Journal: Cell Death & Disease

Article Title: C1q-TNF-related protein-3 attenuates pressure overload-induced cardiac hypertrophy by suppressing the p38/CREB pathway and p38-induced ER stress

doi: 10.1038/s41419-019-1749-0

Figure Lengend Snippet: a Representative western blot of CTRP3 levels in different tissues of WT mice and Ctrp3 -KO mice ( n = 3 mice per group). b The HW/BW ratio in animals after 4 weeks of TAC ( n = 5–8 mice per group). c–e The left ventricular ejection fraction (LVEF), IVSd, and LVPWd, accordingly, determined by analyzing the echocardiographic images ( n = 12–14 mice per group). f Representative images of the gross murine heart and sections stained with hematoxylin and eosin (HE), and wheat germ agglutinin (WGA) ( n = 5–8 mice per group). g The mean cross-sectional area of cardiomyocytes from the indicated groups ( n ≥ 100 cells per group). h Representative images of the murine heart sections (after 4 weeks of TAC) stained with Masson stain, arranged with the perivascular area at the top and the interstitial area at the bottom ( n = 5–8 mice per group). i The LV collagen volume in different groups ( n ≥ 40 fields per group). j Real-time polymerase chain reaction (real-time PCR) analysis of the expression of genes encoding hypertrophic markers α-MHC, β-MHC, ANP, BNP, Acta-1, IL-6, and Rcan1.4, and the fibrotic markers TGF-β1, collagen-I, and collagen-III in each group ( n = 6 mice per group). b – j The data were analyzed by one-way ANOVA. ** p < 0.01 vs. SHAM, # p < 0.05 vs. TAC. In the bar graphs, the data are presented as the mean ± standard error of the mean (SEM)

Article Snippet: Some NRCMs were also treated with CTRP3 (5 μg/ml) in the presence of PE for 24 h. Before PE treatment, some NRCMs were pretreated respectively with 1 μM SB203580 or 1 μM 666–15 (CREB inhibitor, purchased from Med Chem Express) for 2 h to inhibit phosphorylation of p38 or CREB .

Techniques: Western Blot, Staining, Real-time Polymerase Chain Reaction, Expressing

Journal: Cell Death & Disease

Article Title: C1q-TNF-related protein-3 attenuates pressure overload-induced cardiac hypertrophy by suppressing the p38/CREB pathway and p38-induced ER stress

doi: 10.1038/s41419-019-1749-0

Figure Lengend Snippet: a Representative western blot and quantification of CTRP3 levels in the heart tissue of WT mice and LV-CTRP3 mice ( n = 3 mice per group). b CTRP3 serum levels in mice infected with LV-NULL or LV-CTRP3 ( n = 3 mice per group). c The HW/BW ratio in animals after 4 weeks of TAC surgery ( n = 5–7 mice per group). d–f LVEF, IVSd, and LVPWd, accordingly, determined by analyzing the echocardiographic images ( n = 12–14 mice per group). g Representative images of the gross murine heart and sections stained with HE and WGA ( n = 5–7 mice per group). h The mean cross-sectional area of cardiomyocytes from the indicated groups ( n ≥ 100 cells per group). i Representative images of the murine heart sections (after 4 weeks of TAC) stained with Masson stain, arranged with the perivascular area at the top and the interstitial area at the bottom ( n = 5–7 mice per group). j The LV collagen volume in different groups ( n ≥ 40 fields per group). k Real-time PCR analysis for the expression of genes encoding the hypertrophic markers α-MHC, β-MHC, ANP, BNP, Acta-1, IL-6, and Rcan1.4, and the fibrotic markers TGF-β1, collagen-I, and collagen-III in each group (n = 6 mice per group). c – k The data were analyzed by one-way ANOVA. * p < 0.05, ** p < 0.01 vs. SHAM, # p < 0.05 vs. TAC; ns, not significant. In the bar graphs, the data are presented as the mean ± SEM

Article Snippet: Some NRCMs were also treated with CTRP3 (5 μg/ml) in the presence of PE for 24 h. Before PE treatment, some NRCMs were pretreated respectively with 1 μM SB203580 or 1 μM 666–15 (CREB inhibitor, purchased from Med Chem Express) for 2 h to inhibit phosphorylation of p38 or CREB .

Techniques: Western Blot, Infection, Staining, Real-time Polymerase Chain Reaction, Expressing

Journal: Cell Death & Disease

Article Title: C1q-TNF-related protein-3 attenuates pressure overload-induced cardiac hypertrophy by suppressing the p38/CREB pathway and p38-induced ER stress

doi: 10.1038/s41419-019-1749-0

Figure Lengend Snippet: a, b Representative western blot (top) and quantification (bottom) of the p38-CREB signaling pathway activity in the hearts of mice with different genotypes (WT, Ctrp3 -KO, and LV-CTRP3) 4 weeks after sham treatment or TAC surgery ( n = 5–6 mice per group). c, d Representative immunofluorescence images of murine heart sections stained with p-p38 (red) and DAPI (blue) (left), and the percentage of p-p38–positive nuclei (right) in the hearts of mice with different genotypes (WT, Ctrp3 -KO, and LV-CTRP3) 4 weeks after sham treatment or TAC surgery ( n = 5–6 mice per group). The data were analyzed by one-way ANOVA. * p < 0.05, ** p < 0.01 vs. SHAM, # p < 0.05 vs. TAC. In the bar graphs, the data are presented as the mean ± SEM

Article Snippet: Some NRCMs were also treated with CTRP3 (5 μg/ml) in the presence of PE for 24 h. Before PE treatment, some NRCMs were pretreated respectively with 1 μM SB203580 or 1 μM 666–15 (CREB inhibitor, purchased from Med Chem Express) for 2 h to inhibit phosphorylation of p38 or CREB .

Techniques: Western Blot, Activity Assay, Immunofluorescence, Staining

Journal: Cell Death & Disease

Article Title: C1q-TNF-related protein-3 attenuates pressure overload-induced cardiac hypertrophy by suppressing the p38/CREB pathway and p38-induced ER stress

doi: 10.1038/s41419-019-1749-0

Figure Lengend Snippet: a Representative western blot (left) and quantification (right) of the p38-CREB signaling pathway activity in NRCMs from the indicated groups ( n = 5 samples per group). b Representative western blot (left) and quantification (right) of the p38-CREB signaling pathway activity in NRCMs from the indicated groups ( n = 5 samples per group). c Left: Representative immunofluorescence images of NRCMs transfected with siRNA or si-CTRP3, and stained with α-actinin (red) and DAPI (blue). The NRCMs were treated with dimethyl sulfoxide (DMSO) or a p38 inhibitor SB203580 (1 μM). Right: The mean cell surface area of NRCMs in the indicated groups ( n ≥ 30 cells per group). d Real-time PCR analysis of the expression of genes encoding the hypertrophic markers β-MHC, ANP, and BNP in the indicated groups ( n = 5 samples per group). e Representative western blot (left), and quantification (right) of p-CREB and CREB levels in NRCMs from the indicated groups ( n = 5 samples per group). f Left: Representative immunofluorescence images of PBS- and CTRP3-treated NRCMs stained with α-actinin (red) and DAPI (blue). The NRCMs were treated with DMSO or SB203580 (1 μM). Right: The mean cell surface area of NRCMs in the indicated groups ( n ≥ 30 cells per group). g Real-time PCR analysis of the expression of genes encoding the hypertrophic markers β-MHC, ANP, and BNP in the indicated groups ( n = 4 samples per group). h Representative western blot (left), and quantification (right) of p-CREB and CREB levels in NRCMs from the indicated groups ( n = 5 samples per group). The data were analyzed by one-way ANOVA. a , and b * p < 0.05, ** p < 0.01 vs. control, # p < 0.05 vs. PE. e , h * p < 0.05 between the two indicated groups; ns, not significant. In the bar graphs, the data are presented as the mean ± SEM

Article Snippet: Some NRCMs were also treated with CTRP3 (5 μg/ml) in the presence of PE for 24 h. Before PE treatment, some NRCMs were pretreated respectively with 1 μM SB203580 or 1 μM 666–15 (CREB inhibitor, purchased from Med Chem Express) for 2 h to inhibit phosphorylation of p38 or CREB .

Techniques: Western Blot, Activity Assay, Immunofluorescence, Transfection, Staining, Real-time Polymerase Chain Reaction, Expressing, Control

Journal: Cell Death & Disease

Article Title: C1q-TNF-related protein-3 attenuates pressure overload-induced cardiac hypertrophy by suppressing the p38/CREB pathway and p38-induced ER stress

doi: 10.1038/s41419-019-1749-0

Figure Lengend Snippet: a Representative western blot of the activity of GRP78, eIF2α, IRE1α, CHOP, and ATF6 in mice hearts from indicated groups. b Statistical diagrams of GRP78, eIF2α, IRE1α, CHOP, and ATF6 protein expression in mice hearts from indicated groups ( n = 6 mice per group). c Representative western blot of the activity of GRP78, eIF2α, IRE1α, CHOP, and ATF6 in mice hearts from indicated groups. d Statistical diagrams of GRP78, eIF2α, IRE1α, CHOP, and ATF6 protein expression in mice hearts from indicated groups ( n = 6 mice per group). e, f Representative immunofluorescence images of murine heart sections stained with GRP78 (red) and DAPI (blue) in the hearts of mice with different genotypes (WT, Ctrp3 -KO, and LV-CTRP3) 4 weeks after sham treatment or TAC surgery ( n = 5–6 mice per group). g Representative western blot (left), and quantification (right) of GRP78, eIF2α, IRE1α, CHOP, and ATF6 in the hearts of mice from the indicated groups ( n = 5 mice per group). The data were analyzed by one-way ANOVA. b , d * p < 0.05, ** p < 0.01 vs. SHAM, # p < 0.05 vs. TAC. g * p < 0.05 and # p < 0.05 between indicated groups. In the bar graphs, the data are presented as the mean ± SEM

Article Snippet: Some NRCMs were also treated with CTRP3 (5 μg/ml) in the presence of PE for 24 h. Before PE treatment, some NRCMs were pretreated respectively with 1 μM SB203580 or 1 μM 666–15 (CREB inhibitor, purchased from Med Chem Express) for 2 h to inhibit phosphorylation of p38 or CREB .

Techniques: Western Blot, Activity Assay, Expressing, Immunofluorescence, Staining

Journal: Cell Death & Disease

Article Title: C1q-TNF-related protein-3 attenuates pressure overload-induced cardiac hypertrophy by suppressing the p38/CREB pathway and p38-induced ER stress

doi: 10.1038/s41419-019-1749-0

Figure Lengend Snippet: a Representative western blot (left) and quantification (right) of the ER stress signaling pathway activity in NRCMs from the indicated groups ( n = 4 samples per group). b Representative western blot (left) and quantification (right) of the p38-CREB and ER stress signaling pathway activity in NRCMs from the indicated groups ( n = 4 samples per group). c Representative western blot (left) and quantification (right) of ER stress and p38-CREB signaling pathway activity, protein expression levels of ANP and β-MHC in NRCMs from the indicated groups ( n = 4 samples per group). * p < 0.05, ** p < 0.01 between indicated groups. In the bar graphs, the data are presented as the mean ± SEM. d Proposed protective mechanism of the role of CTRP3 in pathological cardiac hypertrophy. CTRP3 inhibits the activation of the p38/CREB signaling pathway and ER stress pathway in cardiomyocytes under pressure overload, thereby alleviating pathological cardiac hypertrophy

Article Snippet: Some NRCMs were also treated with CTRP3 (5 μg/ml) in the presence of PE for 24 h. Before PE treatment, some NRCMs were pretreated respectively with 1 μM SB203580 or 1 μM 666–15 (CREB inhibitor, purchased from Med Chem Express) for 2 h to inhibit phosphorylation of p38 or CREB .

Techniques: Western Blot, Activity Assay, Expressing, Activation Assay

Journal: Heliyon

Article Title: Obesity alters adipose tissue response to fasting and refeeding in women: A study on lipolytic and endocrine dynamics and acute insulin resistance

doi: 10.1016/j.heliyon.2024.e37875

Figure Lengend Snippet: Key resources table

Article Snippet: Human CTRP3 ELISA DuoSet Kit , R&D systems Biotechne , Cat# DY7925-05.

Techniques: Recombinant, Enzyme-linked Immunosorbent Assay, Software

Journal: BMJ Open Diabetes Research & Care

Article Title: Plasma C1q/tumor necrosis factor-related protein-3 concentrations are associated with diabetic peripheral neuropathy

doi: 10.1136/bmjdrc-2021-002746

Figure Lengend Snippet: Plasma C1q/tumor necrosis factor-related protein-3 (CTRP3) concentrations in patients without diabetic peripheral neuropathy (non-DPN) and with DPN. Data are presented as means±SD; ***p<0.001 compared with non-DPN.

Article Snippet: The plasma CTRP3 concentrations were determined by ELISA with specific antibody against CTRP3 (Proteintech, Wuhan, China) according to standard protocols.

Techniques: Clinical Proteomics

Journal: BMJ Open Diabetes Research & Care

Article Title: Plasma C1q/tumor necrosis factor-related protein-3 concentrations are associated with diabetic peripheral neuropathy

doi: 10.1136/bmjdrc-2021-002746

Figure Lengend Snippet: The results of the nerve conduction testing from groups divided according to plasma CTRP3 tertiles

Article Snippet: The plasma CTRP3 concentrations were determined by ELISA with specific antibody against CTRP3 (Proteintech, Wuhan, China) according to standard protocols.

Techniques: Clinical Proteomics

Journal: BMJ Open Diabetes Research & Care

Article Title: Plasma C1q/tumor necrosis factor-related protein-3 concentrations are associated with diabetic peripheral neuropathy

doi: 10.1136/bmjdrc-2021-002746

Figure Lengend Snippet: Scatter plots showing the correlations of plasma C1q/tumor necrosis factor-related protein-3 (CTRP3) concentrations with nerve conduction parameters. The correlations were assessed by Pearson’s correlation test. M represents motor, S represents sensory, L represents left, R represents right, T represents tibia, P represents peroneal and Su represents sural.

Article Snippet: The plasma CTRP3 concentrations were determined by ELISA with specific antibody against CTRP3 (Proteintech, Wuhan, China) according to standard protocols.

Techniques: Clinical Proteomics

Journal: Redox Biology

Article Title: Melatonin improves cardiac function in a mouse model of heart failure with preserved ejection fraction

doi: 10.1016/j.redox.2018.07.007

Figure Lengend Snippet: Melatonin increased myocardial CTRP3 expression in obese mice. (A-B) Representative blots and results for myocardial CTRP3 expression (n = 6 per group). (C) Representative images of myocardial CTRP3 immunostaining. (D-E) CTRP3 expression in H9c2 cells. H9c2 cells were treated with melatonin for 15 min, after which they were collected for blot detection. Data are expressed as the mean ± SD of six independent experiments (D-E). Differences were compared by one-way ANOVA followed by Tukey's post hoc test. * P < 0.05 compared with the ND+vehicle group, # P < 0.05 compared with the HFD+vehicle group.

Article Snippet: Circulating CTRP3 levels were determined by commercial ELISA kit (Aviva Systems Biology, San Diego, CA) according to manufacturer's instructions.

Techniques: Expressing, Immunostaining

Journal: Redox Biology

Article Title: Melatonin improves cardiac function in a mouse model of heart failure with preserved ejection fraction

doi: 10.1016/j.redox.2018.07.007

Figure Lengend Snippet: Melatonin caused adipocytes to secrete CTRP3 without affecting adiponectin expression or inflammation. (A) CTRP3 expression in 3T3-L1 adipocytes. 3T3-L1 adipocytes were subjected to treatment with melatonin (10 μmol/L) at different time points and then collected for blot detection. (B-C) Representative images and results for CTRP3 immunostaining in adipose tissue after melatonin treatment (n = 5 per group). (D) Circulating CTRP3 levels after melatonin treatment (n = 6 per group). (E) The level of adiponectin in adipose tissues (n = 5 per group). Data are expressed as the mean ± SD of six independent experiments (A). Differences were compared by one-way ANOVA followed by Tukey's post hoc test. * P < 0.05.

Article Snippet: Circulating CTRP3 levels were determined by commercial ELISA kit (Aviva Systems Biology, San Diego, CA) according to manufacturer's instructions.

Techniques: Expressing, Immunostaining

Journal: Redox Biology

Article Title: Melatonin improves cardiac function in a mouse model of heart failure with preserved ejection fraction

doi: 10.1016/j.redox.2018.07.007

Figure Lengend Snippet: Depleting circulating CTRP3 using a CTRP3 antibody largely abolished melatonin-mediated protection against diastolic dysfunction. (A) LVEDP after melatonin treatment (n = 5 per group). (B) -dP/dt with melatonin treatment (n = 5 per group). (C) Alterations in the Tau index after melatonin treatment (n = 5 per group). (D) The level of 4-HNE (n = 5 per group). (E-F) The mRNA levels of Sod2 and Gpx (n = 5 per group). All data are expressed as the mean ± SD. Differences were compared by one-way ANOVA followed by Tukey's post hoc test. * P < 0.05.

Article Snippet: Circulating CTRP3 levels were determined by commercial ELISA kit (Aviva Systems Biology, San Diego, CA) according to manufacturer's instructions.

Techniques:

Journal: Redox Biology

Article Title: Melatonin improves cardiac function in a mouse model of heart failure with preserved ejection fraction

doi: 10.1016/j.redox.2018.07.007

Figure Lengend Snippet: Adipocyte-derived CTRP3 activated Nrf2 to prevent oxidative stress and cell apoptosis. (A) CTRP3 expression in the pooled adipocyte medium. 3T3-L1 adipocytes were treated melatonin (10 μmol/L) or vehicle for 24 h, after which the medium was collected to detect CTRP3 expression. ConM-V: conditioned medium in which adipocytes treated with vehicle were cultured; ConM-M: conditioned medium in which adipocytes treated with melatonin were cultured. (B-C) Nrf2, HO-1 and SOD2 expression in H9c2 cells. H9c2 cells were exposed to ConM-M for different time periods and then collected for blot detection. (D) Immunostaining of Nrf2 in H9c2 cells. H9c2 cells were exposed to ConM-V or ConM-M for 4 h and then collected for blot detection. (E-F) CTRP3 deficiency in adipocytes largely abolished the effects ConM-M on Nrf2 and HO-1 expression in H9c2 cells. (G) Cell viability in all the groups. (H) Sod2 mRNA levels in H9c2 cells. (I) DCFH-DA staining and TUNEL staining. rhCTRP3, recombinant human CTRP3. All data are expressed as the mean ± SD of six independent experiments. Differences were compared by one-way ANOVA followed by Tukey's post hoc test. * P < 0.05.

Article Snippet: Circulating CTRP3 levels were determined by commercial ELISA kit (Aviva Systems Biology, San Diego, CA) according to manufacturer's instructions.

Techniques: Derivative Assay, Expressing, Cell Culture, Immunostaining, Staining, TUNEL Assay, Recombinant

Journal: Redox Biology

Article Title: Melatonin improves cardiac function in a mouse model of heart failure with preserved ejection fraction

doi: 10.1016/j.redox.2018.07.007

Figure Lengend Snippet: miR-200a was closely associated with Nrf2 activation. (A) Nrf2-related miRNA levels. H9c2 cells were exposed to ConM-V or ConM-M for 24 h and then collected for further analysis. (B) miR-93a, miR-193b and miR-200a levels after rhCTRP3 treatment. (C) Keap1 mRNA levels. (D–F) Nrf2 and HO-1 protein levels. rhCTRP3, recombinant human CTRP3. All data are expressed as the mean ± SD of six independent experiments. Differences were compared by one-way ANOVA followed by Tukey's post hoc test. * P < 0.05.

Article Snippet: Circulating CTRP3 levels were determined by commercial ELISA kit (Aviva Systems Biology, San Diego, CA) according to manufacturer's instructions.

Techniques: Activation Assay, Recombinant

Journal: Diabetes Therapy

Article Title: Astragaloside IV Regulates Insulin Resistance and Inflammatory Response of Adipocytes via Modulating CTRP3 and PI3K/AKT Signaling

doi: 10.1007/s13300-022-01312-1

Figure Lengend Snippet: Actions of AS-IV on the CTRP3 expression in adipocytes. A Effects of AS-IV on CTRP3 mRNA expression in adipocytes. B Actions of AS-IV on CTRP3 protein level in adipocytes. C Effects of CTRP3 siRNA or si-NC transfection on CTRP3 mRNA expression in adipocytes. D Effects of CTRP3 siRNA or si-NC transfection on CTRP3 protein level in adipocytes. N = 3. ** P < 0.01 and *** P < 0.001

Article Snippet: The siRNA that targets CTRP3 (5′- TGGATTTCGUGGUUACCAATT-3′) was synthesized by RiboBio (Guangzhou, China), and siRNA with the scrambled sequence (5′-GTTCAGTTCAGGTTAGTATCT-3′) was used as control siRNA.

Techniques: Expressing, Transfection

Journal: Diabetes Therapy

Article Title: Astragaloside IV Regulates Insulin Resistance and Inflammatory Response of Adipocytes via Modulating CTRP3 and PI3K/AKT Signaling

doi: 10.1007/s13300-022-01312-1

Figure Lengend Snippet: Effects of CTRP3 silencing on the insulin resistance and inflammatory response in adipocytes treated with AS-IV. A Effects of CTRP3 silencing on glucose consumption in AS-IV stimulated AS-IV are shown. B Effects of CTRP3 silencing on IL-6 mRNA expression in AS-IV stimulated AS-IV are shown. C Effects of CTRP3 silencing on TNF-α mRNA expression in AS-IV stimulated AS-IV are shown. D Effects of CTRP3 silencing on IL-6 protein levels in AS-IV stimulated AS-IV are shown. E Effects of CTRP3 silencing on TNF-α protein level in AS-IV stimulated AS-IV are shown. F Effects of CTRP3 silencing on GLUT-4 mRNA expression in AS-IV stimulated AS-IV are shown. * P < 0.05, ** P < 0.01 and *** P < 0.001

Article Snippet: The siRNA that targets CTRP3 (5′- TGGATTTCGUGGUUACCAATT-3′) was synthesized by RiboBio (Guangzhou, China), and siRNA with the scrambled sequence (5′-GTTCAGTTCAGGTTAGTATCT-3′) was used as control siRNA.

Techniques: Expressing

Journal: Diabetes Therapy

Article Title: Astragaloside IV Regulates Insulin Resistance and Inflammatory Response of Adipocytes via Modulating CTRP3 and PI3K/AKT Signaling

doi: 10.1007/s13300-022-01312-1

Figure Lengend Snippet: Effects of CTRP3 silencing on the PI3K/AKT signaling in adipocytes treated with AS-IV. Protein expression levels of p-PI3K, PI3K, p-AKT and AKT are shown. N = 3. * P < 0.05, ** P < 0.01 and *** P < 0.001

Article Snippet: The siRNA that targets CTRP3 (5′- TGGATTTCGUGGUUACCAATT-3′) was synthesized by RiboBio (Guangzhou, China), and siRNA with the scrambled sequence (5′-GTTCAGTTCAGGTTAGTATCT-3′) was used as control siRNA.

Techniques: Expressing

Journal: Diabetes Therapy

Article Title: Astragaloside IV Regulates Insulin Resistance and Inflammatory Response of Adipocytes via Modulating CTRP3 and PI3K/AKT Signaling

doi: 10.1007/s13300-022-01312-1

Figure Lengend Snippet:

Article Snippet: The siRNA that targets CTRP3 (5′- TGGATTTCGUGGUUACCAATT-3′) was synthesized by RiboBio (Guangzhou, China), and siRNA with the scrambled sequence (5′-GTTCAGTTCAGGTTAGTATCT-3′) was used as control siRNA.

Techniques: Concentration Assay, Expressing, Activity Assay, Inhibition

Journal: International Journal of Molecular Sciences

Article Title: Downregulation of CTRP-3 by Weight Loss In Vivo and by Bile Acids and Incretins in Adipocytes In Vitro

doi: 10.3390/ijms21218168

Figure Lengend Snippet: Human CTRP-3 serum levels in obesity as measured by different ELISA kit suppliers. Serum data from the present study (human CTRP-3 ELISA Kit from R&D Systems, Wiesbaden, Germany) are depicted together with data published by Deng et al. ( Diabetol Metab. Syndr. , 2015 [ 14 ]; ELISA Kit from Aviscera Bioscience, Santa Clara, CA, USA), Wolf et al. ( PLoS ONE , 2015 [ 13 ]; ELISA Kit from AdipoGen, Incheon, Korea), and Jain et al. ( Int. J. Endocrinol. Metab. , 2019 [ 24 ]; ELISA Kit from Wuhan EIAab Science Co.). BS, bariatric surgery (present study); LCD, low calorie diet (present study).

Article Snippet: Obesity subgroup ( n = 180) , 28.02 ± 1.65 , 94.53 ± 43.94 , CTRP-3 ELISA Aviscera Bioscience, Santa Clara, CA, USA , Deng, W. et al. , [ ] .

Techniques: Enzyme-linked Immunosorbent Assay

Journal: Acta Cardiologica Sinica

Article Title: Complement C1q/Tumor Necrosis Factor-Related Protein-3 (CTRP3) is Significantly Decreased in Patients with Heart Failure and Closely Related with Ventricular Tachycardia

doi: 10.6515/ACS.202105_37(3).20201019B

Figure Lengend Snippet: Demographic and laboratory findings of patients with HFrEF and healthy controls

Article Snippet: For measuring the serum CTRP3 levels, CTRP3 (human) competitive enzyme-linked immunosorbent assay (ELISA) kit (Adipogen, South Korea, Cat# AG-45A0042EK-KI01) were used.

Techniques:

Journal: Acta Cardiologica Sinica

Article Title: Complement C1q/Tumor Necrosis Factor-Related Protein-3 (CTRP3) is Significantly Decreased in Patients with Heart Failure and Closely Related with Ventricular Tachycardia

doi: 10.6515/ACS.202105_37(3).20201019B

Figure Lengend Snippet: Demographic and laboratory findings of HFrEF patients according to presence of ventricular tachycardia

Article Snippet: For measuring the serum CTRP3 levels, CTRP3 (human) competitive enzyme-linked immunosorbent assay (ELISA) kit (Adipogen, South Korea, Cat# AG-45A0042EK-KI01) were used.

Techniques:

Journal: Acta Cardiologica Sinica

Article Title: Complement C1q/Tumor Necrosis Factor-Related Protein-3 (CTRP3) is Significantly Decreased in Patients with Heart Failure and Closely Related with Ventricular Tachycardia

doi: 10.6515/ACS.202105_37(3).20201019B

Figure Lengend Snippet: Variable regression analysis for the detection of HFrEF patients with ventricular tachycardia

Article Snippet: For measuring the serum CTRP3 levels, CTRP3 (human) competitive enzyme-linked immunosorbent assay (ELISA) kit (Adipogen, South Korea, Cat# AG-45A0042EK-KI01) were used.

Techniques:

Journal: Acta Cardiologica Sinica

Article Title: Complement C1q/Tumor Necrosis Factor-Related Protein-3 (CTRP3) is Significantly Decreased in Patients with Heart Failure and Closely Related with Ventricular Tachycardia

doi: 10.6515/ACS.202105_37(3).20201019B

Figure Lengend Snippet: ROC analysis of serum CTRP3 level in predicting the presence of ventricular tachycardia for patients with heart failure with reduced ejection fraction. AUROC, area under the receiver operating characteristic; CI, confidence interval; CTRP3, complement C1q/tumor necrosis factor (TNF)-related protein-3; ROC, receiver operating characteristic curve; VT, ventricular tachycardia.

Article Snippet: For measuring the serum CTRP3 levels, CTRP3 (human) competitive enzyme-linked immunosorbent assay (ELISA) kit (Adipogen, South Korea, Cat# AG-45A0042EK-KI01) were used.

Techniques:

Journal: Frontiers in Cellular Neuroscience

Article Title: C1q/Tumor Necrosis Factor-Related Protein-3 Attenuates Brain Injury after Intracerebral Hemorrhage via AMPK-Dependent Pathway in Rat

doi: 10.3389/fncel.2016.00237

Figure Lengend Snippet: Primers used in qRT-PCR .

Article Snippet: Adult rats were split at random into the following four groups: sham-operated (sham) group, ICH group, ICH + vehicle group and ICH + recombinant CTRP3 (rCTRP3, Chimerigen, USA) group. rCTRP3 was injected intracerebroventricularly (80 μg/kg) 30 min after ICH and then three times per week until the animals were killed.

Techniques:

Journal: Frontiers in Cellular Neuroscience

Article Title: C1q/Tumor Necrosis Factor-Related Protein-3 Attenuates Brain Injury after Intracerebral Hemorrhage via AMPK-Dependent Pathway in Rat

doi: 10.3389/fncel.2016.00237

Figure Lengend Snippet: Effects of CTRP3 treatment on brain water content 7 days after ICH. (A) Brain water content in ipsilateral (Ipsi) and contralateral (Contra) hemispheres 7 days after ICH in rats treated with rCTRP3. (B) Brain water content in ipsilateral (Ipsi) and contralateral (Contra) hemispheres 7 days after ICH in rats treated with Lenti-CTRP3. Values are mean ± SEM. n = 8 per group. * p < 0.05 vs. sham; # p < 0.05 vs. vehicle or Lenti.null. CTRP3, C1q/tumor necrosis factor-related protein-3; rCTRP3, recombinant CTRP3; Lenti.CTRP3, Lentivirus overexpression of CTRP3; ICH, intracerebral hemorrhage.

Article Snippet: Adult rats were split at random into the following four groups: sham-operated (sham) group, ICH group, ICH + vehicle group and ICH + recombinant CTRP3 (rCTRP3, Chimerigen, USA) group. rCTRP3 was injected intracerebroventricularly (80 μg/kg) 30 min after ICH and then three times per week until the animals were killed.

Techniques: Recombinant, Over Expression

Journal: Frontiers in Cellular Neuroscience

Article Title: C1q/Tumor Necrosis Factor-Related Protein-3 Attenuates Brain Injury after Intracerebral Hemorrhage via AMPK-Dependent Pathway in Rat

doi: 10.3389/fncel.2016.00237

Figure Lengend Snippet: Effects of CTRP3 treatment on neurological functions 7 days after ICH. All animals after ICH showed significant neurological deficits based on performance on the modified Garcia (A) , beam balance (B) and wire hanging (C) tests. Rats treated with rCTRP3 showed reduced neurological deficits in all three tests. Treatment with Lenti-CTRP3 starting 2 weeks before induction of ICH showed a tendency to ameliorate neurological deficits (D–F) . Values are mean ± SEM. n = 9 per group. * p < 0.05 vs. sham; ** p < 0.01 vs. sham; # p < 0.05 vs. vehicle or Lenti.null. CTRP3, C1q/tumor necrosis factor-related protein-3; rCTRP3, recombinant CTRP3; Lenti-CTRP3, Lentivirus overexpression of CTRP3; ICH, intracerebral hemorrhage.

Article Snippet: Adult rats were split at random into the following four groups: sham-operated (sham) group, ICH group, ICH + vehicle group and ICH + recombinant CTRP3 (rCTRP3, Chimerigen, USA) group. rCTRP3 was injected intracerebroventricularly (80 μg/kg) 30 min after ICH and then three times per week until the animals were killed.

Techniques: Modification, Recombinant, Over Expression

Journal: Frontiers in Cellular Neuroscience

Article Title: C1q/Tumor Necrosis Factor-Related Protein-3 Attenuates Brain Injury after Intracerebral Hemorrhage via AMPK-Dependent Pathway in Rat

doi: 10.3389/fncel.2016.00237

Figure Lengend Snippet: Effects of CTRP3 treatment on ICH-induced blood-brain barrier (BBB) damage 7 days after ICH. (A) Quantification of Evans blue dye extravasation (blue staining) in the ipsilateral (Ipsi) and contralateral (Contra) hemispheres 7 days after ICH in rats treated with rCTRP3. (B) Quantification of Evans blue dye extravasation (blue staining) in ipsilateral (Ipsi) and contralateral (Contra) hemispheres 7 days after ICH in rats treated with Lenti-CTRP3. Values are mean ± SEM. n = 6 per group. ** p < 0.01 vs. sham; # p < 0.05 vs. vehicle or Lenti.null. CTRP3, C1q/tumor necrosis factor-related protein-3; rCTRP3, recombinant CTRP3; Lenti-CTRP3, Lentivirus overexpression of CTRP3; ICH, intracerebral hemorrhage.

Article Snippet: Adult rats were split at random into the following four groups: sham-operated (sham) group, ICH group, ICH + vehicle group and ICH + recombinant CTRP3 (rCTRP3, Chimerigen, USA) group. rCTRP3 was injected intracerebroventricularly (80 μg/kg) 30 min after ICH and then three times per week until the animals were killed.

Techniques: Staining, Recombinant, Over Expression

Journal: Frontiers in Cellular Neuroscience

Article Title: C1q/Tumor Necrosis Factor-Related Protein-3 Attenuates Brain Injury after Intracerebral Hemorrhage via AMPK-Dependent Pathway in Rat

doi: 10.3389/fncel.2016.00237

Figure Lengend Snippet: CTRP3 encourages angiogenesis in the hematoma border zone 7 days after ICH. (A) Capillary density computed by immunohistochemical staining for CD31 (brown) in the perifocal region in ICH (b) , rCTRP3 (c) and Lenti-CTRP3 (d) 7 days after ICH. A control brain section demonstrates a normal distribution of microvessels in the same region (a) . Bar = 100 μm. (B) Bar graph showing the number of brown stained capillaries 7 days after ICH. Values are mean ± SEM. n = 5 per group. * p < 0.05 vs. sham; ** p < 0.01 vs. sham; # p < 0.05 vs. ICH. CTRP3, C1q/tumor necrosis factor-related protein-3; rCTRP3, recombinant CTRP3; Lenti-CTRP3, Lentivirus overexpression of CTRP3; ICH, intracerebral hemorrhage; CD31, platelet endothelial cell adhesion molecule-1.

Article Snippet: Adult rats were split at random into the following four groups: sham-operated (sham) group, ICH group, ICH + vehicle group and ICH + recombinant CTRP3 (rCTRP3, Chimerigen, USA) group. rCTRP3 was injected intracerebroventricularly (80 μg/kg) 30 min after ICH and then three times per week until the animals were killed.

Techniques: Immunohistochemical staining, Staining, Control, Recombinant, Over Expression

Journal: Frontiers in Cellular Neuroscience

Article Title: C1q/Tumor Necrosis Factor-Related Protein-3 Attenuates Brain Injury after Intracerebral Hemorrhage via AMPK-Dependent Pathway in Rat

doi: 10.3389/fncel.2016.00237

Figure Lengend Snippet: CTRP3 upregulates pAMPK/HIF-1α/vascular endothelial growth factor (VEGF) axis protein expression in the hematoma border zone 7 days after ICH. (A) Western blot analysis of the effect of rCTRP3 on CTRP3, phosphorylated (p) AMP-activated protein kinase (AMPK; Thr172)/AMPK, HIF-1α and VEGF-A. (B–E) Representative ratios of CTRP3, p-AMPK, HIF-1α and VEGF-A protein expression. (F) Western blot analysis of the effect of Lenti-CTRP3 on CTRP3, phosphorylated (p) AMPK (Thr172)/AMPK, HIF-1α and VEGF-A. (G–J) Representative ratios of CTRP3, p-AMPK, HIF-1α and VEGF-A protein expression. Values are mean ± SEM. n = 4 per group. * p < 0.05 vs. sham; ## p < 0.01 vs. vehicle or Lenti.null. CTRP3, C1q/tumor necrosis factor-related protein-3; rCTRP3, recombinant CTRP3; Lenti-CTRP3, Lentivirus overexpression of CTRP3; ICH, intracerebral hemorrhage.

Article Snippet: Adult rats were split at random into the following four groups: sham-operated (sham) group, ICH group, ICH + vehicle group and ICH + recombinant CTRP3 (rCTRP3, Chimerigen, USA) group. rCTRP3 was injected intracerebroventricularly (80 μg/kg) 30 min after ICH and then three times per week until the animals were killed.

Techniques: Expressing, Western Blot, Recombinant, Over Expression

Journal: Frontiers in Cellular Neuroscience

Article Title: C1q/Tumor Necrosis Factor-Related Protein-3 Attenuates Brain Injury after Intracerebral Hemorrhage via AMPK-Dependent Pathway in Rat

doi: 10.3389/fncel.2016.00237

Figure Lengend Snippet: Quantitative RT-PCR analysis of HIF-1α and VEGF-A mRNA levels in the hematoma border zone 7 days after ICH. (A–C) Quantitative RT-PCR analysis of the effect of rCTRP3 on CTRP3, HIF-1α and VEGF-A mRNA levels. (D–F) Quantitative RT-PCR analysis of the effect of rCTRP3 on CTRP3, HIF-1α and VEGF-A mRNA levels. Values are mean ± SEM. n = 4–6 per group. * p < 0.05 vs. sham; ** p < 0.01 vs. sham; ## p < 0.01 vs. vehicle or Lenti.null. CTRP3, C1q/tumor necrosis factor-related protein-3; rCTRP3, recombinant CTRP3; Lenti.CTRP3, Lentivirus overexpression of CTRP3; ICH, intracerebral hemorrhage.

Article Snippet: Adult rats were split at random into the following four groups: sham-operated (sham) group, ICH group, ICH + vehicle group and ICH + recombinant CTRP3 (rCTRP3, Chimerigen, USA) group. rCTRP3 was injected intracerebroventricularly (80 μg/kg) 30 min after ICH and then three times per week until the animals were killed.

Techniques: Quantitative RT-PCR, Recombinant, Over Expression

Journal: Frontiers in Cellular Neuroscience

Article Title: C1q/Tumor Necrosis Factor-Related Protein-3 Attenuates Brain Injury after Intracerebral Hemorrhage via AMPK-Dependent Pathway in Rat

doi: 10.3389/fncel.2016.00237

Figure Lengend Snippet: CTRP3 promotes angiogenesis via an AMPK-dependent signaling mechanism. (A) Western blot analysis of the effects of COM.C and CBO on rCTRP3-induced p-AMPK, HIF-1α and VEGF-A expression. (B–D) Representative ratios of p-AMPK, HIF-1α and VEGF-A protein expression. (E) Modified Garcia test analysis of the effects of COM.C and CBO on neurological function improvement induced by rCTRP3. (F) Evans blue dye extravasation analysis of the effects of COM.C and CBO on ICH-induced BBB damage reduced by rCTRP3. (G) Immunohistochemical staining analysis of the effects of COM.C and CBO on angiogenesis induced by rCTRP3. Capillary density measured by immunohistochemical staining for CD31 (brown) in the perifocal region in ICH (a) , rCTRP3 (b) , COM.C (c) and CBO (d) 7 days after ICH. (H) Bar graph showing the number of brown stained capillaries. Values are mean ± SEM. n = 4–6 per group. ** p < 0.01 vs. ICH; # p < 0.05 vs. rCTRP3; ## p < 0.01 vs. rCTRP3; & p < 0.05 vs. COM.C. CTRP3, C1q/tumor necrosis factor-related protein-3; rCTRP3, recombinant CTRP3; Lenti-CTRP3, Lentivirus overexpression of CTRP3; ICH, intracerebral hemorrhage; COM.C, compound C; CBO, CBO-P11.

Article Snippet: Adult rats were split at random into the following four groups: sham-operated (sham) group, ICH group, ICH + vehicle group and ICH + recombinant CTRP3 (rCTRP3, Chimerigen, USA) group. rCTRP3 was injected intracerebroventricularly (80 μg/kg) 30 min after ICH and then three times per week until the animals were killed.

Techniques: Western Blot, Expressing, Modification, Immunohistochemical staining, Staining, Recombinant, Over Expression