of hub differentially expressed genes in baicalein-treated KTC-1 cells. (A) Protein-protein interaction network of hub differentially expressed genes all BA-treated groups (50, 100, 150 μM) versus the control group. (B) Hierarchical clustering of hub differentially expressed genes using the RobustRankAggreg method. (C) Boxplot illustrates the significant differences in PLAU and F3 mRNA levels between thyroid carcinoma and matched normal thyroid samples. (D) Boxplot showing the mRNA levels of EGR1, CCN2, TRIB3, H2AC6, and VCAM1 in thyroid carcinoma compared to matched normal thyroid samples, with no significant differences observed. (E) PLAU expression correlates with tumor stage, but it is not linked to overall survival and disease-free survival. (F) F3 expression correlates with tumor stage, overall survival, and disease-free survival. (G) Immunohistochemical analysis of PLAU expression in papillary thyroid carcinoma versus normal thyroid tissues from the HPA database. * p < 0.05.

Article Snippet: BC-11 hydrobromide, a PLAU inhibitor (PLAUi), was obtained from Tocris, Biotechnology (Bristol, UK).

Techniques: Control, Expressing, Immunohistochemical staining

PLAU facilitates baicalein-induced suppression in KTC-1 cells. (A) Molecular docking was employed to simulate the interaction between baicalein and PLAU. (B) Serum levels of urokinase-type plasminogen activator and Plau mRNA expression in cancerous tissues from patients with papillary thyroid carcinoma comparing those without metastasis to those with metastasis or BRAF mutation. (C) Levels of urokinase-type plasminogen activator in the supernatant of the culture medium. (D) Plau mRNA expression in KTC-1 cells. (E) Densitometric quantification of the PLAU/GAPDH protein ratio. (F) Immunofluorescent staining and quantitative analysis of PLAU expression in KTC-1 cells. Scale bar, 20 μm. (G) Representative transmission electron microscope images of KTC-1 cells. Scale bar, 5.0 μm, 1.0 μm, or 0.5 μm. (H) Representative scanning electron microscope images of KTC-1 cells. Scale bar, 50 μm, 10 μm, or 5 μm. Ctrl, control group with DMSO; BA, baicalein 100 μM; PLAUi, PLAU inhibitor (BC-11 hydrobromide); BA+PLAUi, combined treatment of baicalein 100 μM and PLAU inhibitor (BC-11 hydrobromide). All data are presented as mean ± S.E.M and analyzed by a one-way ANOVA with Turkey t test. All images is representative of three experiments. ns, not statistically; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Journal: Frontiers in Endocrinology

Article Title: Baicalein inhibits the progression of thyroid cancer by suppressing the TPL2/MEK2/ERK2 pathway

doi: 10.3389/fendo.2026.1739944

Figure Lengend Snippet: PLAU facilitates baicalein-induced suppression in KTC-1 cells. (A) Molecular docking was employed to simulate the interaction between baicalein and PLAU. (B) Serum levels of urokinase-type plasminogen activator and Plau mRNA expression in cancerous tissues from patients with papillary thyroid carcinoma comparing those without metastasis to those with metastasis or BRAF mutation. (C) Levels of urokinase-type plasminogen activator in the supernatant of the culture medium. (D) Plau mRNA expression in KTC-1 cells. (E) Densitometric quantification of the PLAU/GAPDH protein ratio. (F) Immunofluorescent staining and quantitative analysis of PLAU expression in KTC-1 cells. Scale bar, 20 μm. (G) Representative transmission electron microscope images of KTC-1 cells. Scale bar, 5.0 μm, 1.0 μm, or 0.5 μm. (H) Representative scanning electron microscope images of KTC-1 cells. Scale bar, 50 μm, 10 μm, or 5 μm. Ctrl, control group with DMSO; BA, baicalein 100 μM; PLAUi, PLAU inhibitor (BC-11 hydrobromide); BA+PLAUi, combined treatment of baicalein 100 μM and PLAU inhibitor (BC-11 hydrobromide). All data are presented as mean ± S.E.M and analyzed by a one-way ANOVA with Turkey t test. All images is representative of three experiments. ns, not statistically; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Article Snippet: BC-11 hydrobromide, a PLAU inhibitor (PLAUi), was obtained from Tocris, Biotechnology (Bristol, UK).

Techniques: Expressing, Mutagenesis, Staining, Transmission Assay, Microscopy, Control

PLAU is associated with the suppression of biological behavior and the reprogramming of Golgi apparatus in KTC-1 cells by baicalein. (A) Immunofluorescent staining and quantitative analysis of apoptotic KTC-1 cells. Scale bar, 20 μm. (B) Cellular apoptosis was assessed using flow cytometry analyses. (C) Cell migration was assessed via cell scratch assays. Scale bar, 200 μm. (D) Cell viability was determined using a cell counting kit-8. (E) Immunofluorescent staining and quantitative analysis the of Golgi apparatus in KTC-1 cells. Scale bar, 20 μm. Ctrl, control group with DMSO; BA, baicalein 100 μM; PLAUi, PLAU inhibitor (BC-11 hydrobromide); BA+PLAUi, combined treatment of baicalein 100 μM and PLAU inhibitor (BC-11 hydrobromide). All data are presented as mean ± S.E.M and analyzed by a one-way ANOVA with Turkey t test. All images is representative of three experiments. ns, not statistically; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Journal: Frontiers in Endocrinology

Article Title: Baicalein inhibits the progression of thyroid cancer by suppressing the TPL2/MEK2/ERK2 pathway

doi: 10.3389/fendo.2026.1739944

Figure Lengend Snippet: PLAU is associated with the suppression of biological behavior and the reprogramming of Golgi apparatus in KTC-1 cells by baicalein. (A) Immunofluorescent staining and quantitative analysis of apoptotic KTC-1 cells. Scale bar, 20 μm. (B) Cellular apoptosis was assessed using flow cytometry analyses. (C) Cell migration was assessed via cell scratch assays. Scale bar, 200 μm. (D) Cell viability was determined using a cell counting kit-8. (E) Immunofluorescent staining and quantitative analysis the of Golgi apparatus in KTC-1 cells. Scale bar, 20 μm. Ctrl, control group with DMSO; BA, baicalein 100 μM; PLAUi, PLAU inhibitor (BC-11 hydrobromide); BA+PLAUi, combined treatment of baicalein 100 μM and PLAU inhibitor (BC-11 hydrobromide). All data are presented as mean ± S.E.M and analyzed by a one-way ANOVA with Turkey t test. All images is representative of three experiments. ns, not statistically; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Article Snippet: BC-11 hydrobromide, a PLAU inhibitor (PLAUi), was obtained from Tocris, Biotechnology (Bristol, UK).

Techniques: Staining, Flow Cytometry, Migration, Cell Counting, Control

Inhibition of PLAU enhances the suppression of the MAPK pathway and Golgi apparatus reprogramming by baicalein in KTC-1 cells. (A) Molecular docking was employed to simulate the interaction between baicalein and key proteins such as ERK2, MEK2, TPL2, and ARF1. (B) qRT-PCR analysis was conducted to assess the expression levels of Erk1 , Erk2 , Mek1 , Mek2 , TPL2 , and Nis mRNA expression in cancer tissues from patients with papillary thyroid carcinoma, comparing those without metastasis to those with metastasis or BRAF mutation. (C) qRT-PCR analysis of the mRNA expression of Erk1 , Erk2 , Mek1 , Mek2 , Tpl2 , Nis, Arf1, and Paqr11 in KTC-1 cells. (D) Relative protein expression of ERK1, ERK2, MEK1, MEK2, and TPL2. Ctrl, control group with DMSO; BA, baicalein 100 μM; PLAUi, PLAU inhibitor (BC-11 hydrobromide); BA+PLAUi, combined treatment of baicalein 100 μM and PLAU inhibitor (BC-11 hydrobromide). All data are presented as mean ± S.E.M and analyzed by a one-way ANOVA with Turkey t test. All images is representative of three experiments. ns, not statistically; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Journal: Frontiers in Endocrinology

Article Title: Baicalein inhibits the progression of thyroid cancer by suppressing the TPL2/MEK2/ERK2 pathway

doi: 10.3389/fendo.2026.1739944

Figure Lengend Snippet: Inhibition of PLAU enhances the suppression of the MAPK pathway and Golgi apparatus reprogramming by baicalein in KTC-1 cells. (A) Molecular docking was employed to simulate the interaction between baicalein and key proteins such as ERK2, MEK2, TPL2, and ARF1. (B) qRT-PCR analysis was conducted to assess the expression levels of Erk1 , Erk2 , Mek1 , Mek2 , TPL2 , and Nis mRNA expression in cancer tissues from patients with papillary thyroid carcinoma, comparing those without metastasis to those with metastasis or BRAF mutation. (C) qRT-PCR analysis of the mRNA expression of Erk1 , Erk2 , Mek1 , Mek2 , Tpl2 , Nis, Arf1, and Paqr11 in KTC-1 cells. (D) Relative protein expression of ERK1, ERK2, MEK1, MEK2, and TPL2. Ctrl, control group with DMSO; BA, baicalein 100 μM; PLAUi, PLAU inhibitor (BC-11 hydrobromide); BA+PLAUi, combined treatment of baicalein 100 μM and PLAU inhibitor (BC-11 hydrobromide). All data are presented as mean ± S.E.M and analyzed by a one-way ANOVA with Turkey t test. All images is representative of three experiments. ns, not statistically; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Article Snippet: BC-11 hydrobromide, a PLAU inhibitor (PLAUi), was obtained from Tocris, Biotechnology (Bristol, UK).

Techniques: Inhibition, Quantitative RT-PCR, Expressing, Mutagenesis, Control

Inhibition of PLAU enhances the tumor growth suppression effect of baicalein in a thyroid cancer xenograft mouse model. (A) Treatment with baicalein resulted in a reduction in tumor size after 28 days ( n = 5). (B) The combination of baicalein and PLAU inhibitor significantly decreased tumor weight. (C) The combination of baicalein and PLAU inhibitor significantly decreased tumor volumes. (D) Body weight fluctuations were tracked in all experimental groups over the study period. (E) Representative images of hematoxylin and eosin stain in the transplanted tumor tissues. (F) qRT-PCR analysis of the mRNA expression of Plau, Erk1, Erk2, Mek1, Mek2, Tpl2, and Nis in the transplanted tumor tissues. (G) Relative protein expression of PLAU, ERK1, ERK2, MEK1, MEK2, and TPL2 in the transplanted tumor tissues. Ctrl, control group with DMSO; BA, baicalein 100 μM; BA+PLAUi, combined treatment of baicalein 100 μM and PLAU inhibitor (BC-11 hydrobromide). For (A) , data are presented as Median with interquartile range and analyzed by a Brown-Forsythe and Welch ANOVA test with Dunnett T3 multiple comparison test. For (C, D) , data are presented as mean ± S.E.M and analyzed by a two way ANOVA test. For (F, G) , data are presented as mean ± S.E.M and analyzed by a one-way ANOVA with Turkey t test. All images is representative of three experiments. ns, not statistically; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Journal: Frontiers in Endocrinology

Article Title: Baicalein inhibits the progression of thyroid cancer by suppressing the TPL2/MEK2/ERK2 pathway

doi: 10.3389/fendo.2026.1739944

Figure Lengend Snippet: Inhibition of PLAU enhances the tumor growth suppression effect of baicalein in a thyroid cancer xenograft mouse model. (A) Treatment with baicalein resulted in a reduction in tumor size after 28 days ( n = 5). (B) The combination of baicalein and PLAU inhibitor significantly decreased tumor weight. (C) The combination of baicalein and PLAU inhibitor significantly decreased tumor volumes. (D) Body weight fluctuations were tracked in all experimental groups over the study period. (E) Representative images of hematoxylin and eosin stain in the transplanted tumor tissues. (F) qRT-PCR analysis of the mRNA expression of Plau, Erk1, Erk2, Mek1, Mek2, Tpl2, and Nis in the transplanted tumor tissues. (G) Relative protein expression of PLAU, ERK1, ERK2, MEK1, MEK2, and TPL2 in the transplanted tumor tissues. Ctrl, control group with DMSO; BA, baicalein 100 μM; BA+PLAUi, combined treatment of baicalein 100 μM and PLAU inhibitor (BC-11 hydrobromide). For (A) , data are presented as Median with interquartile range and analyzed by a Brown-Forsythe and Welch ANOVA test with Dunnett T3 multiple comparison test. For (C, D) , data are presented as mean ± S.E.M and analyzed by a two way ANOVA test. For (F, G) , data are presented as mean ± S.E.M and analyzed by a one-way ANOVA with Turkey t test. All images is representative of three experiments. ns, not statistically; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Article Snippet: BC-11 hydrobromide, a PLAU inhibitor (PLAUi), was obtained from Tocris, Biotechnology (Bristol, UK).

Techniques: Inhibition, H&E Stain, Quantitative RT-PCR, Expressing, Control, Comparison

(A) Pearson correlation between body mass index (BMI) and uPA levels in human adipose tissues. N=12. (B) The relative uPA levels in the adipose tissues of patients before and 2 years after bariatric surgery. Data was analyzed by paired t-test. N=5. (C) SDS-PAGE zymography gels and (D) quantification of uPA activity within eWAT of Plau WT/WT mice fed LFD or HFD for 0, 14 or 20 weeks. N=3–9. (E) Level of Plau (uPA) mRNA expression within eWAT of Plau WT/WT mice fed LFD or HFD for 0, 14 or 20 weeks. N=3–9. Data are expressed as mean±SEM and analyzed by one-way ANOVA and Fisher’s LSD test (D, E). tPA: tissue plasminogen activator.

Journal: Arteriosclerosis, thrombosis, and vascular biology

Article Title: Urokinase plasminogen activator deficiency delays the development of obesity and metabolic sequelae

doi: 10.1161/ATVBAHA.125.324017

Figure Lengend Snippet: (A) Pearson correlation between body mass index (BMI) and uPA levels in human adipose tissues. N=12. (B) The relative uPA levels in the adipose tissues of patients before and 2 years after bariatric surgery. Data was analyzed by paired t-test. N=5. (C) SDS-PAGE zymography gels and (D) quantification of uPA activity within eWAT of Plau WT/WT mice fed LFD or HFD for 0, 14 or 20 weeks. N=3–9. (E) Level of Plau (uPA) mRNA expression within eWAT of Plau WT/WT mice fed LFD or HFD for 0, 14 or 20 weeks. N=3–9. Data are expressed as mean±SEM and analyzed by one-way ANOVA and Fisher’s LSD test (D, E). tPA: tissue plasminogen activator.

Article Snippet: The mRNA levels of Plau (Mm00447054_m1), Adgre1 ( Mm00802529_m1 ), Tnfa (Mm00443258_m1) , Pparg (Mm00440940_m1) , Cd36 (Mm00432403_m1), Cidea (Mm00432554_m1), Il6 (Mm00446190_m1), Il1b (Mm00434228_m1) and F3 (Mm00438855_m1) were determined using TaqMan gene expression assays (Applied Biosystems) on an ABI StepOne Plus or a QuantStudio3 sequence detection system (Applied Biosystems).

Techniques: SDS Page, Zymography, Activity Assay, Expressing

(A) Mean body weight over time of Plau WT/WT and Plau KO/KO mice for 14 weeks. N=4–9. (B) Distribution of body weight, (C) total eWAT mass and (D) eWAT adipocyte area of Plau WT/WT and Plau KO/KO mice after 14 weeks on diet. N=4–9. (E) Representative F4/80-stained sections of eWAT isolated from Plau WT/WT and Plau KO/KO mice and (F) quantification of the % area positive for F4/80 after 14 weeks on diet. Arrows indicate crown-like structures. N=4–9. Levels of mRNA encoding (G) Adgre1 and (H) Tnfa in eWAT of Plau WT/WT and Plau KO/KO mice after 14 weeks on diet. N=4–9 (I) Mean body weight over time of Plau WT/WT and Plau KO/KO mice for 20 weeks. N=3–8. (J) Distribution of body weight, (K) total eWAT mass and (L) eWAT adipocyte area of Plau WT/WT and Plau KO/KO mice after 20 weeks on diet. N=3–8. (M) Representative F4/80-stained sections of eWAT isolated from Plau WT/WT and Plau KO/KO mice and (N) quantification of the % area positive for F4/80 after 20 weeks on diet. Arrows indicate crown-like structures. N=3–8. Levels of mRNA encoding (O) Adgre1 and (P) Tnfa in eWAT of Plau WT/WT and Plau KO/KO mice after 20 weeks on diet. N=3–8. Data are expressed as mean±SEM and analyzed by two-way ANOVA and Fisher’s LSD test (B-D, F-H, J-L, N-P).

Journal: Arteriosclerosis, thrombosis, and vascular biology

Article Title: Urokinase plasminogen activator deficiency delays the development of obesity and metabolic sequelae

doi: 10.1161/ATVBAHA.125.324017

Figure Lengend Snippet: (A) Mean body weight over time of Plau WT/WT and Plau KO/KO mice for 14 weeks. N=4–9. (B) Distribution of body weight, (C) total eWAT mass and (D) eWAT adipocyte area of Plau WT/WT and Plau KO/KO mice after 14 weeks on diet. N=4–9. (E) Representative F4/80-stained sections of eWAT isolated from Plau WT/WT and Plau KO/KO mice and (F) quantification of the % area positive for F4/80 after 14 weeks on diet. Arrows indicate crown-like structures. N=4–9. Levels of mRNA encoding (G) Adgre1 and (H) Tnfa in eWAT of Plau WT/WT and Plau KO/KO mice after 14 weeks on diet. N=4–9 (I) Mean body weight over time of Plau WT/WT and Plau KO/KO mice for 20 weeks. N=3–8. (J) Distribution of body weight, (K) total eWAT mass and (L) eWAT adipocyte area of Plau WT/WT and Plau KO/KO mice after 20 weeks on diet. N=3–8. (M) Representative F4/80-stained sections of eWAT isolated from Plau WT/WT and Plau KO/KO mice and (N) quantification of the % area positive for F4/80 after 20 weeks on diet. Arrows indicate crown-like structures. N=3–8. Levels of mRNA encoding (O) Adgre1 and (P) Tnfa in eWAT of Plau WT/WT and Plau KO/KO mice after 20 weeks on diet. N=3–8. Data are expressed as mean±SEM and analyzed by two-way ANOVA and Fisher’s LSD test (B-D, F-H, J-L, N-P).

Techniques: Staining, Isolation

(A) Total liver mass, (B) liver to body weight ratio, (C) circulating alanine aminotransferase (ALT) activity and (D) level of hepatic triglyceride of Plau WT/WT and Plau KO/KO mice after 14 weeks on diet. N=4–9. (E) Representative H&E-stained sections of livers isolated from Plau WT/WT and Plau KO/KO mice after 14 weeks on diet. Levels of mRNA encoding (F) Pparg , (G) Cidea and (H) Cd36 in livers of Plau WT/WT and Plau KO/KO mice after 14 weeks on diet. N=4–9. (I) Circulating levels of total cholesterol in Plau WT/WT and Plau KO/KO mice after 14 weeks on diet. N=4–9. (J) Total liver mass, (K) liver to body weight ratio, (L) circulating ALT activity and (M) level of hepatic triglyceride of Plau WT/WT and Plau KO/KO mice after 20 weeks on diet. N=3–8. (N) Representative H&E-stained sections of livers isolated from Plau WT/WT and Plau KO/KO mice after 20 weeks on diet. N=3–8. Levels of mRNA encoding (O) Pparg , (P) Cidea and (Q) Cd36 in livers of Plau WT/WT and Plau KO/KO mice after 20 weeks on diet. N=3–8. (R) Circulating levels of total cholesterol in Plau WT/WT and Plau KO/KO mice after 20 weeks on diet. N=3–8. Data are expressed as mean±SEM and analyzed by two-way ANOVA and Fisher’s LSD test (A-D, F-M, O-R).

Journal: Arteriosclerosis, thrombosis, and vascular biology

Article Title: Urokinase plasminogen activator deficiency delays the development of obesity and metabolic sequelae

doi: 10.1161/ATVBAHA.125.324017

Figure Lengend Snippet: (A) Total liver mass, (B) liver to body weight ratio, (C) circulating alanine aminotransferase (ALT) activity and (D) level of hepatic triglyceride of Plau WT/WT and Plau KO/KO mice after 14 weeks on diet. N=4–9. (E) Representative H&E-stained sections of livers isolated from Plau WT/WT and Plau KO/KO mice after 14 weeks on diet. Levels of mRNA encoding (F) Pparg , (G) Cidea and (H) Cd36 in livers of Plau WT/WT and Plau KO/KO mice after 14 weeks on diet. N=4–9. (I) Circulating levels of total cholesterol in Plau WT/WT and Plau KO/KO mice after 14 weeks on diet. N=4–9. (J) Total liver mass, (K) liver to body weight ratio, (L) circulating ALT activity and (M) level of hepatic triglyceride of Plau WT/WT and Plau KO/KO mice after 20 weeks on diet. N=3–8. (N) Representative H&E-stained sections of livers isolated from Plau WT/WT and Plau KO/KO mice after 20 weeks on diet. N=3–8. Levels of mRNA encoding (O) Pparg , (P) Cidea and (Q) Cd36 in livers of Plau WT/WT and Plau KO/KO mice after 20 weeks on diet. N=3–8. (R) Circulating levels of total cholesterol in Plau WT/WT and Plau KO/KO mice after 20 weeks on diet. N=3–8. Data are expressed as mean±SEM and analyzed by two-way ANOVA and Fisher’s LSD test (A-D, F-M, O-R).

Techniques: Activity Assay, Staining, Isolation

(A) The total number of cells, and (B) total number of macrophages in the peritoneal lavage fluid collected 72 hours after intraperitoneal injection of 1 mL of 4% thioglycolate. N=3. (C) SDS-PAGE zymography gel and (D) quantification of uPA activity in peritoneal lavage fluid isolated from Plau WT/WT , Plau fl/fl , Plau KO/KO and Plau −/− mice following a 72 hours thioglycolate challenge. N=3. Data are expressed as mean±SEM and analyzed by one-way ANOVA and Tukey’s test (A, B, D). Levels of mRNA encoding (E) Il6 (IL-6), (F) Il1b (IL-1β) and (G) F3 (tissue factor) in thioglycolate-induced peritoneal macrophages with and without lipopolysaccharide (LPS; 1 μg/mL). N=5. Levels of mRNA encoding (H) Il6 , (I) Il1b and (J) F3 in thioglycolate-induced peritoneal macrophages with and without stimulation with zymosan A (1 mg/mL). N=5–6. (K) Generation of reactive oxygen species in thioglycolate-induced peritoneal macrophages following stimulation with zymosan A (1 mg/mL). N=5–6. Levels of mRNA encoding (L) Il6 , (M) Il1b and (N) F3 in bone marrow-derived macrophages (BMDMs) with and without stimulation with LPS (1 μg/mL) or zymosan A (1 mg/mL). N=4–5. (O) Generation of reactive oxygen species in BMDMs following stimulation with LPS (1 μg/mL) or zymosan A (1 mg/mL). N=5. Data are expressed as mean±SEM and analyzed by two-way ANOVA and Fisher’s LSD test (E-O).

Journal: Arteriosclerosis, thrombosis, and vascular biology

Article Title: Urokinase plasminogen activator deficiency delays the development of obesity and metabolic sequelae

doi: 10.1161/ATVBAHA.125.324017

Figure Lengend Snippet: (A) The total number of cells, and (B) total number of macrophages in the peritoneal lavage fluid collected 72 hours after intraperitoneal injection of 1 mL of 4% thioglycolate. N=3. (C) SDS-PAGE zymography gel and (D) quantification of uPA activity in peritoneal lavage fluid isolated from Plau WT/WT , Plau fl/fl , Plau KO/KO and Plau −/− mice following a 72 hours thioglycolate challenge. N=3. Data are expressed as mean±SEM and analyzed by one-way ANOVA and Tukey’s test (A, B, D). Levels of mRNA encoding (E) Il6 (IL-6), (F) Il1b (IL-1β) and (G) F3 (tissue factor) in thioglycolate-induced peritoneal macrophages with and without lipopolysaccharide (LPS; 1 μg/mL). N=5. Levels of mRNA encoding (H) Il6 , (I) Il1b and (J) F3 in thioglycolate-induced peritoneal macrophages with and without stimulation with zymosan A (1 mg/mL). N=5–6. (K) Generation of reactive oxygen species in thioglycolate-induced peritoneal macrophages following stimulation with zymosan A (1 mg/mL). N=5–6. Levels of mRNA encoding (L) Il6 , (M) Il1b and (N) F3 in bone marrow-derived macrophages (BMDMs) with and without stimulation with LPS (1 μg/mL) or zymosan A (1 mg/mL). N=4–5. (O) Generation of reactive oxygen species in BMDMs following stimulation with LPS (1 μg/mL) or zymosan A (1 mg/mL). N=5. Data are expressed as mean±SEM and analyzed by two-way ANOVA and Fisher’s LSD test (E-O).

Techniques: In Vitro, Injection, SDS Page, Zymography, Activity Assay, Isolation, Derivative Assay

Journal: Arteriosclerosis, thrombosis, and vascular biology

Article Title: Urokinase plasminogen activator deficiency delays the development of obesity and metabolic sequelae

doi: 10.1161/ATVBAHA.125.324017

Techniques: Activity Assay, Injection, SDS Page, Zymography, Isolation, Expressing

(A) Mean body weight over time of Plau fl/fl /LysM Cre- and Plau fl/fl /LysM Cre+ mice mice. N=4–9. (B) Total eWAT mass and (C) eWAT adipocyte area of Plau fl/fl /LysM Cre- and Plau fl/fl /LysM Cre+ mice after 14 weeks on diet. N=4–9. (D) Quantification of the % area positive for F4/80 and (E) representative F4/80-stained sections of eWAT isolated from Plau fl/fl /LysM Cre- and Plau fl/fl /LysM Cre+ mice after 14 weeks on diet. Arrows indicate crown-like structures. N=4–9. (F) Circulating levels of total cholesterol in Plau fl/fl /LysM Cre- and Plau fl/fl /LysM Cre+ mice after 14 weeks on diet. N=4–9. (G) Total liver mass, (H) liver to body weight ratio and (I) level of hepatic triglyceride of Plau fl/fl /LysM Cre- and Plau fl/fl /LysM Cre+ mice after 14 weeks on diet. N=4–9. (J) Representative H&E-stained sections of livers isolated from Plau fl/fl /LysM Cre- and Plau fl/fl /LysM Cre+ mice after 14 weeks on diet. N=4–9. Data are expressed as mean±SEM and analyzed by two-way ANOVA and Fisher’s LSD test (B-D, F-I).

Journal: Arteriosclerosis, thrombosis, and vascular biology

Article Title: Urokinase plasminogen activator deficiency delays the development of obesity and metabolic sequelae

doi: 10.1161/ATVBAHA.125.324017

Figure Lengend Snippet: (A) Mean body weight over time of Plau fl/fl /LysM Cre- and Plau fl/fl /LysM Cre+ mice mice. N=4–9. (B) Total eWAT mass and (C) eWAT adipocyte area of Plau fl/fl /LysM Cre- and Plau fl/fl /LysM Cre+ mice after 14 weeks on diet. N=4–9. (D) Quantification of the % area positive for F4/80 and (E) representative F4/80-stained sections of eWAT isolated from Plau fl/fl /LysM Cre- and Plau fl/fl /LysM Cre+ mice after 14 weeks on diet. Arrows indicate crown-like structures. N=4–9. (F) Circulating levels of total cholesterol in Plau fl/fl /LysM Cre- and Plau fl/fl /LysM Cre+ mice after 14 weeks on diet. N=4–9. (G) Total liver mass, (H) liver to body weight ratio and (I) level of hepatic triglyceride of Plau fl/fl /LysM Cre- and Plau fl/fl /LysM Cre+ mice after 14 weeks on diet. N=4–9. (J) Representative H&E-stained sections of livers isolated from Plau fl/fl /LysM Cre- and Plau fl/fl /LysM Cre+ mice after 14 weeks on diet. N=4–9. Data are expressed as mean±SEM and analyzed by two-way ANOVA and Fisher’s LSD test (B-D, F-I).

Techniques: Staining, Isolation

In vitro experiments confirming ellagic acid (EA) target on PLAU to regulate NF-κB signaling pathway in corneal endothelial cells. ( A – C ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in H 2 O 2 -treated B4G12 cells, with or without EA treatment. The relative protein expression levels are shown for B PLAU and C the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( D – F ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in UVA-irradiated B4G12 cells, with or without EA treatment. Relative protein expression levels are shown for E PLAU and F the ratio of phospho-NF-κB p65 to total NF-κB p65 ( n = 3). ( G – I ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 following siPLAU treatment in H 2 O 2 -treated B4G12 cells, with or without EA. Relative protein expression levels are presented for G PLAU and I the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( J ) Schematic diagram illustrating the proposed anti-inflammatory and anti-oxidant mechanisms of EA in FECD, highlighting its role in modulating the NF-κB pathway. All data are presented as mean ± SD. * P < 0.05, ** P < 0.01 by 1-way ANOVA with Tukey’s post hoc test.

Journal: Investigative Ophthalmology & Visual Science

Article Title: Integrated Transcriptomics and Experimental Validation Reveal That Ellagic Acid Alleviates Fuchs Endothelial Corneal Dystrophy via PLAU/NF-κB Signaling

doi: 10.1167/iovs.67.1.31

Figure Lengend Snippet: In vitro experiments confirming ellagic acid (EA) target on PLAU to regulate NF-κB signaling pathway in corneal endothelial cells. ( A – C ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in H 2 O 2 -treated B4G12 cells, with or without EA treatment. The relative protein expression levels are shown for B PLAU and C the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( D – F ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in UVA-irradiated B4G12 cells, with or without EA treatment. Relative protein expression levels are shown for E PLAU and F the ratio of phospho-NF-κB p65 to total NF-κB p65 ( n = 3). ( G – I ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 following siPLAU treatment in H 2 O 2 -treated B4G12 cells, with or without EA. Relative protein expression levels are presented for G PLAU and I the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( J ) Schematic diagram illustrating the proposed anti-inflammatory and anti-oxidant mechanisms of EA in FECD, highlighting its role in modulating the NF-κB pathway. All data are presented as mean ± SD. * P < 0.05, ** P < 0.01 by 1-way ANOVA with Tukey’s post hoc test.

Article Snippet: Primary antibodies against PLAU (Proteintech, China; #17968-1-AP), NF-κB p65 (Abcam, UK; #ab32536), phospho-NF-κB p65 (S536; Abcam, UK; #ab76302), GAPDH (ABclonal, China; #AC002), and β-Actin (ABclonal, China; #AC004) were applied overnight at 4°C.

Techniques: In Vitro, Western Blot, Expressing, Irradiation

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