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Right ventricular myocardium gene expression (A) and protein levels (B) , and circulating plasma mediator levels (C) in chronic thromboembolic pulmonary hypertension (CTEPH) and sham (sham). Gene expression data depicts genes involved in myofilament remodeling (MYH6 and MYH7, α- and β-myosin heavy chain isoforms, respectively), extracellular matrix fibrosis (COL1A1 and COL3A1, type I and III collagen chains, respectively), Ca 2+ -handling (ATP2A2, sarcoendoplasmic reticulum calcium ATPase 2; RYR2, cardiac ryanodine receptor), and neurohumoral mediators (NPPB, B-type natriuretic peptide; EDN1, endothelin-1; TNF, tumor necrosis factor-α). Data were averaged upon normalization for 2 internal control genes, GAPDH (glyceraldehyde-3-phosphate dehydrogenase) and RPL4 (ribosomal protein L4). Calcium-handling protein levels of sarcoendoplasmic reticulum Ca2+-ATPase 2a (SERCA2a) normalized for GAPDH and phospho-phospholamban (PLB) normalized for total PLB and representative Western blot bands are presented in (B) , whilst mediator plasma levels <t>of</t> <t>N-terminal</t> <t>pro–B-type</t> natriuretic peptide (NT-proBNP) and endothelin-1 (ET-1) are presented in panel C. In panels A and B data are presented relative to Sham reference levels (dashed lines). * P < 0.05 vs. Sham by Student's t -test or Mann–Whitney U -test, according to assumptions ( n = 6 and 7 in Sham and CTEPH, respectively).

N Terminal Pro, supplied by Cusabio, used in various techniques. Bioz Stars score: 93/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 9 article reviews

n terminal pro - by Bioz Stars, 2026-06

93/100 stars

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1) Product Images from "A swine model of severe chronic thromboembolic pulmonary hypertension induced by repeated pulmonary artery long suture injection"

Article Title: A swine model of severe chronic thromboembolic pulmonary hypertension induced by repeated pulmonary artery long suture injection

Journal: Frontiers in Cardiovascular Medicine

doi: 10.3389/fcvm.2025.1736958

Figure Legend Snippet: Right ventricular myocardium gene expression (A) and protein levels (B) , and circulating plasma mediator levels (C) in chronic thromboembolic pulmonary hypertension (CTEPH) and sham (sham). Gene expression data depicts genes involved in myofilament remodeling (MYH6 and MYH7, α- and β-myosin heavy chain isoforms, respectively), extracellular matrix fibrosis (COL1A1 and COL3A1, type I and III collagen chains, respectively), Ca 2+ -handling (ATP2A2, sarcoendoplasmic reticulum calcium ATPase 2; RYR2, cardiac ryanodine receptor), and neurohumoral mediators (NPPB, B-type natriuretic peptide; EDN1, endothelin-1; TNF, tumor necrosis factor-α). Data were averaged upon normalization for 2 internal control genes, GAPDH (glyceraldehyde-3-phosphate dehydrogenase) and RPL4 (ribosomal protein L4). Calcium-handling protein levels of sarcoendoplasmic reticulum Ca2+-ATPase 2a (SERCA2a) normalized for GAPDH and phospho-phospholamban (PLB) normalized for total PLB and representative Western blot bands are presented in (B) , whilst mediator plasma levels of N-terminal pro–B-type natriuretic peptide (NT-proBNP) and endothelin-1 (ET-1) are presented in panel C. In panels A and B data are presented relative to Sham reference levels (dashed lines). * P < 0.05 vs. Sham by Student's t -test or Mann–Whitney U -test, according to assumptions ( n = 6 and 7 in Sham and CTEPH, respectively).

Techniques Used: Gene Expression, Clinical Proteomics, Control, Western Blot, MANN-WHITNEY

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BW of offspring rats from 1-day to 16-week-old (A). Heart damages in offspring at the age of 8 and 16 weeks, including the ratios (B) LVW/BW, (C) HW/BW and (D) NT-proBNP level in serum. Concentration of Ang II in (E) left ventricle and (F) serum. Data are presented as mean ± SD. n=10 in each group (A-C) and n=7 in each group (D-F). *P<0.05, **P<0.01 vs Con. BW, body weight; HW, heart weight; LVW, left ventricular weight; NT-proBNP, N-terminal pro-brain natriuretic peptide; Ang II, angiotensin II; Con, control; LPS, lipopolysaccharide.

Journal: Molecular Medicine Reports

Article Title: Prenatal lipopolysaccharide exposure programs cardiac fibrosis via dysregulating of connexin 43 in offspring rats

doi: 10.3892/mmr.2026.13830

Figure Lengend Snippet: BW of offspring rats from 1-day to 16-week-old (A). Heart damages in offspring at the age of 8 and 16 weeks, including the ratios (B) LVW/BW, (C) HW/BW and (D) NT-proBNP level in serum. Concentration of Ang II in (E) left ventricle and (F) serum. Data are presented as mean ± SD. n=10 in each group (A-C) and n=7 in each group (D-F). *P<0.05, **P<0.01 vs Con. BW, body weight; HW, heart weight; LVW, left ventricular weight; NT-proBNP, N-terminal pro-brain natriuretic peptide; Ang II, angiotensin II; Con, control; LPS, lipopolysaccharide.

Article Snippet: Serum concentrations of N-terminal pro-BNP (NT-proBNP; cat. no. E-EL-R3023) and Ang II, along with myocardial tissue levels of Ang II (cat. no. E-EL-R1430c), were quantified using commercial ELISA kits (Elabscience Biotechnology Co., Ltd.) following manufacturer protocols.

Techniques: Concentration Assay, Control

SLC31A1 is abundantly expressed in post-AMI HF mouse models, silencing of which mitigates post-AMI HF by inhibiting cardiomyocyte apoptosis. (A, B) LVEF and LVEDP detected by echocardiography, n = 12; (C) The serum NT-proBNP level measured by ELISA, n = 12; (D) Representative images of TTC-stained heart sections and quantification of myocardial infarction, n = 6; (E) Cardiomyocyte apoptosis assessed by TUNEL staining, n = 6; (F) Sorting of macrophages (F4/80 + /CD11b + ) by flow cytometry; (G) mRNA expression of SLC31A1 determined by RT-qPCR, n = 12; (H) The level of SLC31A1 protein determined by western blot, n = 3. Data were described as mean ± standard deviation, with multi-group comparisons conducted by one-way ANOVA, followed by Tukey’s post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Frontiers in Immunology

Article Title: SLC31A1 knockdown mitigates post-MI heart failure via regulation of copper metabolism

doi: 10.3389/fimmu.2026.1707203

Figure Lengend Snippet: SLC31A1 is abundantly expressed in post-AMI HF mouse models, silencing of which mitigates post-AMI HF by inhibiting cardiomyocyte apoptosis. (A, B) LVEF and LVEDP detected by echocardiography, n = 12; (C) The serum NT-proBNP level measured by ELISA, n = 12; (D) Representative images of TTC-stained heart sections and quantification of myocardial infarction, n = 6; (E) Cardiomyocyte apoptosis assessed by TUNEL staining, n = 6; (F) Sorting of macrophages (F4/80 + /CD11b + ) by flow cytometry; (G) mRNA expression of SLC31A1 determined by RT-qPCR, n = 12; (H) The level of SLC31A1 protein determined by western blot, n = 3. Data were described as mean ± standard deviation, with multi-group comparisons conducted by one-way ANOVA, followed by Tukey’s post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Levels of N-terminal pro-brain natriuretic peptide (NT-proBNP), IL-1β, tumor necrosis factor-α (TNF-α) and HMGB1 were measured in the mouse serum and cell supernatants using ELISA kits (Elabscience) (NT-proBNP kit: E-EL-M0834; IL-1β kit: E-EL-M0037; TNF-α kit: E-EL-M3063; HMGB1 kit: E-EL-M0676).

Techniques: Enzyme-linked Immunosorbent Assay, Staining, TUNEL Assay, Flow Cytometry, Expressing, Quantitative RT-PCR, Western Blot, Standard Deviation

SLC31A1 knockdown arrests cuproptosis and HMGB1 release by regulating copper metabolism imbalance, alleviating inflammatory responses in macrophages of mice with HF after AMI. (A-C) Cu 2+ level, ATP content and SDH activity in mouse macrophages determined by kits; (D) Levels of cuproptosis-related proteins FDX1 and DLAT in mouse macrophages measured by western blot; (E) Mitochondrial damage in cells detected by TEM; Levels of HMGB1 (F) , IL-1β (G) , and TNF-α (H) in mouse serum measured by ELISA. n = 12. Data were described as mean ± standard deviation, with multi-group comparisons conducted by one-way ANOVA, followed by Tukey’s post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Frontiers in Immunology

Article Title: SLC31A1 knockdown mitigates post-MI heart failure via regulation of copper metabolism

doi: 10.3389/fimmu.2026.1707203

Figure Lengend Snippet: SLC31A1 knockdown arrests cuproptosis and HMGB1 release by regulating copper metabolism imbalance, alleviating inflammatory responses in macrophages of mice with HF after AMI. (A-C) Cu 2+ level, ATP content and SDH activity in mouse macrophages determined by kits; (D) Levels of cuproptosis-related proteins FDX1 and DLAT in mouse macrophages measured by western blot; (E) Mitochondrial damage in cells detected by TEM; Levels of HMGB1 (F) , IL-1β (G) , and TNF-α (H) in mouse serum measured by ELISA. n = 12. Data were described as mean ± standard deviation, with multi-group comparisons conducted by one-way ANOVA, followed by Tukey’s post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques: Knockdown, Activity Assay, Western Blot, Enzyme-linked Immunosorbent Assay, Standard Deviation

ATTM inhibits cuproptosis in macrophages, impedes cardiomyocyte apoptosis and relieves HF after AMI in mice. (A-C) Cu 2+ level, ATP content, and SDH activity in mouse macrophages determined by kits, n = 12; (D) Levels of cuproptosis-related proteins FDX1 and DLAT in mouse macrophages measured by western blot, n = 12; (E) Mitochondrial damage in cells assessed by TEM; Levels of HMGB1 (F) , IL-1β (G) , and TNF-α (H) in mouse serum measured by ELISA, n = 12; LVEF (I) and LVEDP (J) detected by echocardiography, n = 12; K, The NT-proBNP level in mouse serum measured by ELISA, n = 12; L, Representative images of TTC-stained heart sections and quantification of myocardial infarction, n = 6; M, Cardiomyocyte apoptosis assessed by TUNEL staining, n = 6. Data were described as mean ± standard deviation, with multi-group comparisons conducted by one-way ANOVA, followed by Tukey’s post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Frontiers in Immunology

Article Title: SLC31A1 knockdown mitigates post-MI heart failure via regulation of copper metabolism

doi: 10.3389/fimmu.2026.1707203

Figure Lengend Snippet: ATTM inhibits cuproptosis in macrophages, impedes cardiomyocyte apoptosis and relieves HF after AMI in mice. (A-C) Cu 2+ level, ATP content, and SDH activity in mouse macrophages determined by kits, n = 12; (D) Levels of cuproptosis-related proteins FDX1 and DLAT in mouse macrophages measured by western blot, n = 12; (E) Mitochondrial damage in cells assessed by TEM; Levels of HMGB1 (F) , IL-1β (G) , and TNF-α (H) in mouse serum measured by ELISA, n = 12; LVEF (I) and LVEDP (J) detected by echocardiography, n = 12; K, The NT-proBNP level in mouse serum measured by ELISA, n = 12; L, Representative images of TTC-stained heart sections and quantification of myocardial infarction, n = 6; M, Cardiomyocyte apoptosis assessed by TUNEL staining, n = 6. Data were described as mean ± standard deviation, with multi-group comparisons conducted by one-way ANOVA, followed by Tukey’s post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques: Activity Assay, Western Blot, Enzyme-linked Immunosorbent Assay, Staining, TUNEL Assay, Standard Deviation

SLC31A1 silencing or ATTM suppresses cuproptosis and inflammatory responses in hypoxia-induced macrophages. (A) Cell viability assessed by CCK-8; (B–D) The Cu 2+ level, ATP content, and SDH activity in RAW264.7 cells determined by kits; (E) Levels of cuproptosis-related proteins FDX1 and DLAT in RAW264.7 cells measured by western blot; (F) Mitochondrial damage in cells assessed by TEM; (G) The LDH activity in RAW264.7 cell supernatants detected by the kit; (H-J) Levels of HMGB1, IL-1β, and TNF-α in RAW264.7 cell supernatants measured by ELISA; (K) SLC31A1 mRNA expression determined by RT-qPCR; (L) The SLC31A1 protein level measured by western blot. All cell-based in vitro experiments were independently repeated three times. Data were described as mean ± standard deviation, with multi-group comparisons conducted by one-way ANOVA, followed by Tukey’s post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Frontiers in Immunology

Article Title: SLC31A1 knockdown mitigates post-MI heart failure via regulation of copper metabolism

doi: 10.3389/fimmu.2026.1707203

Figure Lengend Snippet: SLC31A1 silencing or ATTM suppresses cuproptosis and inflammatory responses in hypoxia-induced macrophages. (A) Cell viability assessed by CCK-8; (B–D) The Cu 2+ level, ATP content, and SDH activity in RAW264.7 cells determined by kits; (E) Levels of cuproptosis-related proteins FDX1 and DLAT in RAW264.7 cells measured by western blot; (F) Mitochondrial damage in cells assessed by TEM; (G) The LDH activity in RAW264.7 cell supernatants detected by the kit; (H-J) Levels of HMGB1, IL-1β, and TNF-α in RAW264.7 cell supernatants measured by ELISA; (K) SLC31A1 mRNA expression determined by RT-qPCR; (L) The SLC31A1 protein level measured by western blot. All cell-based in vitro experiments were independently repeated three times. Data were described as mean ± standard deviation, with multi-group comparisons conducted by one-way ANOVA, followed by Tukey’s post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques: CCK-8 Assay, Activity Assay, Western Blot, Enzyme-linked Immunosorbent Assay, Expressing, Quantitative RT-PCR, In Vitro, Standard Deviation

SLC31A1 is implicated in cuproptosis in macrophages through regulation of the NLRP3/HMGB1 pathway. (A) NLRP3 mRNA expression determined by RT-qPCR; (B) NLRP3, cleaved caspase-1 and ASC protein levels measured by western blot; (C) Cell viability evaluated by CCK-8; (D-F) The Cu 2+ level, ATP content, and SDH activity in RAW264.7 cells assessed by kits; (G) Levels of cuproptosis-related proteins FDX1 and DLAT in RAW264.7 cells determined by western blot; (H) Mitochondrial damage in cells assessed by TEM; (I) The LDH activity in RAW264.7 cell supernatants detected by a kit; (J-L) Levels of HMGB1, IL-1β, and TNF-α in RAW264.7 cell supernatants measured by ELISA. All cell-based in vitro experiments were independently repeated three times. Data were described as mean ± standard deviation, with multi-group comparisons conducted by one-way ANOVA, followed by Tukey’s post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Frontiers in Immunology

Article Title: SLC31A1 knockdown mitigates post-MI heart failure via regulation of copper metabolism

doi: 10.3389/fimmu.2026.1707203

Figure Lengend Snippet: SLC31A1 is implicated in cuproptosis in macrophages through regulation of the NLRP3/HMGB1 pathway. (A) NLRP3 mRNA expression determined by RT-qPCR; (B) NLRP3, cleaved caspase-1 and ASC protein levels measured by western blot; (C) Cell viability evaluated by CCK-8; (D-F) The Cu 2+ level, ATP content, and SDH activity in RAW264.7 cells assessed by kits; (G) Levels of cuproptosis-related proteins FDX1 and DLAT in RAW264.7 cells determined by western blot; (H) Mitochondrial damage in cells assessed by TEM; (I) The LDH activity in RAW264.7 cell supernatants detected by a kit; (J-L) Levels of HMGB1, IL-1β, and TNF-α in RAW264.7 cell supernatants measured by ELISA. All cell-based in vitro experiments were independently repeated three times. Data were described as mean ± standard deviation, with multi-group comparisons conducted by one-way ANOVA, followed by Tukey’s post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques: Expressing, Quantitative RT-PCR, Western Blot, CCK-8 Assay, Activity Assay, Enzyme-linked Immunosorbent Assay, In Vitro, Standard Deviation

Activation of the NLRP3/HMGB1 pathway partly counteracts the protection against macrophage cuproptosis and cardiomyocyte apoptosis mediated by SLC31A1 knockdown in mice with post-AMI HF. (A) NLRP3 mRNA expression in mouse macrophages determined by RT-qPCR, n = 12; (B) NLRP3, cleaved caspase-1 and ASC protein levels in mouse macrophages measured by western blot, n = 12; (C-E) The Cu 2+ level, ATP content, and SDH activity in mouse macrophages assessed by kits, n = 12; (F) Levels of cuproptosis-related proteins FDX1 and DLAT in mouse macrophages determined by western blot, n = 12; (G) Mitochondrial damage in cells assessed by TEM; (H-J) Levels of HMGB1, IL-1β, and TNF-α in mouse serum measured by ELISA, n = 12; (K-L) LVEF and LVEDP detected by echocardiography, n = 12; (M) The NT-proBNP level in mouse serum measured by ELISA, n = 12; (N) Representative images of TTC-stained heart sections and quantification of myocardial infarction, n = 6; (O) Cardiomyocyte apoptosis evaluated by TUNEL staining, n = 6. Data were described as mean ± standard deviation, with multi-group comparisons conducted by one-way ANOVA, followed by Tukey’s post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Frontiers in Immunology

Article Title: SLC31A1 knockdown mitigates post-MI heart failure via regulation of copper metabolism

doi: 10.3389/fimmu.2026.1707203

Figure Lengend Snippet: Activation of the NLRP3/HMGB1 pathway partly counteracts the protection against macrophage cuproptosis and cardiomyocyte apoptosis mediated by SLC31A1 knockdown in mice with post-AMI HF. (A) NLRP3 mRNA expression in mouse macrophages determined by RT-qPCR, n = 12; (B) NLRP3, cleaved caspase-1 and ASC protein levels in mouse macrophages measured by western blot, n = 12; (C-E) The Cu 2+ level, ATP content, and SDH activity in mouse macrophages assessed by kits, n = 12; (F) Levels of cuproptosis-related proteins FDX1 and DLAT in mouse macrophages determined by western blot, n = 12; (G) Mitochondrial damage in cells assessed by TEM; (H-J) Levels of HMGB1, IL-1β, and TNF-α in mouse serum measured by ELISA, n = 12; (K-L) LVEF and LVEDP detected by echocardiography, n = 12; (M) The NT-proBNP level in mouse serum measured by ELISA, n = 12; (N) Representative images of TTC-stained heart sections and quantification of myocardial infarction, n = 6; (O) Cardiomyocyte apoptosis evaluated by TUNEL staining, n = 6. Data were described as mean ± standard deviation, with multi-group comparisons conducted by one-way ANOVA, followed by Tukey’s post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques: Activation Assay, Knockdown, Expressing, Quantitative RT-PCR, Western Blot, Activity Assay, Enzyme-linked Immunosorbent Assay, Staining, TUNEL Assay, Standard Deviation

Journal: Frontiers in Cardiovascular Medicine

Article Title: A swine model of severe chronic thromboembolic pulmonary hypertension induced by repeated pulmonary artery long suture injection

doi: 10.3389/fcvm.2025.1736958

Figure Lengend Snippet: Right ventricular myocardium gene expression (A) and protein levels (B) , and circulating plasma mediator levels (C) in chronic thromboembolic pulmonary hypertension (CTEPH) and sham (sham). Gene expression data depicts genes involved in myofilament remodeling (MYH6 and MYH7, α- and β-myosin heavy chain isoforms, respectively), extracellular matrix fibrosis (COL1A1 and COL3A1, type I and III collagen chains, respectively), Ca 2+ -handling (ATP2A2, sarcoendoplasmic reticulum calcium ATPase 2; RYR2, cardiac ryanodine receptor), and neurohumoral mediators (NPPB, B-type natriuretic peptide; EDN1, endothelin-1; TNF, tumor necrosis factor-α). Data were averaged upon normalization for 2 internal control genes, GAPDH (glyceraldehyde-3-phosphate dehydrogenase) and RPL4 (ribosomal protein L4). Calcium-handling protein levels of sarcoendoplasmic reticulum Ca2+-ATPase 2a (SERCA2a) normalized for GAPDH and phospho-phospholamban (PLB) normalized for total PLB and representative Western blot bands are presented in (B) , whilst mediator plasma levels of N-terminal pro–B-type natriuretic peptide (NT-proBNP) and endothelin-1 (ET-1) are presented in panel C. In panels A and B data are presented relative to Sham reference levels (dashed lines). * P < 0.05 vs. Sham by Student's t -test or Mann–Whitney U -test, according to assumptions ( n = 6 and 7 in Sham and CTEPH, respectively).

Article Snippet: Previously aliquoted plasma samples were thawed on ice and assayed for N-terminal pro–B-type natriuretic peptide (NT-proBNP; CSB-EQ027465PI, Cusabio) and endothelin-1 (ET-1; ADI-900-020A, Enzo Life Sciences Inc) in duplicate according to the manufacturer's instructions.

Techniques: Gene Expression, Clinical Proteomics, Control, Western Blot, MANN-WHITNEY

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1) Product Images from "A swine model of severe chronic thromboembolic pulmonary hypertension induced by repeated pulmonary artery long suture injection"

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