mouse igf 1 Search Results


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(A) Differentially expressed genes and overall expression trends of cortical neurons from seven different groups. “D vs A”: log₂FC of KCls vs Control, “G vs D”: log₂FC of MDZs vs KCls. (B) Gene expression profiles of commonly secreted neuronal factors under KCl, and MDZ conditions. <t>IGF1</t> is highlighted by a red dashed line. (C) Validation of IGF1and BDNF expression by RT-qPCR. n.s. P >0.05, * P < 0.05, ** P < 0.01, **** P < 0.0001. n=3. (D-E) Representative images and quantification of EdU assay after IGFBP3 experiment in GL261 cells. Scale bar = 100 μm. (F-G) Representative images and quantification of EdU assay after Linsitinib (OSI-906) treated experiments in GL261 cells. Scale bar = 200 μm. (H-I) Activation of the IGF1 downstream PI3K/AKT signaling pathway in glioma cells and its quantitative analysis. (J-K) PI3K/AKT signaling pathway change after IGFBP3 incubation in glioma cells. n.s. P >0.05, * P< 0.05, ** P< 0.01, *** P< 0.001, **** P< 0.0001. n=3.
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(A) Differentially expressed genes and overall expression trends of cortical neurons from seven different groups. “D vs A”: log₂FC of KCls vs Control, “G vs D”: log₂FC of MDZs vs KCls. (B) Gene expression profiles of commonly secreted neuronal factors under KCl, and MDZ conditions. <t>IGF1</t> is highlighted by a red dashed line. (C) Validation of IGF1and BDNF expression by RT-qPCR. n.s. P >0.05, * P < 0.05, ** P < 0.01, **** P < 0.0001. n=3. (D-E) Representative images and quantification of EdU assay after IGFBP3 experiment in GL261 cells. Scale bar = 100 μm. (F-G) Representative images and quantification of EdU assay after Linsitinib (OSI-906) treated experiments in GL261 cells. Scale bar = 200 μm. (H-I) Activation of the IGF1 downstream PI3K/AKT signaling pathway in glioma cells and its quantitative analysis. (J-K) PI3K/AKT signaling pathway change after IGFBP3 incubation in glioma cells. n.s. P >0.05, * P< 0.05, ** P< 0.01, *** P< 0.001, **** P< 0.0001. n=3.
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(A) Differentially expressed genes and overall expression trends of cortical neurons from seven different groups. “D vs A”: log₂FC of KCls vs Control, “G vs D”: log₂FC of MDZs vs KCls. (B) Gene expression profiles of commonly secreted neuronal factors under KCl, and MDZ conditions. <t>IGF1</t> is highlighted by a red dashed line. (C) Validation of IGF1and BDNF expression by RT-qPCR. n.s. P >0.05, * P < 0.05, ** P < 0.01, **** P < 0.0001. n=3. (D-E) Representative images and quantification of EdU assay after IGFBP3 experiment in GL261 cells. Scale bar = 100 μm. (F-G) Representative images and quantification of EdU assay after Linsitinib (OSI-906) treated experiments in GL261 cells. Scale bar = 200 μm. (H-I) Activation of the IGF1 downstream PI3K/AKT signaling pathway in glioma cells and its quantitative analysis. (J-K) PI3K/AKT signaling pathway change after IGFBP3 incubation in glioma cells. n.s. P >0.05, * P< 0.05, ** P< 0.01, *** P< 0.001, **** P< 0.0001. n=3.
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(A) Differentially expressed genes and overall expression trends of cortical neurons from seven different groups. “D vs A”: log₂FC of KCls vs Control, “G vs D”: log₂FC of MDZs vs KCls. (B) Gene expression profiles of commonly secreted neuronal factors under KCl, and MDZ conditions. <t>IGF1</t> is highlighted by a red dashed line. (C) Validation of IGF1and BDNF expression by RT-qPCR. n.s. P >0.05, * P < 0.05, ** P < 0.01, **** P < 0.0001. n=3. (D-E) Representative images and quantification of EdU assay after IGFBP3 experiment in GL261 cells. Scale bar = 100 μm. (F-G) Representative images and quantification of EdU assay after Linsitinib (OSI-906) treated experiments in GL261 cells. Scale bar = 200 μm. (H-I) Activation of the IGF1 downstream PI3K/AKT signaling pathway in glioma cells and its quantitative analysis. (J-K) PI3K/AKT signaling pathway change after IGFBP3 incubation in glioma cells. n.s. P >0.05, * P< 0.05, ** P< 0.01, *** P< 0.001, **** P< 0.0001. n=3.
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(A) Differentially expressed genes and overall expression trends of cortical neurons from seven different groups. “D vs A”: log₂FC of KCls vs Control, “G vs D”: log₂FC of MDZs vs KCls. (B) Gene expression profiles of commonly secreted neuronal factors under KCl, and MDZ conditions. <t>IGF1</t> is highlighted by a red dashed line. (C) Validation of IGF1and BDNF expression by RT-qPCR. n.s. P >0.05, * P < 0.05, ** P < 0.01, **** P < 0.0001. n=3. (D-E) Representative images and quantification of EdU assay after IGFBP3 experiment in GL261 cells. Scale bar = 100 μm. (F-G) Representative images and quantification of EdU assay after Linsitinib (OSI-906) treated experiments in GL261 cells. Scale bar = 200 μm. (H-I) Activation of the IGF1 downstream PI3K/AKT signaling pathway in glioma cells and its quantitative analysis. (J-K) PI3K/AKT signaling pathway change after IGFBP3 incubation in glioma cells. n.s. P >0.05, * P< 0.05, ** P< 0.01, *** P< 0.001, **** P< 0.0001. n=3.
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(A) Differentially expressed genes and overall expression trends of cortical neurons from seven different groups. “D vs A”: log₂FC of KCls vs Control, “G vs D”: log₂FC of MDZs vs KCls. (B) Gene expression profiles of commonly secreted neuronal factors under KCl, and MDZ conditions. <t>IGF1</t> is highlighted by a red dashed line. (C) Validation of IGF1and BDNF expression by RT-qPCR. n.s. P >0.05, * P < 0.05, ** P < 0.01, **** P < 0.0001. n=3. (D-E) Representative images and quantification of EdU assay after IGFBP3 experiment in GL261 cells. Scale bar = 100 μm. (F-G) Representative images and quantification of EdU assay after Linsitinib (OSI-906) treated experiments in GL261 cells. Scale bar = 200 μm. (H-I) Activation of the IGF1 downstream PI3K/AKT signaling pathway in glioma cells and its quantitative analysis. (J-K) PI3K/AKT signaling pathway change after IGFBP3 incubation in glioma cells. n.s. P >0.05, * P< 0.05, ** P< 0.01, *** P< 0.001, **** P< 0.0001. n=3.
Igf 1, supplied by R&D Systems, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Figure 7. TRPV4 regulates <t>IGF1</t> expression in CCR2– macrophages and is required for coronary angiogenesis (A) Immunostaining for IGF1 (white) and CD68 (red) in control and Tnnt2DK210/DK210 hearts treated with vehicle, TRPV4 inhibitor, or TRPV4 agonist. Scale bar: 20 mm. (B) Quantification of IGF1 protein expression (% IGF1+ macrophages, IGF1 MFI) in control and Tnnt2DK210/DK210 hearts treated with vehicle, TRPV4 inhibitor, or TRPV4 agonist. MFI, mean florescent intensity. n = 5 per group. *p < 0.05 compared to vehicle-treated control hearts. **p < 0.05 compared to vehicle-treated Tnnt2DK210/DK210 hearts. (ANOVA, post hoc Tukey). (C) Low-magnification H&E images of control and Tnnt2DK210/DK210 hearts treated with vehicle or TRPV4 inhibitor for 2 weeks beginning at 6 weeks of age. n = 4 per group. Scale bar: 200 mm. (D) Quantification of the ratio of compact to trabecular myocardium in control and Tnnt2DK210/DK210 hearts treated with vehicle or TRPV4 inhibitor. *p < 0.05 compared to vehicle-treated control hearts (ANOVA, post hoc Tukey). (E) LV ejection fraction and LV chamber dimensions in control and Tnnt2DK210/DK210 mice treated with vehicle or TRPV4 inhibitor for 2 weeks beginning at 6 weeks of age. n = 5 per group. *p < 0.05 compared to vehicle-treated control hearts (ANOVA, post hoc Tukey).
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Figure 7. TRPV4 regulates <t>IGF1</t> expression in CCR2– macrophages and is required for coronary angiogenesis (A) Immunostaining for IGF1 (white) and CD68 (red) in control and Tnnt2DK210/DK210 hearts treated with vehicle, TRPV4 inhibitor, or TRPV4 agonist. Scale bar: 20 mm. (B) Quantification of IGF1 protein expression (% IGF1+ macrophages, IGF1 MFI) in control and Tnnt2DK210/DK210 hearts treated with vehicle, TRPV4 inhibitor, or TRPV4 agonist. MFI, mean florescent intensity. n = 5 per group. *p < 0.05 compared to vehicle-treated control hearts. **p < 0.05 compared to vehicle-treated Tnnt2DK210/DK210 hearts. (ANOVA, post hoc Tukey). (C) Low-magnification H&E images of control and Tnnt2DK210/DK210 hearts treated with vehicle or TRPV4 inhibitor for 2 weeks beginning at 6 weeks of age. n = 4 per group. Scale bar: 200 mm. (D) Quantification of the ratio of compact to trabecular myocardium in control and Tnnt2DK210/DK210 hearts treated with vehicle or TRPV4 inhibitor. *p < 0.05 compared to vehicle-treated control hearts (ANOVA, post hoc Tukey). (E) LV ejection fraction and LV chamber dimensions in control and Tnnt2DK210/DK210 mice treated with vehicle or TRPV4 inhibitor for 2 weeks beginning at 6 weeks of age. n = 5 per group. *p < 0.05 compared to vehicle-treated control hearts (ANOVA, post hoc Tukey).
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Figure 7. TRPV4 regulates <t>IGF1</t> expression in CCR2– macrophages and is required for coronary angiogenesis (A) Immunostaining for IGF1 (white) and CD68 (red) in control and Tnnt2DK210/DK210 hearts treated with vehicle, TRPV4 inhibitor, or TRPV4 agonist. Scale bar: 20 mm. (B) Quantification of IGF1 protein expression (% IGF1+ macrophages, IGF1 MFI) in control and Tnnt2DK210/DK210 hearts treated with vehicle, TRPV4 inhibitor, or TRPV4 agonist. MFI, mean florescent intensity. n = 5 per group. *p < 0.05 compared to vehicle-treated control hearts. **p < 0.05 compared to vehicle-treated Tnnt2DK210/DK210 hearts. (ANOVA, post hoc Tukey). (C) Low-magnification H&E images of control and Tnnt2DK210/DK210 hearts treated with vehicle or TRPV4 inhibitor for 2 weeks beginning at 6 weeks of age. n = 4 per group. Scale bar: 200 mm. (D) Quantification of the ratio of compact to trabecular myocardium in control and Tnnt2DK210/DK210 hearts treated with vehicle or TRPV4 inhibitor. *p < 0.05 compared to vehicle-treated control hearts (ANOVA, post hoc Tukey). (E) LV ejection fraction and LV chamber dimensions in control and Tnnt2DK210/DK210 mice treated with vehicle or TRPV4 inhibitor for 2 weeks beginning at 6 weeks of age. n = 5 per group. *p < 0.05 compared to vehicle-treated control hearts (ANOVA, post hoc Tukey).
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Figure 7. TRPV4 regulates <t>IGF1</t> expression in CCR2– macrophages and is required for coronary angiogenesis (A) Immunostaining for IGF1 (white) and CD68 (red) in control and Tnnt2DK210/DK210 hearts treated with vehicle, TRPV4 inhibitor, or TRPV4 agonist. Scale bar: 20 mm. (B) Quantification of IGF1 protein expression (% IGF1+ macrophages, IGF1 MFI) in control and Tnnt2DK210/DK210 hearts treated with vehicle, TRPV4 inhibitor, or TRPV4 agonist. MFI, mean florescent intensity. n = 5 per group. *p < 0.05 compared to vehicle-treated control hearts. **p < 0.05 compared to vehicle-treated Tnnt2DK210/DK210 hearts. (ANOVA, post hoc Tukey). (C) Low-magnification H&E images of control and Tnnt2DK210/DK210 hearts treated with vehicle or TRPV4 inhibitor for 2 weeks beginning at 6 weeks of age. n = 4 per group. Scale bar: 200 mm. (D) Quantification of the ratio of compact to trabecular myocardium in control and Tnnt2DK210/DK210 hearts treated with vehicle or TRPV4 inhibitor. *p < 0.05 compared to vehicle-treated control hearts (ANOVA, post hoc Tukey). (E) LV ejection fraction and LV chamber dimensions in control and Tnnt2DK210/DK210 mice treated with vehicle or TRPV4 inhibitor for 2 weeks beginning at 6 weeks of age. n = 5 per group. *p < 0.05 compared to vehicle-treated control hearts (ANOVA, post hoc Tukey).
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Image Search Results


(A) Differentially expressed genes and overall expression trends of cortical neurons from seven different groups. “D vs A”: log₂FC of KCls vs Control, “G vs D”: log₂FC of MDZs vs KCls. (B) Gene expression profiles of commonly secreted neuronal factors under KCl, and MDZ conditions. IGF1 is highlighted by a red dashed line. (C) Validation of IGF1and BDNF expression by RT-qPCR. n.s. P >0.05, * P < 0.05, ** P < 0.01, **** P < 0.0001. n=3. (D-E) Representative images and quantification of EdU assay after IGFBP3 experiment in GL261 cells. Scale bar = 100 μm. (F-G) Representative images and quantification of EdU assay after Linsitinib (OSI-906) treated experiments in GL261 cells. Scale bar = 200 μm. (H-I) Activation of the IGF1 downstream PI3K/AKT signaling pathway in glioma cells and its quantitative analysis. (J-K) PI3K/AKT signaling pathway change after IGFBP3 incubation in glioma cells. n.s. P >0.05, * P< 0.05, ** P< 0.01, *** P< 0.001, **** P< 0.0001. n=3.

Journal: bioRxiv

Article Title: Midazolam suppresses glioma progression by attenuating neuronal activity and downregulating IGF1 signaling

doi: 10.64898/2026.03.31.715727

Figure Lengend Snippet: (A) Differentially expressed genes and overall expression trends of cortical neurons from seven different groups. “D vs A”: log₂FC of KCls vs Control, “G vs D”: log₂FC of MDZs vs KCls. (B) Gene expression profiles of commonly secreted neuronal factors under KCl, and MDZ conditions. IGF1 is highlighted by a red dashed line. (C) Validation of IGF1and BDNF expression by RT-qPCR. n.s. P >0.05, * P < 0.05, ** P < 0.01, **** P < 0.0001. n=3. (D-E) Representative images and quantification of EdU assay after IGFBP3 experiment in GL261 cells. Scale bar = 100 μm. (F-G) Representative images and quantification of EdU assay after Linsitinib (OSI-906) treated experiments in GL261 cells. Scale bar = 200 μm. (H-I) Activation of the IGF1 downstream PI3K/AKT signaling pathway in glioma cells and its quantitative analysis. (J-K) PI3K/AKT signaling pathway change after IGFBP3 incubation in glioma cells. n.s. P >0.05, * P< 0.05, ** P< 0.01, *** P< 0.001, **** P< 0.0001. n=3.

Article Snippet: The concentrations of IGF1 in Neu-CMs were quantified using a commercial Mouse/Rat IGF1 ELISA Kit (Multi Sciences, China) according to the manufacturer’s instructions.

Techniques: Expressing, Control, Gene Expression, Biomarker Discovery, Quantitative RT-PCR, EdU Assay, Activation Assay, Incubation

(A) Overall distribution of IGF1 - related genes in all samples. (B) Standardized expression profile and function annotation of IGF1co-expression genes. (C-D) Over-representation enrichment analysis of genes of interest using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases in KCl treated group and MDZ treated group, respectively. (E) Fuzzy cluster analysis identifying five distinct expression patterns of genes participated in MAPK signaling pathway. (F) Transcriptional activity of Fos was evaluated using a univariable linear model. (G) Predicted c-Fos binding motif within the Igf1 promoter region identified using the JASPAR database. (H) ChIP-qPCR analysis assessing c-Fos enrichment at the predicted regulatory region. * P <0.05, ** P < 0.01, **** P< 0.0001. n=3.

Journal: bioRxiv

Article Title: Midazolam suppresses glioma progression by attenuating neuronal activity and downregulating IGF1 signaling

doi: 10.64898/2026.03.31.715727

Figure Lengend Snippet: (A) Overall distribution of IGF1 - related genes in all samples. (B) Standardized expression profile and function annotation of IGF1co-expression genes. (C-D) Over-representation enrichment analysis of genes of interest using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases in KCl treated group and MDZ treated group, respectively. (E) Fuzzy cluster analysis identifying five distinct expression patterns of genes participated in MAPK signaling pathway. (F) Transcriptional activity of Fos was evaluated using a univariable linear model. (G) Predicted c-Fos binding motif within the Igf1 promoter region identified using the JASPAR database. (H) ChIP-qPCR analysis assessing c-Fos enrichment at the predicted regulatory region. * P <0.05, ** P < 0.01, **** P< 0.0001. n=3.

Article Snippet: The concentrations of IGF1 in Neu-CMs were quantified using a commercial Mouse/Rat IGF1 ELISA Kit (Multi Sciences, China) according to the manufacturer’s instructions.

Techniques: Expressing, Activity Assay, Binding Assay, ChIP-qPCR

Figure 7. TRPV4 regulates IGF1 expression in CCR2– macrophages and is required for coronary angiogenesis (A) Immunostaining for IGF1 (white) and CD68 (red) in control and Tnnt2DK210/DK210 hearts treated with vehicle, TRPV4 inhibitor, or TRPV4 agonist. Scale bar: 20 mm. (B) Quantification of IGF1 protein expression (% IGF1+ macrophages, IGF1 MFI) in control and Tnnt2DK210/DK210 hearts treated with vehicle, TRPV4 inhibitor, or TRPV4 agonist. MFI, mean florescent intensity. n = 5 per group. *p < 0.05 compared to vehicle-treated control hearts. **p < 0.05 compared to vehicle-treated Tnnt2DK210/DK210 hearts. (ANOVA, post hoc Tukey). (C) Low-magnification H&E images of control and Tnnt2DK210/DK210 hearts treated with vehicle or TRPV4 inhibitor for 2 weeks beginning at 6 weeks of age. n = 4 per group. Scale bar: 200 mm. (D) Quantification of the ratio of compact to trabecular myocardium in control and Tnnt2DK210/DK210 hearts treated with vehicle or TRPV4 inhibitor. *p < 0.05 compared to vehicle-treated control hearts (ANOVA, post hoc Tukey). (E) LV ejection fraction and LV chamber dimensions in control and Tnnt2DK210/DK210 mice treated with vehicle or TRPV4 inhibitor for 2 weeks beginning at 6 weeks of age. n = 5 per group. *p < 0.05 compared to vehicle-treated control hearts (ANOVA, post hoc Tukey).

Journal: Immunity

Article Title: Resident cardiac macrophages mediate adaptive myocardial remodeling.

doi: 10.1016/j.immuni.2021.07.003

Figure Lengend Snippet: Figure 7. TRPV4 regulates IGF1 expression in CCR2– macrophages and is required for coronary angiogenesis (A) Immunostaining for IGF1 (white) and CD68 (red) in control and Tnnt2DK210/DK210 hearts treated with vehicle, TRPV4 inhibitor, or TRPV4 agonist. Scale bar: 20 mm. (B) Quantification of IGF1 protein expression (% IGF1+ macrophages, IGF1 MFI) in control and Tnnt2DK210/DK210 hearts treated with vehicle, TRPV4 inhibitor, or TRPV4 agonist. MFI, mean florescent intensity. n = 5 per group. *p < 0.05 compared to vehicle-treated control hearts. **p < 0.05 compared to vehicle-treated Tnnt2DK210/DK210 hearts. (ANOVA, post hoc Tukey). (C) Low-magnification H&E images of control and Tnnt2DK210/DK210 hearts treated with vehicle or TRPV4 inhibitor for 2 weeks beginning at 6 weeks of age. n = 4 per group. Scale bar: 200 mm. (D) Quantification of the ratio of compact to trabecular myocardium in control and Tnnt2DK210/DK210 hearts treated with vehicle or TRPV4 inhibitor. *p < 0.05 compared to vehicle-treated control hearts (ANOVA, post hoc Tukey). (E) LV ejection fraction and LV chamber dimensions in control and Tnnt2DK210/DK210 mice treated with vehicle or TRPV4 inhibitor for 2 weeks beginning at 6 weeks of age. n = 5 per group. *p < 0.05 compared to vehicle-treated control hearts (ANOVA, post hoc Tukey).

Article Snippet: Primary antibodies used were: CD68 clone FA-11 1:400 (Biolegend Cat# 137001), GFP (AbcamCat# ab13970), RFP (Abcam Cat# ab62341), cardiac actin clone AC1-20.4.2 (Sigma Cat# A9357), a-actinin clone BM-75.2 (Sigma Cat# A5044), Ki67 (Abcam Cat# ab15580), CD34 clone MEC14.7 (Abcam Cat# ab8158), Cx43 (Cell Signaling Cat# 3512), Paxillin clone Y113 (Abcam Cat# ab32084), Pan-Cadherin (Cell Signaling Cat# 4068), Claudin I (Cell Signaling cat# 13255), Desmoplakin I/II clone DP2.15 (Abcam Cat# ab16434), IGF1 (R&D systems Cat# AF791), CYR61 (R&D systems Cat# AF4055), Ly6G clone 1A8 (BD Cat# 551459), HCN4 (Fisher Cat# PA5-111878), FAK (Abcam, Cat# ab76496), and TRPV4 clone 1B2.6 (Millipore Cat# MABS466).

Techniques: Expressing, Immunostaining, Control