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mouse primary proximal renal tubular epithelial cells  (Cell Biologics Inc)

 
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    Cell Biologics Inc mouse primary proximal renal tubular epithelial cells
    Mouse Primary Proximal Renal Tubular Epithelial Cells, supplied by Cell Biologics Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+primary+proximal+renal+tubular+epithelial+cells/mouse+primary+proximal+renal+tubular+epithelial+cells/pm37179213-54-0-10
    Average 90 stars, based on 1 article reviews
    mouse primary proximal renal tubular epithelial cells - by Bioz Stars, 2026-09
    90/100 stars

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    Article Title: MircoRNA-322-5p promotes lipopolysaccharide-induced acute kidney injury mouse models and mouse primary proximal renal tubular epithelial cell injury by regulating T-box transcription factor 21/mitogen-activated protein kinase/extracellular signal-related kinase axis
    Article Snippet: Mouse primary proximal renal tubular epithelial cells were procured from Cell Biologics, Inc.



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    Cell Biologics Inc mouse primary proximal renal tubular epithelial cells
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    Cell Biologics Inc mouse proximal renal tubular epithelial primary cells
    Effect of GSK′872 on renal function and pathological changes in LPS-induced acute kidney injury. C57BL/6 mice were randomly divided into three groups (n=6). Mice in the LPS group were treated with LPS intraperitoneally (10 mg/kg) for 24 h. Mice in the GKS′872 group were intraperitoneally injected with the RIPK3 inhibitor GSK′872 (5 µM/kg) for 30 min prior to LPS exposure. (A) Serum BUN and creatinine were determined in the three groups. (B) Representative images of periodic acid-Schiff-stained kidney sections. Magnification, ×200 (inset, magnification, ×400). The red arrows indicate vacuolar deformation and swelling of renal tubular <t>epithelial</t> cells. (C) Quantification of tubular injury. The percentage of injured renal tubules was determined for each animal by histology scoring as described in the materials and methods section. (D) Electron microscopy of mitochondria in mouse renal tubular epithelial cells (magnification ×10,000). The red arrows point to swelling and deformation of mitochondria. *P<0.01 vs. CON; # P<0.01 vs. LPS. BUN, blood urea nitrogen; CON, control; LPS, lipopolysaccharide.
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    https://www.bioz.com/product/mouse+primary+proximal+renal+tubular+epithelial+cells/mouse+primary+proximal+renal+tubular+epithelial+cells/pmc06625383-76-0-10
    Average 90 stars, based on 1 article reviews
    mouse proximal renal tubular epithelial primary cells - by Bioz Stars, 2026-09
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    Effect of GSK′872 on renal function and pathological changes in LPS-induced acute kidney injury. C57BL/6 mice were randomly divided into three groups (n=6). Mice in the LPS group were treated with LPS intraperitoneally (10 mg/kg) for 24 h. Mice in the GKS′872 group were intraperitoneally injected with the RIPK3 inhibitor GSK′872 (5 µM/kg) for 30 min prior to LPS exposure. (A) Serum BUN and creatinine were determined in the three groups. (B) Representative images of periodic acid-Schiff-stained kidney sections. Magnification, ×200 (inset, magnification, ×400). The red arrows indicate vacuolar deformation and swelling of renal tubular epithelial cells. (C) Quantification of tubular injury. The percentage of injured renal tubules was determined for each animal by histology scoring as described in the materials and methods section. (D) Electron microscopy of mitochondria in mouse renal tubular epithelial cells (magnification ×10,000). The red arrows point to swelling and deformation of mitochondria. *P<0.01 vs. CON; # P<0.01 vs. LPS. BUN, blood urea nitrogen; CON, control; LPS, lipopolysaccharide.

    Journal: Molecular Medicine Reports

    Article Title: RIPK3 mediates renal tubular epithelial cell apoptosis in endotoxin-induced acute kidney injury

    doi: 10.3892/mmr.2019.10416

    Figure Lengend Snippet: Effect of GSK′872 on renal function and pathological changes in LPS-induced acute kidney injury. C57BL/6 mice were randomly divided into three groups (n=6). Mice in the LPS group were treated with LPS intraperitoneally (10 mg/kg) for 24 h. Mice in the GKS′872 group were intraperitoneally injected with the RIPK3 inhibitor GSK′872 (5 µM/kg) for 30 min prior to LPS exposure. (A) Serum BUN and creatinine were determined in the three groups. (B) Representative images of periodic acid-Schiff-stained kidney sections. Magnification, ×200 (inset, magnification, ×400). The red arrows indicate vacuolar deformation and swelling of renal tubular epithelial cells. (C) Quantification of tubular injury. The percentage of injured renal tubules was determined for each animal by histology scoring as described in the materials and methods section. (D) Electron microscopy of mitochondria in mouse renal tubular epithelial cells (magnification ×10,000). The red arrows point to swelling and deformation of mitochondria. *P<0.01 vs. CON; # P<0.01 vs. LPS. BUN, blood urea nitrogen; CON, control; LPS, lipopolysaccharide.

    Article Snippet: Mouse proximal renal tubular epithelial primary cells were purchased from Cell Biologics, Inc.

    Techniques: Injection, Staining, Electron Microscopy, Control

    LPS increases the expression of RIPK3 in renal tubular epithelial cells in a time-dependent manner. (A) RIPK3 mRNA expression in renal tubular epithelial cells stimulated with 40 µg/ml LPS for 6, 12, 24 or 48 h. (B) RIPK3 protein expression in renal tubular epithelial cells treated with LPS for 6, 12, 24 or 48 h. (C) Quantification of RIPK3 protein expression. *P<0.01 vs. respective CON. RIPK3, receptor-interacting protein kinase 3; CON, control; LPS, lipopolysaccharide.

    Journal: Molecular Medicine Reports

    Article Title: RIPK3 mediates renal tubular epithelial cell apoptosis in endotoxin-induced acute kidney injury

    doi: 10.3892/mmr.2019.10416

    Figure Lengend Snippet: LPS increases the expression of RIPK3 in renal tubular epithelial cells in a time-dependent manner. (A) RIPK3 mRNA expression in renal tubular epithelial cells stimulated with 40 µg/ml LPS for 6, 12, 24 or 48 h. (B) RIPK3 protein expression in renal tubular epithelial cells treated with LPS for 6, 12, 24 or 48 h. (C) Quantification of RIPK3 protein expression. *P<0.01 vs. respective CON. RIPK3, receptor-interacting protein kinase 3; CON, control; LPS, lipopolysaccharide.

    Article Snippet: Mouse proximal renal tubular epithelial primary cells were purchased from Cell Biologics, Inc.

    Techniques: Expressing, Control

    siRNA targeting RIPK3 and the RIPK3 inhibitor GSK′872 reduce the levels of apoptosis in renal tubular epithelial cells following LPS stimulation. Mouse proximal renal tubular epithelial cells in the LPS group were stimulated with 40 µg/ml LPS for 24 h. The RIPK3 kinase inhibitor GSK′872 was added to cells 1 h prior to LPS stimulation in the LPS + GSK′872 group. The LPS + RIPK3-siRNA group was transfected with 5 nM RIPK3-siRNA prior to LPS stimulation. The control group was treated with an equal volume of DMSO. (A) Levels of apoptosis were determined using flow cytometry. (B) Quantification of tubular epithelial cell apoptosis. (C) Western blot analysis for the expression of Bax in cultured tubular epithelial cells that have undergone different treatments. (D) Western blotting for the expression of C-caspase-3 and full-length Caspase-3 in different groups. C-caspase-3 and full-length caspase-3 were from different membrane. (E) The expression level of RIPK3 in siRNA-transfected renal tubular epithelial cells. *P<0.01 vs. CON; # P<0.01 vs. LPS. PI, propidium iodide; CON, control; LPS, lipopolysaccharide; RIPK3, receptor-interacting protein kinase 3; siRNA, small interfering RNA; siNC, negative control siRNA; C-caspase-3, cleaved caspase-3.

    Journal: Molecular Medicine Reports

    Article Title: RIPK3 mediates renal tubular epithelial cell apoptosis in endotoxin-induced acute kidney injury

    doi: 10.3892/mmr.2019.10416

    Figure Lengend Snippet: siRNA targeting RIPK3 and the RIPK3 inhibitor GSK′872 reduce the levels of apoptosis in renal tubular epithelial cells following LPS stimulation. Mouse proximal renal tubular epithelial cells in the LPS group were stimulated with 40 µg/ml LPS for 24 h. The RIPK3 kinase inhibitor GSK′872 was added to cells 1 h prior to LPS stimulation in the LPS + GSK′872 group. The LPS + RIPK3-siRNA group was transfected with 5 nM RIPK3-siRNA prior to LPS stimulation. The control group was treated with an equal volume of DMSO. (A) Levels of apoptosis were determined using flow cytometry. (B) Quantification of tubular epithelial cell apoptosis. (C) Western blot analysis for the expression of Bax in cultured tubular epithelial cells that have undergone different treatments. (D) Western blotting for the expression of C-caspase-3 and full-length Caspase-3 in different groups. C-caspase-3 and full-length caspase-3 were from different membrane. (E) The expression level of RIPK3 in siRNA-transfected renal tubular epithelial cells. *P<0.01 vs. CON; # P<0.01 vs. LPS. PI, propidium iodide; CON, control; LPS, lipopolysaccharide; RIPK3, receptor-interacting protein kinase 3; siRNA, small interfering RNA; siNC, negative control siRNA; C-caspase-3, cleaved caspase-3.

    Article Snippet: Mouse proximal renal tubular epithelial primary cells were purchased from Cell Biologics, Inc.

    Techniques: Transfection, Control, Flow Cytometry, Western Blot, Expressing, Cell Culture, Membrane, Small Interfering RNA, Negative Control