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Procell Inc mouse cardiac muscle cell line hl
CRIF1 was downregulated in the AF mice. ( A ) Atrial tissue of mice was stained with hematoxylin and eosin (H&E) to display the morphological structure. CRIF1 expression in the atrial tissue of mice was detected using immunohistochemistry (200×). ( B ) The CRIF1 mRNA levels in the atrial tissue were detected by RT-qPCR. The mice cardiac muscle cell <t>line</t> <t>HL-1</t> was treated with Ang II (0, 0.1, 0.2, 0.5, 1 and 2 μM) for 24 h. ( C ) The CRIF1 mRNA expression was determined by RT-qPCR. Data are presented as mean ± SD (n=8 mice in each group). t -test was applied. ***P<0.001 vs control group.
Mouse Cardiac Muscle Cell Line Hl, supplied by Procell Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse+cardiac+muscle+cell+line+hl/pmc13264984-66-1-10?v=Procell+Inc
Average 86 stars, based on 1 article reviews
mouse cardiac muscle cell line hl - by Bioz Stars, 2026-06
86/100 stars

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1) Product Images from "Protective Effects of CR6-Interacting Factor 1 Against Angiotensin II-Induced Atrial Fibrillation by Regulating the SIRT1/eNOS Signaling Pathway and Cardiomyocyte Remodeling"

Article Title: Protective Effects of CR6-Interacting Factor 1 Against Angiotensin II-Induced Atrial Fibrillation by Regulating the SIRT1/eNOS Signaling Pathway and Cardiomyocyte Remodeling

Journal: Journal of Inflammation Research

doi: 10.2147/JIR.S596132

CRIF1 was downregulated in the AF mice. ( A ) Atrial tissue of mice was stained with hematoxylin and eosin (H&E) to display the morphological structure. CRIF1 expression in the atrial tissue of mice was detected using immunohistochemistry (200×). ( B ) The CRIF1 mRNA levels in the atrial tissue were detected by RT-qPCR. The mice cardiac muscle cell line HL-1 was treated with Ang II (0, 0.1, 0.2, 0.5, 1 and 2 μM) for 24 h. ( C ) The CRIF1 mRNA expression was determined by RT-qPCR. Data are presented as mean ± SD (n=8 mice in each group). t -test was applied. ***P<0.001 vs control group.
Figure Legend Snippet: CRIF1 was downregulated in the AF mice. ( A ) Atrial tissue of mice was stained with hematoxylin and eosin (H&E) to display the morphological structure. CRIF1 expression in the atrial tissue of mice was detected using immunohistochemistry (200×). ( B ) The CRIF1 mRNA levels in the atrial tissue were detected by RT-qPCR. The mice cardiac muscle cell line HL-1 was treated with Ang II (0, 0.1, 0.2, 0.5, 1 and 2 μM) for 24 h. ( C ) The CRIF1 mRNA expression was determined by RT-qPCR. Data are presented as mean ± SD (n=8 mice in each group). t -test was applied. ***P<0.001 vs control group.

Techniques Used: Staining, Expressing, Immunohistochemistry, Quantitative RT-PCR, Control

Overexpression of CRIF1 activates the SIRT1/eNOS pathway in cardiomyocytes treated with Ang II. HL-1 cells were transfected with pcDNA3.1-CRIF1 (OE-CRIF1) or vector for 24 h, and then treated with Ang II (1 μM) for an additional 24 h. The mRNA expression levels of ( A ) CRIF1, ( B ) SIRT1 and ( C ) eNOS were evaluated using RT-qPCR. HL-1 cells were transfected with pcDNA3.1-CRIF1 (OE-CRIF1) or vector for 24 h, and were then cotreated with a SIRT1 inhibitor EX527 (10 μM) and Ang II (1 μM) for further 24 h. ( D ) The cell apoptosis was assessed by staining with TUNEL and DAPI, and observed under a fluorescence microscope (200 X). ( E ) Apoptosis was quantified by calculating TUNEL positive cells (normalized to DAPI-stained cells). Data are presented as mean ± SD in triplicates. ***P<0.001 vs control group; ### P<0.001 vs Ang II+Vector group; $$$ P<0.001 vs OE-CRIF1 group.
Figure Legend Snippet: Overexpression of CRIF1 activates the SIRT1/eNOS pathway in cardiomyocytes treated with Ang II. HL-1 cells were transfected with pcDNA3.1-CRIF1 (OE-CRIF1) or vector for 24 h, and then treated with Ang II (1 μM) for an additional 24 h. The mRNA expression levels of ( A ) CRIF1, ( B ) SIRT1 and ( C ) eNOS were evaluated using RT-qPCR. HL-1 cells were transfected with pcDNA3.1-CRIF1 (OE-CRIF1) or vector for 24 h, and were then cotreated with a SIRT1 inhibitor EX527 (10 μM) and Ang II (1 μM) for further 24 h. ( D ) The cell apoptosis was assessed by staining with TUNEL and DAPI, and observed under a fluorescence microscope (200 X). ( E ) Apoptosis was quantified by calculating TUNEL positive cells (normalized to DAPI-stained cells). Data are presented as mean ± SD in triplicates. ***P<0.001 vs control group; ### P<0.001 vs Ang II+Vector group; $$$ P<0.001 vs OE-CRIF1 group.

Techniques Used: Over Expression, Transfection, Plasmid Preparation, Expressing, Quantitative RT-PCR, Staining, TUNEL Assay, Fluorescence, Microscopy, Control

CRIF1 overexpression inhibits Ang II–induced hypertrophy of HL-1 cells. ( A ) Cells were stained with α-actinin antibody and observed under a fluorescence microscope. Representative images are shown (200×). RT-qPCR was used to assess the mRNA expression levels of hypertrophy-related genes, including ( B ) ANP, ( C ) BNP, and ( D ) β-MHC. Data are presented as mean ± SD in triplicate. ***P<0.001 vs control group; ### P<0.001 vs Ang II+Vector group; $$$ P<0.001 vs OE-CRIF1 group.
Figure Legend Snippet: CRIF1 overexpression inhibits Ang II–induced hypertrophy of HL-1 cells. ( A ) Cells were stained with α-actinin antibody and observed under a fluorescence microscope. Representative images are shown (200×). RT-qPCR was used to assess the mRNA expression levels of hypertrophy-related genes, including ( B ) ANP, ( C ) BNP, and ( D ) β-MHC. Data are presented as mean ± SD in triplicate. ***P<0.001 vs control group; ### P<0.001 vs Ang II+Vector group; $$$ P<0.001 vs OE-CRIF1 group.

Techniques Used: Over Expression, Staining, Fluorescence, Microscopy, Quantitative RT-PCR, Expressing, Control, Plasmid Preparation

CRIF1 overexpression suppresses Ang II–induced inflammation in cardiomyocytes. ( A – C ) RT-qPCR was used to determine the mRNA levels of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6. ( D – F ) ELISA was used to measure the levels of TNF-α, IL-1β, and IL-6 in the culture medium of HL-1 cells. Data are presented as mean ± SD in triplicate. ***P<0.001 vs control group; ### P<0.001 vs Ang II+Vector group; $$$ P<0.001 vs OE-CRIF1 group.
Figure Legend Snippet: CRIF1 overexpression suppresses Ang II–induced inflammation in cardiomyocytes. ( A – C ) RT-qPCR was used to determine the mRNA levels of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6. ( D – F ) ELISA was used to measure the levels of TNF-α, IL-1β, and IL-6 in the culture medium of HL-1 cells. Data are presented as mean ± SD in triplicate. ***P<0.001 vs control group; ### P<0.001 vs Ang II+Vector group; $$$ P<0.001 vs OE-CRIF1 group.

Techniques Used: Over Expression, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Control, Plasmid Preparation

Overexpression of CRIF1 inhibits intracellular ROS generation and oxidative stress in cardiomyocytes treated with Ang II. ( A ) Cells were stained with DHE, and representative images of intracellular ROS are shown (200×). ( B ) The extent of intracellular ROS was quantified by counting DHE-positive cells (normalized to DAPI-stained cells). Cell lysates of HL-1 cells were used to detect the oxidative stress markers: ( C ) MDA, ( D ) SOD, ( E ) CAT, and ( F ) NO. Data are presented as mean ± SD in triplicate. ***P<0.001 vs control group; ### P<0.001 vs Ang II+Vector group; $$$ P<0.001 vs OE-CRIF1 group.
Figure Legend Snippet: Overexpression of CRIF1 inhibits intracellular ROS generation and oxidative stress in cardiomyocytes treated with Ang II. ( A ) Cells were stained with DHE, and representative images of intracellular ROS are shown (200×). ( B ) The extent of intracellular ROS was quantified by counting DHE-positive cells (normalized to DAPI-stained cells). Cell lysates of HL-1 cells were used to detect the oxidative stress markers: ( C ) MDA, ( D ) SOD, ( E ) CAT, and ( F ) NO. Data are presented as mean ± SD in triplicate. ***P<0.001 vs control group; ### P<0.001 vs Ang II+Vector group; $$$ P<0.001 vs OE-CRIF1 group.

Techniques Used: Over Expression, Staining, Control, Plasmid Preparation



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CRIF1 was downregulated in the AF mice. ( A ) Atrial tissue of mice was stained with hematoxylin and eosin (H&E) to display the morphological structure. CRIF1 expression in the atrial tissue of mice was detected using immunohistochemistry (200×). ( B ) The CRIF1 mRNA levels in the atrial tissue were detected by RT-qPCR. The mice cardiac muscle cell line HL-1 was treated with Ang II (0, 0.1, 0.2, 0.5, 1 and 2 μM) for 24 h. ( C ) The CRIF1 mRNA expression was determined by RT-qPCR. Data are presented as mean ± SD (n=8 mice in each group). t -test was applied. ***P<0.001 vs control group.

Journal: Journal of Inflammation Research

Article Title: Protective Effects of CR6-Interacting Factor 1 Against Angiotensin II-Induced Atrial Fibrillation by Regulating the SIRT1/eNOS Signaling Pathway and Cardiomyocyte Remodeling

doi: 10.2147/JIR.S596132

Figure Lengend Snippet: CRIF1 was downregulated in the AF mice. ( A ) Atrial tissue of mice was stained with hematoxylin and eosin (H&E) to display the morphological structure. CRIF1 expression in the atrial tissue of mice was detected using immunohistochemistry (200×). ( B ) The CRIF1 mRNA levels in the atrial tissue were detected by RT-qPCR. The mice cardiac muscle cell line HL-1 was treated with Ang II (0, 0.1, 0.2, 0.5, 1 and 2 μM) for 24 h. ( C ) The CRIF1 mRNA expression was determined by RT-qPCR. Data are presented as mean ± SD (n=8 mice in each group). t -test was applied. ***P<0.001 vs control group.

Article Snippet: The mouse cardiac muscle cell line HL-1 was purchased from Procell (CL-0605, China).

Techniques: Staining, Expressing, Immunohistochemistry, Quantitative RT-PCR, Control

Overexpression of CRIF1 activates the SIRT1/eNOS pathway in cardiomyocytes treated with Ang II. HL-1 cells were transfected with pcDNA3.1-CRIF1 (OE-CRIF1) or vector for 24 h, and then treated with Ang II (1 μM) for an additional 24 h. The mRNA expression levels of ( A ) CRIF1, ( B ) SIRT1 and ( C ) eNOS were evaluated using RT-qPCR. HL-1 cells were transfected with pcDNA3.1-CRIF1 (OE-CRIF1) or vector for 24 h, and were then cotreated with a SIRT1 inhibitor EX527 (10 μM) and Ang II (1 μM) for further 24 h. ( D ) The cell apoptosis was assessed by staining with TUNEL and DAPI, and observed under a fluorescence microscope (200 X). ( E ) Apoptosis was quantified by calculating TUNEL positive cells (normalized to DAPI-stained cells). Data are presented as mean ± SD in triplicates. ***P<0.001 vs control group; ### P<0.001 vs Ang II+Vector group; $$$ P<0.001 vs OE-CRIF1 group.

Journal: Journal of Inflammation Research

Article Title: Protective Effects of CR6-Interacting Factor 1 Against Angiotensin II-Induced Atrial Fibrillation by Regulating the SIRT1/eNOS Signaling Pathway and Cardiomyocyte Remodeling

doi: 10.2147/JIR.S596132

Figure Lengend Snippet: Overexpression of CRIF1 activates the SIRT1/eNOS pathway in cardiomyocytes treated with Ang II. HL-1 cells were transfected with pcDNA3.1-CRIF1 (OE-CRIF1) or vector for 24 h, and then treated with Ang II (1 μM) for an additional 24 h. The mRNA expression levels of ( A ) CRIF1, ( B ) SIRT1 and ( C ) eNOS were evaluated using RT-qPCR. HL-1 cells were transfected with pcDNA3.1-CRIF1 (OE-CRIF1) or vector for 24 h, and were then cotreated with a SIRT1 inhibitor EX527 (10 μM) and Ang II (1 μM) for further 24 h. ( D ) The cell apoptosis was assessed by staining with TUNEL and DAPI, and observed under a fluorescence microscope (200 X). ( E ) Apoptosis was quantified by calculating TUNEL positive cells (normalized to DAPI-stained cells). Data are presented as mean ± SD in triplicates. ***P<0.001 vs control group; ### P<0.001 vs Ang II+Vector group; $$$ P<0.001 vs OE-CRIF1 group.

Article Snippet: The mouse cardiac muscle cell line HL-1 was purchased from Procell (CL-0605, China).

Techniques: Over Expression, Transfection, Plasmid Preparation, Expressing, Quantitative RT-PCR, Staining, TUNEL Assay, Fluorescence, Microscopy, Control

CRIF1 overexpression inhibits Ang II–induced hypertrophy of HL-1 cells. ( A ) Cells were stained with α-actinin antibody and observed under a fluorescence microscope. Representative images are shown (200×). RT-qPCR was used to assess the mRNA expression levels of hypertrophy-related genes, including ( B ) ANP, ( C ) BNP, and ( D ) β-MHC. Data are presented as mean ± SD in triplicate. ***P<0.001 vs control group; ### P<0.001 vs Ang II+Vector group; $$$ P<0.001 vs OE-CRIF1 group.

Journal: Journal of Inflammation Research

Article Title: Protective Effects of CR6-Interacting Factor 1 Against Angiotensin II-Induced Atrial Fibrillation by Regulating the SIRT1/eNOS Signaling Pathway and Cardiomyocyte Remodeling

doi: 10.2147/JIR.S596132

Figure Lengend Snippet: CRIF1 overexpression inhibits Ang II–induced hypertrophy of HL-1 cells. ( A ) Cells were stained with α-actinin antibody and observed under a fluorescence microscope. Representative images are shown (200×). RT-qPCR was used to assess the mRNA expression levels of hypertrophy-related genes, including ( B ) ANP, ( C ) BNP, and ( D ) β-MHC. Data are presented as mean ± SD in triplicate. ***P<0.001 vs control group; ### P<0.001 vs Ang II+Vector group; $$$ P<0.001 vs OE-CRIF1 group.

Article Snippet: The mouse cardiac muscle cell line HL-1 was purchased from Procell (CL-0605, China).

Techniques: Over Expression, Staining, Fluorescence, Microscopy, Quantitative RT-PCR, Expressing, Control, Plasmid Preparation

CRIF1 overexpression suppresses Ang II–induced inflammation in cardiomyocytes. ( A – C ) RT-qPCR was used to determine the mRNA levels of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6. ( D – F ) ELISA was used to measure the levels of TNF-α, IL-1β, and IL-6 in the culture medium of HL-1 cells. Data are presented as mean ± SD in triplicate. ***P<0.001 vs control group; ### P<0.001 vs Ang II+Vector group; $$$ P<0.001 vs OE-CRIF1 group.

Journal: Journal of Inflammation Research

Article Title: Protective Effects of CR6-Interacting Factor 1 Against Angiotensin II-Induced Atrial Fibrillation by Regulating the SIRT1/eNOS Signaling Pathway and Cardiomyocyte Remodeling

doi: 10.2147/JIR.S596132

Figure Lengend Snippet: CRIF1 overexpression suppresses Ang II–induced inflammation in cardiomyocytes. ( A – C ) RT-qPCR was used to determine the mRNA levels of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6. ( D – F ) ELISA was used to measure the levels of TNF-α, IL-1β, and IL-6 in the culture medium of HL-1 cells. Data are presented as mean ± SD in triplicate. ***P<0.001 vs control group; ### P<0.001 vs Ang II+Vector group; $$$ P<0.001 vs OE-CRIF1 group.

Article Snippet: The mouse cardiac muscle cell line HL-1 was purchased from Procell (CL-0605, China).

Techniques: Over Expression, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Control, Plasmid Preparation

Overexpression of CRIF1 inhibits intracellular ROS generation and oxidative stress in cardiomyocytes treated with Ang II. ( A ) Cells were stained with DHE, and representative images of intracellular ROS are shown (200×). ( B ) The extent of intracellular ROS was quantified by counting DHE-positive cells (normalized to DAPI-stained cells). Cell lysates of HL-1 cells were used to detect the oxidative stress markers: ( C ) MDA, ( D ) SOD, ( E ) CAT, and ( F ) NO. Data are presented as mean ± SD in triplicate. ***P<0.001 vs control group; ### P<0.001 vs Ang II+Vector group; $$$ P<0.001 vs OE-CRIF1 group.

Journal: Journal of Inflammation Research

Article Title: Protective Effects of CR6-Interacting Factor 1 Against Angiotensin II-Induced Atrial Fibrillation by Regulating the SIRT1/eNOS Signaling Pathway and Cardiomyocyte Remodeling

doi: 10.2147/JIR.S596132

Figure Lengend Snippet: Overexpression of CRIF1 inhibits intracellular ROS generation and oxidative stress in cardiomyocytes treated with Ang II. ( A ) Cells were stained with DHE, and representative images of intracellular ROS are shown (200×). ( B ) The extent of intracellular ROS was quantified by counting DHE-positive cells (normalized to DAPI-stained cells). Cell lysates of HL-1 cells were used to detect the oxidative stress markers: ( C ) MDA, ( D ) SOD, ( E ) CAT, and ( F ) NO. Data are presented as mean ± SD in triplicate. ***P<0.001 vs control group; ### P<0.001 vs Ang II+Vector group; $$$ P<0.001 vs OE-CRIF1 group.

Article Snippet: The mouse cardiac muscle cell line HL-1 was purchased from Procell (CL-0605, China).

Techniques: Over Expression, Staining, Control, Plasmid Preparation