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Developmental Studies Hybridoma Bank collagen type 1a1
Collagen Type 1a1, supplied by Developmental Studies Hybridoma Bank, used in various techniques. Bioz Stars score: 94/100, based on 12 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/collagen+type+1a1/pmc13049610-453-10-15?v=Developmental+Studies+Hybridoma+Bank
Average 94 stars, based on 12 article reviews

collagen type 1a1 - by Bioz Stars, 2026-07

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Figure 1. SCN5A knockdown promotes the expression of ﬁbrogenic signaling (A) Upper panel: Knockdown of SCN5A gene in human cardiac ﬁbroblasts by targeting SCN5A gene using shRNA lentivirus. Lower panel: ﬁbroblast grown after SCN5A gene knockdown and morphology analyzed microscopically, Scale bar 350 mm (representative pictures shown). (B) The protein expression of Nav1.5 after the knockdown of the SCN5A gene in HCF represents a 50% decrease in Nav1.5 protein expression. Data are expressed as mean G SEM, paired t-test, **p < 0.01, n = 5 independent experiments. (C) Representatives immunoblot and quantitative analysis showing the expression of pro-Col1agen 1A1, a-SMA, and ﬁbronectin in SCN5A knockdown and control HCF normalized with the internal control group. Data are expressed as mean G SEM, paired t-test, **p < 0.01, ***p < 0.001, n = 6 independent experiments. (D) There were higher soluble collagen-type 1 levels measured in a conditioned medium (serum-free) of SCN5A knockdown HCF than that from control cells Data are expressed as mean G SEM, paired t-test, ***p < 0.001, n = 6 independent experiments. SCN5A shRNA: SCN5A knockdown HCF.

Journal: iScience

Article Title: MicroRNA-452-5p regulates fibrogenesis via targeting TGF-β/SMAD4 axis in SCN5A-knockdown human cardiac fibroblasts.

doi: 10.1016/j.isci.2024.110084

Figure Lengend Snippet: Figure 1. SCN5A knockdown promotes the expression of ﬁbrogenic signaling (A) Upper panel: Knockdown of SCN5A gene in human cardiac ﬁbroblasts by targeting SCN5A gene using shRNA lentivirus. Lower panel: ﬁbroblast grown after SCN5A gene knockdown and morphology analyzed microscopically, Scale bar 350 mm (representative pictures shown). (B) The protein expression of Nav1.5 after the knockdown of the SCN5A gene in HCF represents a 50% decrease in Nav1.5 protein expression. Data are expressed as mean G SEM, paired t-test, **p < 0.01, n = 5 independent experiments. (C) Representatives immunoblot and quantitative analysis showing the expression of pro-Col1agen 1A1, a-SMA, and ﬁbronectin in SCN5A knockdown and control HCF normalized with the internal control group. Data are expressed as mean G SEM, paired t-test, **p < 0.01, ***p < 0.001, n = 6 independent experiments. (D) There were higher soluble collagen-type 1 levels measured in a conditioned medium (serum-free) of SCN5A knockdown HCF than that from control cells Data are expressed as mean G SEM, paired t-test, ***p < 0.001, n = 6 independent experiments. SCN5A shRNA: SCN5A knockdown HCF.

Article Snippet: Next, the membranes were incubated with primary antibodies targeting pro-Collagen type 1A1, SMAD4, LaminB, and b-actin (Santa Cruz, sc-293182, sc-7966, sc6216, and sc4778, respectively); a-SMA (Abcam, ab7817); Nav1.5 (Almone Labs, AC-005); Fibronectin (Millipore,MAB1940); TGF-beta receptor I (Sigma, SAB1300113); TGF-b1, TGF-beta receptor II, phosphoSMAD2/3 (Cell signaling, 3711, 11888, and 8828, respectively); as well as GAPDH (Mbl, M171).

Techniques: Knockdown, Expressing, shRNA, Western Blot, Control

Figure 4. MiR-452-5p mimic restored the ﬁbrogenic phenotype in SCN5A knockdown HCF (A) Immunoblot and quantitative analysis of the expression in protein levels of pro-Collagen type 1A1 and ﬁbronectin in control, and SCN5A knockdown HCF, miR-NTC, and miR-452-5p-mimic groups. Data are expressed as mean G SEM, paired t-test, **p < 0.01, n = 6 independent experiments). (B) Soluble collagen-type1 level measured in conditioned medium from SCN5A knockdown HCF as compared to control and SCN5A knockdown HCF treated without or with miR-NTC and miR-452-5p mimic. Data are expressed as mean G SEM, paired t-test, *p < 0.05, **p < 0.01, n = 5 independent experiments. (C) Immunohistochemistry shows increased expression of a-SMA in SCN5A knockdown HCF and this expression was signiﬁcantly reduced upon the treatment of miR-452-5p mimic as compared to both control and miR-NTC groups. a-SMA (green), DAPI (blue). Scale bar: 90 mm. (D) Immunoblots and quantitative analysis of a-SMA in SCN5A knockdown HCF as compared to control and SCN5A knockdown HCF, miR-NTC, and miR-452-5p- mimic groups. Data are expressed as mean G SEM, paired t-test, **p < 0.01. ***p < 0.001, n = 6 independent experiments. (E) Representative images of migration at 0 h and 10 h post-wounding. Scale bar: 300 mm. Graph showing the cell migration distances (mm) of control, SCN5A knockdown HCF, miR-NTC, and miR-452-5p mimic treated groups. Data are expressed as mean G SEM, paired t-test, ***p < 0.001, n = 10 independent experiments. SCN5A shRNA: SCN5A knockdown HCF. miR-NTC: miR negative control.

Journal: iScience

Article Title: MicroRNA-452-5p regulates fibrogenesis via targeting TGF-β/SMAD4 axis in SCN5A-knockdown human cardiac fibroblasts.

doi: 10.1016/j.isci.2024.110084

Figure Lengend Snippet: Figure 4. MiR-452-5p mimic restored the ﬁbrogenic phenotype in SCN5A knockdown HCF (A) Immunoblot and quantitative analysis of the expression in protein levels of pro-Collagen type 1A1 and ﬁbronectin in control, and SCN5A knockdown HCF, miR-NTC, and miR-452-5p-mimic groups. Data are expressed as mean G SEM, paired t-test, **p < 0.01, n = 6 independent experiments). (B) Soluble collagen-type1 level measured in conditioned medium from SCN5A knockdown HCF as compared to control and SCN5A knockdown HCF treated without or with miR-NTC and miR-452-5p mimic. Data are expressed as mean G SEM, paired t-test, *p < 0.05, **p < 0.01, n = 5 independent experiments. (C) Immunohistochemistry shows increased expression of a-SMA in SCN5A knockdown HCF and this expression was signiﬁcantly reduced upon the treatment of miR-452-5p mimic as compared to both control and miR-NTC groups. a-SMA (green), DAPI (blue). Scale bar: 90 mm. (D) Immunoblots and quantitative analysis of a-SMA in SCN5A knockdown HCF as compared to control and SCN5A knockdown HCF, miR-NTC, and miR-452-5p- mimic groups. Data are expressed as mean G SEM, paired t-test, **p < 0.01. ***p < 0.001, n = 6 independent experiments. (E) Representative images of migration at 0 h and 10 h post-wounding. Scale bar: 300 mm. Graph showing the cell migration distances (mm) of control, SCN5A knockdown HCF, miR-NTC, and miR-452-5p mimic treated groups. Data are expressed as mean G SEM, paired t-test, ***p < 0.001, n = 10 independent experiments. SCN5A shRNA: SCN5A knockdown HCF. miR-NTC: miR negative control.

Techniques: Knockdown, Western Blot, Expressing, Control, Immunohistochemistry, Migration, shRNA, Negative Control

Figure 8. Systemic delivery of AAV miR452 ameliorates ﬁbrosis in isoproterenol-induced HF rats (A) Nav1.5 protein expression in left ventricular tissues of HF and control rats. Data are expressed as mean G SEM, paired t-test, **p < 0.01, n = 3 independent experiments. (B) MiR-452-5p mimic delivery through AAV9 increased the miR-452 expression in left ventricular tissues which was initially reduced after HF development as compared to control, measured via qRT-PCR. Data are expressed as mean G SEM, one-way ANOVA followed by Tukey’s multiple comparison test, ***p < 0.001, n = 5–6 independent experiments. (C) Immunoblots and quantitative analysis of pro-collagen type 1a1, ﬁbronectin, a-SMA in LV tissues of HF, and AAV miR452 compared with control. Data are expressed as mean G SEM, one-way ANOVA followed by Tukey’s multiple comparison test, *p < 0.05, **p < 0.01, ***p < 0.001, n = 5–6 independent experiments. (D) Immunoblots and quantitative analysis of TGF-b signaling including TGF-b1, TGF-bRI, RII, p-SMAD2/3, SMAD4 in LV tissues of HF (induced by subcutaneous injection of isoproterenol 100 mg/kg once a week for 2 weeks) and HF rats treated with AAV miR452 (3.0 x1010 genome copies per rat via tail vein, once a week for 2 weeks) compared with control (received normal saline). Data are represented as mean G SEM, one-way ANOVA followed by Tukey’s multiple comparison test, *p < 0.05, **p < 0.01, ***p < 0.001, n = 5–6 independent experiments.

Journal: iScience

Article Title: MicroRNA-452-5p regulates fibrogenesis via targeting TGF-β/SMAD4 axis in SCN5A-knockdown human cardiac fibroblasts.

doi: 10.1016/j.isci.2024.110084

Figure Lengend Snippet: Figure 8. Systemic delivery of AAV miR452 ameliorates ﬁbrosis in isoproterenol-induced HF rats (A) Nav1.5 protein expression in left ventricular tissues of HF and control rats. Data are expressed as mean G SEM, paired t-test, **p < 0.01, n = 3 independent experiments. (B) MiR-452-5p mimic delivery through AAV9 increased the miR-452 expression in left ventricular tissues which was initially reduced after HF development as compared to control, measured via qRT-PCR. Data are expressed as mean G SEM, one-way ANOVA followed by Tukey’s multiple comparison test, ***p < 0.001, n = 5–6 independent experiments. (C) Immunoblots and quantitative analysis of pro-collagen type 1a1, ﬁbronectin, a-SMA in LV tissues of HF, and AAV miR452 compared with control. Data are expressed as mean G SEM, one-way ANOVA followed by Tukey’s multiple comparison test, *p < 0.05, **p < 0.01, ***p < 0.001, n = 5–6 independent experiments. (D) Immunoblots and quantitative analysis of TGF-b signaling including TGF-b1, TGF-bRI, RII, p-SMAD2/3, SMAD4 in LV tissues of HF (induced by subcutaneous injection of isoproterenol 100 mg/kg once a week for 2 weeks) and HF rats treated with AAV miR452 (3.0 x1010 genome copies per rat via tail vein, once a week for 2 weeks) compared with control (received normal saline). Data are represented as mean G SEM, one-way ANOVA followed by Tukey’s multiple comparison test, *p < 0.05, **p < 0.01, ***p < 0.001, n = 5–6 independent experiments.

Techniques: Expressing, Control, Quantitative RT-PCR, Comparison, Western Blot, Injection, Saline

Figure 9. The proposed mechanism of shielding potential of miR-452-5p in cardiac ﬁbroblasts against SCN5A knockdown escalated cardiac ﬁbrogenesis The expression level of miR-452-5p in normal HCF serves to restrain the activity of SMAD4 protein by binding to the 3ˊUTR of SMAD4 mRNA, therefore limiting its activity. However, in the case of SCN5A knockdown, the quantity of miR-452-5p is considerably reduced, impairing its capacity to bind with 30UTR of SMAD4 mRNA and thereby increasing SMAD4 activity. The increase in SMAD4 activity causes the TGF-b to be overexpressed which activates the canonical TGF-b signaling pathway by increasing the phosphorylation of downstream signal transducers SMAD2 and SMAD3. Following phosphorylation, these form a heterodimer with SMAD4 and translocate into the nucleus, where they increase the expression of ﬁbrogenesis-related genes such as pro-Collagen 1A1, ﬁbronectin, and ﬁbroblasts differentiation by overexpressing a-SMA, and increased cell migration leading to cumulative effect on ﬁbrogenesis in SCN5A knockdown condition.

Journal: iScience

Article Title: MicroRNA-452-5p regulates fibrogenesis via targeting TGF-β/SMAD4 axis in SCN5A-knockdown human cardiac fibroblasts.

doi: 10.1016/j.isci.2024.110084

Figure Lengend Snippet: Figure 9. The proposed mechanism of shielding potential of miR-452-5p in cardiac ﬁbroblasts against SCN5A knockdown escalated cardiac ﬁbrogenesis The expression level of miR-452-5p in normal HCF serves to restrain the activity of SMAD4 protein by binding to the 3ˊUTR of SMAD4 mRNA, therefore limiting its activity. However, in the case of SCN5A knockdown, the quantity of miR-452-5p is considerably reduced, impairing its capacity to bind with 30UTR of SMAD4 mRNA and thereby increasing SMAD4 activity. The increase in SMAD4 activity causes the TGF-b to be overexpressed which activates the canonical TGF-b signaling pathway by increasing the phosphorylation of downstream signal transducers SMAD2 and SMAD3. Following phosphorylation, these form a heterodimer with SMAD4 and translocate into the nucleus, where they increase the expression of ﬁbrogenesis-related genes such as pro-Collagen 1A1, ﬁbronectin, and ﬁbroblasts differentiation by overexpressing a-SMA, and increased cell migration leading to cumulative effect on ﬁbrogenesis in SCN5A knockdown condition.

Techniques: Knockdown, Expressing, Activity Assay, Protein Binding, Phospho-proteomics, Migration

SCN5A knockdown promotes the expression of fibrogenic signaling (A) Upper panel: Knockdown of SCN5A gene in human cardiac fibroblasts by targeting SCN5A gene using shRNA lentivirus. Lower panel : fibroblast grown after SCN5A gene knockdown and morphology analyzed microscopically, Scale bar 350 μm (representative pictures shown). (B) The protein expression of Nav1.5 after the knockdown of the SCN5A gene in HCF represents a 50% decrease in Nav1.5 protein expression. Data are expressed as mean ± SEM, paired t-test, ∗∗ p < 0.01, n = 5 independent experiments. (C) Representatives immunoblot and quantitative analysis showing the expression of pro-Col1agen 1A1, α-SMA, and fibronectin in SCN5A knockdown and control HCF normalized with the internal control group. Data are expressed as mean ± SEM, paired t-test, ∗∗ p < 0.01, ∗∗∗ p < 0.001, n = 6 independent experiments. (D) There were higher soluble collagen-type 1 levels measured in a conditioned medium (serum-free) of SCN5A knockdown HCF than that from control cells Data are expressed as mean ± SEM, paired t-test, ∗∗∗ p < 0.001, n = 6 independent experiments. SCN5A shRNA: SCN5A knockdown HCF.

Journal: iScience

Article Title: MicroRNA-452-5p regulates fibrogenesis via targeting TGF-β/SMAD4 axis in SCN5A-knockdown human cardiac fibroblasts

doi: 10.1016/j.isci.2024.110084

Figure Lengend Snippet: SCN5A knockdown promotes the expression of fibrogenic signaling (A) Upper panel: Knockdown of SCN5A gene in human cardiac fibroblasts by targeting SCN5A gene using shRNA lentivirus. Lower panel : fibroblast grown after SCN5A gene knockdown and morphology analyzed microscopically, Scale bar 350 μm (representative pictures shown). (B) The protein expression of Nav1.5 after the knockdown of the SCN5A gene in HCF represents a 50% decrease in Nav1.5 protein expression. Data are expressed as mean ± SEM, paired t-test, ∗∗ p < 0.01, n = 5 independent experiments. (C) Representatives immunoblot and quantitative analysis showing the expression of pro-Col1agen 1A1, α-SMA, and fibronectin in SCN5A knockdown and control HCF normalized with the internal control group. Data are expressed as mean ± SEM, paired t-test, ∗∗ p < 0.01, ∗∗∗ p < 0.001, n = 6 independent experiments. (D) There were higher soluble collagen-type 1 levels measured in a conditioned medium (serum-free) of SCN5A knockdown HCF than that from control cells Data are expressed as mean ± SEM, paired t-test, ∗∗∗ p < 0.001, n = 6 independent experiments. SCN5A shRNA: SCN5A knockdown HCF.

Article Snippet: Anti-Pro-Collagen type 1A1 , Santa Cruz , Cat# sc-293182; RRID: AB_2797597.

Techniques: Knockdown, Expressing, shRNA, Western Blot, Control

MiR-452-5p mimic restored the fibrogenic phenotype in SCN5A knockdown HCF (A) Immunoblot and quantitative analysis of the expression in protein levels of pro-Collagen type 1A1 and fibronectin in control, and SCN5A knockdown HCF, miR-NTC, and miR-452-5p-mimic groups. Data are expressed as mean ± SEM, paired t-test, ∗∗ p < 0.01, n = 6 independent experiments). (B) Soluble collagen-type1 level measured in conditioned medium from SCN5A knockdown HCF as compared to control and SCN5A knockdown HCF treated without or with miR-NTC and miR-452-5p mimic. Data are expressed as mean ± SEM, paired t-test, ∗ p < 0.05, ∗∗ p < 0.01, n = 5 independent experiments. (C) Immunohistochemistry shows increased expression of α-SMA in SCN5A knockdown HCF and this expression was significantly reduced upon the treatment of miR-452-5p mimic as compared to both control and miR-NTC groups. α-SMA (green), DAPI (blue). Scale bar: 90 μm. (D) Immunoblots and quantitative analysis of α-SMA in SCN5A knockdown HCF as compared to control and SCN5A knockdown HCF, miR-NTC, and miR-452-5p-mimic groups. Data are expressed as mean ± SEM, paired t-test, ∗∗ p < 0.01. ∗∗∗ p < 0.001, n = 6 independent experiments. (E) Representative images of migration at 0 h and 10 h post-wounding. Scale bar: 300 μm. Graph showing the cell migration distances (μm) of control, SCN5A knockdown HCF, miR-NTC, and miR-452-5p mimic treated groups. Data are expressed as mean ± SEM, paired t-test, ∗∗∗ p < 0.001, n = 10 independent experiments. SCN5A shRNA: SCN5A knockdown HCF. miR-NTC: miR negative control.

Journal: iScience

Article Title: MicroRNA-452-5p regulates fibrogenesis via targeting TGF-β/SMAD4 axis in SCN5A-knockdown human cardiac fibroblasts

doi: 10.1016/j.isci.2024.110084

Figure Lengend Snippet: MiR-452-5p mimic restored the fibrogenic phenotype in SCN5A knockdown HCF (A) Immunoblot and quantitative analysis of the expression in protein levels of pro-Collagen type 1A1 and fibronectin in control, and SCN5A knockdown HCF, miR-NTC, and miR-452-5p-mimic groups. Data are expressed as mean ± SEM, paired t-test, ∗∗ p < 0.01, n = 6 independent experiments). (B) Soluble collagen-type1 level measured in conditioned medium from SCN5A knockdown HCF as compared to control and SCN5A knockdown HCF treated without or with miR-NTC and miR-452-5p mimic. Data are expressed as mean ± SEM, paired t-test, ∗ p < 0.05, ∗∗ p < 0.01, n = 5 independent experiments. (C) Immunohistochemistry shows increased expression of α-SMA in SCN5A knockdown HCF and this expression was significantly reduced upon the treatment of miR-452-5p mimic as compared to both control and miR-NTC groups. α-SMA (green), DAPI (blue). Scale bar: 90 μm. (D) Immunoblots and quantitative analysis of α-SMA in SCN5A knockdown HCF as compared to control and SCN5A knockdown HCF, miR-NTC, and miR-452-5p-mimic groups. Data are expressed as mean ± SEM, paired t-test, ∗∗ p < 0.01. ∗∗∗ p < 0.001, n = 6 independent experiments. (E) Representative images of migration at 0 h and 10 h post-wounding. Scale bar: 300 μm. Graph showing the cell migration distances (μm) of control, SCN5A knockdown HCF, miR-NTC, and miR-452-5p mimic treated groups. Data are expressed as mean ± SEM, paired t-test, ∗∗∗ p < 0.001, n = 10 independent experiments. SCN5A shRNA: SCN5A knockdown HCF. miR-NTC: miR negative control.

Article Snippet: Anti-Pro-Collagen type 1A1 , Santa Cruz , Cat# sc-293182; RRID: AB_2797597.

Techniques: Knockdown, Western Blot, Expressing, Control, Immunohistochemistry, Migration, shRNA, Negative Control

Systemic delivery of AAV miR452 ameliorates fibrosis in isoproterenol-induced HF rats (A) Nav1.5 protein expression in left ventricular tissues of HF and control rats. Data are expressed as mean ± SEM, paired t-test, ∗∗ p < 0.01, n = 3 independent experiments. (B) MiR-452-5p mimic delivery through AAV9 increased the miR-452 expression in left ventricular tissues which was initially reduced after HF development as compared to control, measured via qRT-PCR. Data are expressed as mean ± SEM, one-way ANOVA followed by Tukey’s multiple comparison test, ∗∗∗ p < 0.001, n = 5–6 independent experiments. (C) Immunoblots and quantitative analysis of pro-collagen type 1a1, fibronectin, α-SMA in LV tissues of HF, and AAV miR452 compared with control. Data are expressed as mean ± SEM, one-way ANOVA followed by Tukey’s multiple comparison test, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, n = 5–6 independent experiments. (D) Immunoblots and quantitative analysis of TGF-β signaling including TGF-β1, TGF-βRI, RII, p -SMAD2/3, SMAD4 in LV tissues of HF (induced by subcutaneous injection of isoproterenol 100 mg/kg once a week for 2 weeks) and HF rats treated with AAV miR452 (3.0 x10 10 genome copies per rat via tail vein, once a week for 2 weeks) compared with control (received normal saline). Data are represented as mean ± SEM, one-way ANOVA followed by Tukey’s multiple comparison test, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, n = 5–6 independent experiments.

Journal: iScience

Article Title: MicroRNA-452-5p regulates fibrogenesis via targeting TGF-β/SMAD4 axis in SCN5A-knockdown human cardiac fibroblasts

doi: 10.1016/j.isci.2024.110084

Figure Lengend Snippet: Systemic delivery of AAV miR452 ameliorates fibrosis in isoproterenol-induced HF rats (A) Nav1.5 protein expression in left ventricular tissues of HF and control rats. Data are expressed as mean ± SEM, paired t-test, ∗∗ p < 0.01, n = 3 independent experiments. (B) MiR-452-5p mimic delivery through AAV9 increased the miR-452 expression in left ventricular tissues which was initially reduced after HF development as compared to control, measured via qRT-PCR. Data are expressed as mean ± SEM, one-way ANOVA followed by Tukey’s multiple comparison test, ∗∗∗ p < 0.001, n = 5–6 independent experiments. (C) Immunoblots and quantitative analysis of pro-collagen type 1a1, fibronectin, α-SMA in LV tissues of HF, and AAV miR452 compared with control. Data are expressed as mean ± SEM, one-way ANOVA followed by Tukey’s multiple comparison test, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, n = 5–6 independent experiments. (D) Immunoblots and quantitative analysis of TGF-β signaling including TGF-β1, TGF-βRI, RII, p -SMAD2/3, SMAD4 in LV tissues of HF (induced by subcutaneous injection of isoproterenol 100 mg/kg once a week for 2 weeks) and HF rats treated with AAV miR452 (3.0 x10 10 genome copies per rat via tail vein, once a week for 2 weeks) compared with control (received normal saline). Data are represented as mean ± SEM, one-way ANOVA followed by Tukey’s multiple comparison test, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, n = 5–6 independent experiments.

Article Snippet: Anti-Pro-Collagen type 1A1 , Santa Cruz , Cat# sc-293182; RRID: AB_2797597.

Techniques: Expressing, Control, Quantitative RT-PCR, Comparison, Western Blot, Injection, Saline

The proposed mechanism of shielding potential of miR-452-5p in cardiac fibroblasts against SCN5A knockdown escalated cardiac fibrogenesis The expression level of miR-452-5p in normal HCF serves to restrain the activity of SMAD4 protein by binding to the 3ˊUTR of SMAD4 mRNA, therefore limiting its activity. However, in the case of SCN5A knockdown, the quantity of miR-452-5p is considerably reduced, impairing its capacity to bind with 3′UTR of SMAD4 mRNA and thereby increasing SMAD4 activity. The increase in SMAD4 activity causes the TGF-β to be overexpressed which activates the canonical TGF-β signaling pathway by increasing the phosphorylation of downstream signal transducers SMAD2 and SMAD3. Following phosphorylation, these form a heterodimer with SMAD4 and translocate into the nucleus, where they increase the expression of fibrogenesis-related genes such as pro-Collagen 1A1, fibronectin, and fibroblasts differentiation by overexpressing α-SMA, and increased cell migration leading to cumulative effect on fibrogenesis in SCN5A knockdown condition.

Journal: iScience

Article Title: MicroRNA-452-5p regulates fibrogenesis via targeting TGF-β/SMAD4 axis in SCN5A-knockdown human cardiac fibroblasts

doi: 10.1016/j.isci.2024.110084

Figure Lengend Snippet: The proposed mechanism of shielding potential of miR-452-5p in cardiac fibroblasts against SCN5A knockdown escalated cardiac fibrogenesis The expression level of miR-452-5p in normal HCF serves to restrain the activity of SMAD4 protein by binding to the 3ˊUTR of SMAD4 mRNA, therefore limiting its activity. However, in the case of SCN5A knockdown, the quantity of miR-452-5p is considerably reduced, impairing its capacity to bind with 3′UTR of SMAD4 mRNA and thereby increasing SMAD4 activity. The increase in SMAD4 activity causes the TGF-β to be overexpressed which activates the canonical TGF-β signaling pathway by increasing the phosphorylation of downstream signal transducers SMAD2 and SMAD3. Following phosphorylation, these form a heterodimer with SMAD4 and translocate into the nucleus, where they increase the expression of fibrogenesis-related genes such as pro-Collagen 1A1, fibronectin, and fibroblasts differentiation by overexpressing α-SMA, and increased cell migration leading to cumulative effect on fibrogenesis in SCN5A knockdown condition.

Article Snippet: Anti-Pro-Collagen type 1A1 , Santa Cruz , Cat# sc-293182; RRID: AB_2797597.

Techniques: Knockdown, Expressing, Activity Assay, Protein Binding, Phospho-proteomics, Migration

Journal: iScience

Article Title: MicroRNA-452-5p regulates fibrogenesis via targeting TGF-β/SMAD4 axis in SCN5A-knockdown human cardiac fibroblasts

doi: 10.1016/j.isci.2024.110084

Figure Lengend Snippet:

Article Snippet: Anti-Pro-Collagen type 1A1 , Santa Cruz , Cat# sc-293182; RRID: AB_2797597.

Techniques: Virus, Recombinant, Transfection, Membrane, Western Blot, Protein Extraction, Reverse Transcription, Qubit Protein Assay, Collagen Assay, Enzyme-linked Immunosorbent Assay, Extraction, Plasmid Preparation, Software, RNA Sequencing

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