Journal: Frontiers in Cell and Developmental Biology

Article Title: An MRTF-A–Sp1–PDE5 Axis Mediates Angiotensin-II-Induced Cardiomyocyte Hypertrophy

doi: 10.3389/fcell.2020.00839

Figure Lengend Snippet: Cardiomyocyte deletion of myocardin-related transcription factor A (MRTF-A) attenuates Ang-II-induced cardiac hypertrophy in mice. MRTF-A conditional knockout (CKO) mice and wild-type (WT) mice were induced to develop cardiac hypertrophy by Ang II infusion as described in section “Materials and Methods.” (A) Immunofluorescence staining was performed with anti-MRTF-A and anti-actinin. (B) Heart weight vs. body weight ratio. (C) Heart weight vs. tibia bone length ratio. (D) Echocardiographic measurements of left ventricular systolic dimension (LVSd). (E) Echocardiographic measurements of left ventricular posterior wall dimension (LVPWd). (F) Echocardiographic measurements of ejection fraction (EF). (G) Echocardiographic measurements of fractional shortening (FS). (H) Cardiac sections were stained with wheat germ agglutinin (WGA). Cross-sectional areas were quantified by Image Pro. (I) Immunohistochemistry (IHC) staining of cardiac sections with anti-MRTF-A, antibrain natriuretic peptide (anti-BNP), and anti-β-major histocompatibility complex (anti-β-MHC) antibodies, Cross-sectional areas were quantified by Image Pro. N = 3–5 mice for the saline groups and N = 5 mice for the Ang II groups. Error bars represent SD. * p < 0.05; ** p < 0.01; *** p < 0.001. Scale bar: 50 μm.

Article Snippet: Western analyses were performed with anti-α-tubulin (Proteintech, Wuhan, China 11224-1, 1:2,000), anti-MRTF-A (Proteintech, China 21166-1, 1:1,000), anti-PDE5 (Proteintech, China 22624-1, 1:1,000), anti-BNP primary antibody (BOSTER, China, 1:1,000 dilution), anti-β-MHC primary antibody (Proteintech, China, 1:1,000 dilution), and anti-Sp1 (Abcam, United Kingdom ab13370, 1:1,000).

Techniques: Knock-Out, Immunofluorescence, Staining, Immunohistochemistry

Journal: International journal of molecular medicine

Article Title: Sphingosine-1-phosphate ameliorates the cardiac hypertrophic response through inhibiting the activity of histone deacetylase-2.

doi: 10.3892/ijmm.2017.3325

Figure Lengend Snippet: Figure 2. Treatment of mice with S1P prevents the development of TAC‑induced cardiac hypertrophy. (A) Representative images of hearts and (B) HW/BW ratios. (C) Histological analysis of cardiomyocytes by hematoxylin and eosin and (D) quantification of cardiomyocyte size. (E) Fluorescein isothiocyanate‑con- jugated wheat germ agglutinin staining and (F) quantification of cardiomyocyte size. (G) Representative immunoblots for cardiac hypertrophic proteins (ANP, BNP and β‑MHC) and (H) semi‑quantification of cardiac hypertrophic proteins. Data are presented as the means ± standard error of the mean (n≥5 for each group). *P<0.05 vs. Sham group; #P<0.05 vs. TAC group. ANP, atrial natriuretic peptide; BNP, brain natriuretic peptide; β‑MHC, β‑myosin heavy chain; BW, body weight; HW, heart weight; S1P, sphingosine‑1‑phosphate; TAC, transverse aortic constriction

Article Snippet: Antibodies against atrial natriuretic peptide (ANP; sc-20158), brain natriuretic peptide (BNP; sc-271185), S1PR2 (sc-25491) and GAPDH (sc-32233) were from Santa Cruz Biotechnology, Inc. (Dallas, TX, USA).

Techniques: Staining, Western Blot

Journal: International journal of molecular medicine

Article Title: Sphingosine-1-phosphate ameliorates the cardiac hypertrophic response through inhibiting the activity of histone deacetylase-2.

doi: 10.3892/ijmm.2017.3325

Figure Lengend Snippet: Figure 3. S1P administration inhibits the PE‑induced cardiac hypertrophic response in vitro. (A and B) Measurement and quantification of the surface area of H9c2 cells following various treatments (magnification, x400). (C and D) Representative immunoblots and semi‑quantification of cardiac hypertrophy‑associated proteins (ANP, BNP and β‑MHC). Data are presented as the means ± standard error of the mean (n≥3 for each experiment). *P<0.05 vs. Con group; #P<0.05 vs. PE group. ANP, atrial natriuretic peptide; BNP, brain natriuretic peptide; β‑MHC, β‑myosin heavy chain; Con, control; PE, phenylephrine; S1P, sphingosine‑1‑phosphate.

Article Snippet: Antibodies against atrial natriuretic peptide (ANP; sc-20158), brain natriuretic peptide (BNP; sc-271185), S1PR2 (sc-25491) and GAPDH (sc-32233) were from Santa Cruz Biotechnology, Inc. (Dallas, TX, USA).

Techniques: In Vitro, Western Blot, Control

Journal: iScience

Article Title: Moderate intensity exercise may protect cardiac function by influencing spleen microbiome composition

doi: 10.1016/j.isci.2023.108635

Figure Lengend Snippet:

Article Snippet: Rabbit anti-BNP , ABclonal , Cat# A2179;.

Techniques: Virus, Recombinant, Software, Flow Cytometry

Journal: Cardiovascular Diagnosis and Therapy

Article Title: The transcription factor PPARA mediates SIRT1 regulation of NCOR1 to protect damaged heart cells

doi: 10.21037/cdt-24-101

Figure Lengend Snippet: SIRT1 protected damaged heart cells. SIRT1 expression was detected by (A) RT-qPCR and (B) Western blot in AC16 and HCMEC cells. (C,D) Apoptosis rates were detected using flow cytometry. (E,F) The contents of ANP, BNP, IL-1β, and IL-18 were detected using ELISA in each group. (G) ROS production, MDA production and SOD activity were measured in each group. Compared with the control group, *P<0.05; compared with the oe-NC group, # P<0.05. n=3. RT-qPCR, reverse transcription-quantitative polymerase chain reaction; HCMEC, human cardiac microvascular endothelial cell; DOX, doxorubicin; oe-NC, overexpression negative control; SIRT1, Sirtuin 1; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; ELISA, enzyme-linked immunosorbent assay; ANP, atrial natriuretic peptide; BNP, brain natriuretic peptide; IL-1β, interleukin-1β; IL-18, interleukin-18; ROS, reactive oxygen species; MDA, malondialdehyde; SOD, superoxide dismutase.

Article Snippet: Human atrial natriuretic peptide (ANP, CSB-E11193h, CUSABIO, Wuhan, China), human brain natriuretic peptide (BNP, CSB-E07970h, CUSABIO), human interleukin 1β (IL-1β, CSB-E08053h, CUSABIO), human interleukin 18 (IL-18, KE00193, Proteintech) were detected using the ELISA kit.

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Activity Assay, Control, Reverse Transcription, Real-time Polymerase Chain Reaction, Over Expression, Negative Control

Journal: Cardiovascular Diagnosis and Therapy

Article Title: The transcription factor PPARA mediates SIRT1 regulation of NCOR1 to protect damaged heart cells

doi: 10.21037/cdt-24-101

Figure Lengend Snippet: SIRT1 targeted the regulation of PPARA and affected heart cells. The expressions of SIRT1 and PPARA were detected by (A) Western blot in each group. Apoptosis rates were detected by (B,C) flow cytometry in each group. The contents of ANP, BNP, IL-1β and IL-18 were detected by (D,E) ELISA in the cell supernatant of each group. The expression of HF marker molecules Myh6 and Myh7 were detected using (F) Western blot. (G) ROS production, MDA production, and SOD activity were detected in each group of cells. (H) Mitochondrial ATP production was detected using a mitochondrial respiratory chain kit. Compared with the control group, *P<0.05; compared with the oe-NC + si-NC group, # P<0.05; compared with the oe-SIRT1 + si-NC group, & P<0.05. n=3. SIRT1, Sirtuin 1; PPARA, peroxisome proliferator-activated receptor α; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; DOX, doxorubicin; oe-NC, overexpression negative control; si-NC, small interfering RNA negative control; HCMEC, human cardiac microvascular endothelial cell; ELISA, enzyme-linked immunosorbent assay; ANP, atrial natriuretic peptide; BNP, brain natriuretic peptide; IL-1β, interleukin-1β; IL-18, interleukin-18; HF, heart failure; Myh6, myosin heavy chain 6; Myh7, myosin heavy chain 7; ROS, reactive oxygen species; MDA, malondialdehyde; SOD, superoxide dismutase; ATP, adenosine triphosphate.

Article Snippet: Human atrial natriuretic peptide (ANP, CSB-E11193h, CUSABIO, Wuhan, China), human brain natriuretic peptide (BNP, CSB-E07970h, CUSABIO), human interleukin 1β (IL-1β, CSB-E08053h, CUSABIO), human interleukin 18 (IL-18, KE00193, Proteintech) were detected using the ELISA kit.

Techniques: Western Blot, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Expressing, Marker, Activity Assay, Control, Over Expression, Negative Control, Small Interfering RNA

Journal: Cardiovascular Diagnosis and Therapy

Article Title: The transcription factor PPARA mediates SIRT1 regulation of NCOR1 to protect damaged heart cells

doi: 10.21037/cdt-24-101

Figure Lengend Snippet: PPARA regulated NCOR1 and protected damaged heart cells. (A) The JASPAR database was used to predict the presence of PPARA binding motifs in the promoter region of NCOR1. (B) ChIP assay was used to validate that the transcription factor PPARA was bound to the NCOR1 promoter region. After AC16s were transfected with oe-PPARA + si-NCOR1 and its negative control, the expressions of PPARA and NCOR1 were detected using (C) Western blot. Cell viability of each group was detected using (D) CCK-8 assay. The apoptosis rates of each group were detected using (E,F) flow cytometry. The contents of ANP, BNP, IL-1β and IL-18 were detected using (G) ELISA in cell supernatant. The expressions of Myh6 and Myh7 were detected by (H) Western blot. (I) ROS production, MDA production, and SOD activity were detected in each group of cells. (J) Mitochondrial ATP production was detected by the kit in cells. Compared with the Control group, *P<0.05; compared with the oe-NC + si-NC group, # P<0.05; compared with the oe-PPARA + si-NC group, & P<0.05. n=3. PPARA, peroxisome proliferator-activated receptor α; NCOR1, nuclear receptor co-repressor 1; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; DOX, doxorubicin; oe-NC, overexpression negative control; si-NC, small interfering RNA negative control; HCMEC, human cardiac microvascular endothelial cell; ChIP, chromatin immunoprecipitation; CCK-8, Cell Counting Kit-8; ELISA, enzyme-linked immunosorbent assay; ANP, atrial natriuretic peptide; BNP, brain natriuretic peptide; IL-1β, interleukin-1β; IL-18, interleukin-18; Myh6, myosin heavy chain 6; Myh7, myosin heavy chain 7; ROS, reactive oxygen species; MDA, malondialdehyde; SOD, superoxide dismutase; ATP, adenosine triphosphate.

Article Snippet: Human atrial natriuretic peptide (ANP, CSB-E11193h, CUSABIO, Wuhan, China), human brain natriuretic peptide (BNP, CSB-E07970h, CUSABIO), human interleukin 1β (IL-1β, CSB-E08053h, CUSABIO), human interleukin 18 (IL-18, KE00193, Proteintech) were detected using the ELISA kit.

Techniques: Binding Assay, Transfection, Negative Control, Western Blot, CCK-8 Assay, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Activity Assay, Control, Over Expression, Small Interfering RNA, Chromatin Immunoprecipitation, Cell Counting