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renal proximal tubular epithelial cell line  (ATCC)


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    ATCC renal proximal tubular epithelial cell line
    Renal Proximal Tubular Epithelial Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 743 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+renal+tubular+epithelial+cell+lines/pm41811824-56-13-25?v=ATCC
    Average 99 stars, based on 743 article reviews
    renal proximal tubular epithelial cell line - by Bioz Stars, 2026-07
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    Schematic illustration of the construction of BPQD@Fer-1 nanoparticles and their application in alleviating TCMR in kidney transplantation. Top panel: Synthesis of black phosphorus quantum dots loaded with Ferrostatin-1 (BPQD@Fer-1) via liquid-phase exfoliation of bulk BP in NMP. The nanoparticles exhibit intrinsic ROS-scavenging capabilities by neutralizing free radicals (e.g., ⋅O 2 −and ⋅OH) through electron (e − ) transfer. Middle panel: In vivo application in a murine kidney transplantation model. Donor kidneys are subjected to cold ischemia and subsequently transplanted. Intravenously administered BPQD@Fer-1 selectively accumulate in the tubular <t>epithelial</t> cells of the kidney allograft. Bottom panel: Intracellular mechanisms and immune microenvironment remodeling. (Left, TCMR group): Severe oxidative stress upregulates intracellular ROS and lipid peroxidation (LPO), triggering ferroptosis in tubular epithelial cells. This leads to the massive release of damage-associated molecular patterns (DAMPs), including high mobility group box 1 (HMGB1), calreticulin (CRT), lactate dehydrogenase (LDH), and adenosine triphosphate (ATP), which subsequently recruit and activate CD8 + T cells, resulting in the upregulation of cytotoxic and pro-inflammatory cytokines (GzmB, IL-2, TNF-α, and IFN-γ). (Right, BPQD@Fer-1 group): The nanoparticles efficiently scavenge ROS, suppress LPO, and block the ferroptotic cascade. The consequent inhibition of DAMPs release restricts CD8 + T cell-mediated cytotoxicity and downregulates the inflammatory cytokine storm, ultimately preserving the kidney allograft.
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    Procell Inc human normal renal tubular epithelial cell line hk 2
    Schematic illustration of the construction of BPQD@Fer-1 nanoparticles and their application in alleviating TCMR in kidney transplantation. Top panel: Synthesis of black phosphorus quantum dots loaded with Ferrostatin-1 (BPQD@Fer-1) via liquid-phase exfoliation of bulk BP in NMP. The nanoparticles exhibit intrinsic ROS-scavenging capabilities by neutralizing free radicals (e.g., ⋅O 2 −and ⋅OH) through electron (e − ) transfer. Middle panel: In vivo application in a murine kidney transplantation model. Donor kidneys are subjected to cold ischemia and subsequently transplanted. Intravenously administered BPQD@Fer-1 selectively accumulate in the tubular <t>epithelial</t> cells of the kidney allograft. Bottom panel: Intracellular mechanisms and immune microenvironment remodeling. (Left, TCMR group): Severe oxidative stress upregulates intracellular ROS and lipid peroxidation (LPO), triggering ferroptosis in tubular epithelial cells. This leads to the massive release of damage-associated molecular patterns (DAMPs), including high mobility group box 1 (HMGB1), calreticulin (CRT), lactate dehydrogenase (LDH), and adenosine triphosphate (ATP), which subsequently recruit and activate CD8 + T cells, resulting in the upregulation of cytotoxic and pro-inflammatory cytokines (GzmB, IL-2, TNF-α, and IFN-γ). (Right, BPQD@Fer-1 group): The nanoparticles efficiently scavenge ROS, suppress LPO, and block the ferroptotic cascade. The consequent inhibition of DAMPs release restricts CD8 + T cell-mediated cytotoxicity and downregulates the inflammatory cytokine storm, ultimately preserving the kidney allograft.
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    ATCC human renal proximal tubular epithelial cell line
    Schematic illustration of the construction of BPQD@Fer-1 nanoparticles and their application in alleviating TCMR in kidney transplantation. Top panel: Synthesis of black phosphorus quantum dots loaded with Ferrostatin-1 (BPQD@Fer-1) via liquid-phase exfoliation of bulk BP in NMP. The nanoparticles exhibit intrinsic ROS-scavenging capabilities by neutralizing free radicals (e.g., ⋅O 2 −and ⋅OH) through electron (e − ) transfer. Middle panel: In vivo application in a murine kidney transplantation model. Donor kidneys are subjected to cold ischemia and subsequently transplanted. Intravenously administered BPQD@Fer-1 selectively accumulate in the tubular <t>epithelial</t> cells of the kidney allograft. Bottom panel: Intracellular mechanisms and immune microenvironment remodeling. (Left, TCMR group): Severe oxidative stress upregulates intracellular ROS and lipid peroxidation (LPO), triggering ferroptosis in tubular epithelial cells. This leads to the massive release of damage-associated molecular patterns (DAMPs), including high mobility group box 1 (HMGB1), calreticulin (CRT), lactate dehydrogenase (LDH), and adenosine triphosphate (ATP), which subsequently recruit and activate CD8 + T cells, resulting in the upregulation of cytotoxic and pro-inflammatory cytokines (GzmB, IL-2, TNF-α, and IFN-γ). (Right, BPQD@Fer-1 group): The nanoparticles efficiently scavenge ROS, suppress LPO, and block the ferroptotic cascade. The consequent inhibition of DAMPs release restricts CD8 + T cell-mediated cytotoxicity and downregulates the inflammatory cytokine storm, ultimately preserving the kidney allograft.
    Human Renal Proximal Tubular Epithelial Cell Line, supplied by ATCC, 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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    ATCC human renal tubular epithelial cell line hk 2 cells
    The therapeutic effects of MSCs in CKD. A Images of H&E staining (scale bar = 100 μm), Masson staining (scale bar = 100 μm), and TEM observation (scale bar = 2 μm) of renal tissue from the Control group, CKD group, and Treatment group, as well as bar charts of the tubular damage score and degree of renal interstitial fibrosis. <t>(B-D)</t> <t>HK-2</t> cells were treated with TGF-β1 and MSCs: Western blotting detection of fibronectin, α- SMA, Col3a1, Col1a1, Col1a2, E-cadherin. * p < 0.05, ** p < 0.01, *** p < 0.001
    Human Renal Tubular Epithelial Cell Line Hk 2 Cells, supplied by ATCC, 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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    ATCC human renal tubular epithelial cell lines
    The therapeutic effects of MSCs in CKD. A Images of H&E staining (scale bar = 100 μm), Masson staining (scale bar = 100 μm), and TEM observation (scale bar = 2 μm) of renal tissue from the Control group, CKD group, and Treatment group, as well as bar charts of the tubular damage score and degree of renal interstitial fibrosis. <t>(B-D)</t> <t>HK-2</t> cells were treated with TGF-β1 and MSCs: Western blotting detection of fibronectin, α- SMA, Col3a1, Col1a1, Col1a2, E-cadherin. * p < 0.05, ** p < 0.01, *** p < 0.001
    Human Renal Tubular Epithelial Cell Lines, supplied by ATCC, 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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    ATCC human renal proximal tubular epithelial cell line hk 2
    The therapeutic effects of MSCs in CKD. A Images of H&E staining (scale bar = 100 μm), Masson staining (scale bar = 100 μm), and TEM observation (scale bar = 2 μm) of renal tissue from the Control group, CKD group, and Treatment group, as well as bar charts of the tubular damage score and degree of renal interstitial fibrosis. <t>(B-D)</t> <t>HK-2</t> cells were treated with TGF-β1 and MSCs: Western blotting detection of fibronectin, α- SMA, Col3a1, Col1a1, Col1a2, E-cadherin. * p < 0.05, ** p < 0.01, *** p < 0.001
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    Image Search Results


    Schematic illustration of the construction of BPQD@Fer-1 nanoparticles and their application in alleviating TCMR in kidney transplantation. Top panel: Synthesis of black phosphorus quantum dots loaded with Ferrostatin-1 (BPQD@Fer-1) via liquid-phase exfoliation of bulk BP in NMP. The nanoparticles exhibit intrinsic ROS-scavenging capabilities by neutralizing free radicals (e.g., ⋅O 2 −and ⋅OH) through electron (e − ) transfer. Middle panel: In vivo application in a murine kidney transplantation model. Donor kidneys are subjected to cold ischemia and subsequently transplanted. Intravenously administered BPQD@Fer-1 selectively accumulate in the tubular epithelial cells of the kidney allograft. Bottom panel: Intracellular mechanisms and immune microenvironment remodeling. (Left, TCMR group): Severe oxidative stress upregulates intracellular ROS and lipid peroxidation (LPO), triggering ferroptosis in tubular epithelial cells. This leads to the massive release of damage-associated molecular patterns (DAMPs), including high mobility group box 1 (HMGB1), calreticulin (CRT), lactate dehydrogenase (LDH), and adenosine triphosphate (ATP), which subsequently recruit and activate CD8 + T cells, resulting in the upregulation of cytotoxic and pro-inflammatory cytokines (GzmB, IL-2, TNF-α, and IFN-γ). (Right, BPQD@Fer-1 group): The nanoparticles efficiently scavenge ROS, suppress LPO, and block the ferroptotic cascade. The consequent inhibition of DAMPs release restricts CD8 + T cell-mediated cytotoxicity and downregulates the inflammatory cytokine storm, ultimately preserving the kidney allograft.

    Journal: Materials Today Bio

    Article Title: Ferrostatin-1-loaded black phosphorus quantum dots (BPQD@Fer-1) nanodelivery system attenuates T cell-mediated rejection after kidney transplantation

    doi: 10.1016/j.mtbio.2026.103292

    Figure Lengend Snippet: Schematic illustration of the construction of BPQD@Fer-1 nanoparticles and their application in alleviating TCMR in kidney transplantation. Top panel: Synthesis of black phosphorus quantum dots loaded with Ferrostatin-1 (BPQD@Fer-1) via liquid-phase exfoliation of bulk BP in NMP. The nanoparticles exhibit intrinsic ROS-scavenging capabilities by neutralizing free radicals (e.g., ⋅O 2 −and ⋅OH) through electron (e − ) transfer. Middle panel: In vivo application in a murine kidney transplantation model. Donor kidneys are subjected to cold ischemia and subsequently transplanted. Intravenously administered BPQD@Fer-1 selectively accumulate in the tubular epithelial cells of the kidney allograft. Bottom panel: Intracellular mechanisms and immune microenvironment remodeling. (Left, TCMR group): Severe oxidative stress upregulates intracellular ROS and lipid peroxidation (LPO), triggering ferroptosis in tubular epithelial cells. This leads to the massive release of damage-associated molecular patterns (DAMPs), including high mobility group box 1 (HMGB1), calreticulin (CRT), lactate dehydrogenase (LDH), and adenosine triphosphate (ATP), which subsequently recruit and activate CD8 + T cells, resulting in the upregulation of cytotoxic and pro-inflammatory cytokines (GzmB, IL-2, TNF-α, and IFN-γ). (Right, BPQD@Fer-1 group): The nanoparticles efficiently scavenge ROS, suppress LPO, and block the ferroptotic cascade. The consequent inhibition of DAMPs release restricts CD8 + T cell-mediated cytotoxicity and downregulates the inflammatory cytokine storm, ultimately preserving the kidney allograft.

    Article Snippet: Human renal tubular epithelial cell line (HK-2) and rat renal tubular epithelial cell line (NRK52E) were purchased from Procell Life Science & Technology Co., Ltd. (Wuhan, China).

    Techniques: Transplantation Assay, In Vivo, Blocking Assay, Inhibition, Preserving

    Single-cell landscape reveals ferroptosis-associated epithelial states and enhanced T-cell activation in TCMR. (A) UMAP visualization of all single cells colored by sample origin (left panel) and cell cluster (right panel). (B) Dot plot showing the expression of canonical marker genes used for cell type annotation across major renal epithelial, immune, and stromal populations. Dot size represents the percentage of cells expressing each gene, and color intensity indicates scaled average expression. (C) UMAP plot annotated by cell type. (D) UMAP plots split by experimental condition (CTRL and TCMR), illustrating comparable global cellular architecture across conditions. (E) Boxplot showing ferroptosis module scores in epithelial cells from CTRL and TCMR groups. Each dot represents a single cell. (F) Ferroptosis scores across epithelial subtypes, including proximal tubule, thick ascending limb, collecting duct principal and intercalated cells, thin limb, and PEC subsets, stratified by condition (CTRL vs TCMR). (G) Heatmap showing average expression of ferroptosis-related genes across epithelial cell types and conditions. Expression values are scaled by gene to highlight relative differences. (H) Boxplot of DAMPs module scores in epithelial cells stratified by ferroptosis state (Ferro_High vs Ferro_Low). (I) Dot plot visualizing the expression profiles of DAMPs-associated genes in epithelial cells, stratified by their ferroptosis states. Dot diameter corresponds to the proportion of cells expressing the target gene, while the color gradient indicates the average expression intensity. (J) Boxplots delineating the variations in T-cell activation scores among the three defined ferroptosis subgroups (Ferro_High, Ferro_Med, and Ferro_Low). (K) Dot plot displaying the expression dynamics of T-cell-related markers across different ferroptosis cohorts. The cellular fraction expressing each gene is represented by dot size, with the mean expression level denoted by color scaling. (L) Boxplot showing cytotoxicity scores in T cells across ferroptosis groups.

    Journal: Materials Today Bio

    Article Title: Ferrostatin-1-loaded black phosphorus quantum dots (BPQD@Fer-1) nanodelivery system attenuates T cell-mediated rejection after kidney transplantation

    doi: 10.1016/j.mtbio.2026.103292

    Figure Lengend Snippet: Single-cell landscape reveals ferroptosis-associated epithelial states and enhanced T-cell activation in TCMR. (A) UMAP visualization of all single cells colored by sample origin (left panel) and cell cluster (right panel). (B) Dot plot showing the expression of canonical marker genes used for cell type annotation across major renal epithelial, immune, and stromal populations. Dot size represents the percentage of cells expressing each gene, and color intensity indicates scaled average expression. (C) UMAP plot annotated by cell type. (D) UMAP plots split by experimental condition (CTRL and TCMR), illustrating comparable global cellular architecture across conditions. (E) Boxplot showing ferroptosis module scores in epithelial cells from CTRL and TCMR groups. Each dot represents a single cell. (F) Ferroptosis scores across epithelial subtypes, including proximal tubule, thick ascending limb, collecting duct principal and intercalated cells, thin limb, and PEC subsets, stratified by condition (CTRL vs TCMR). (G) Heatmap showing average expression of ferroptosis-related genes across epithelial cell types and conditions. Expression values are scaled by gene to highlight relative differences. (H) Boxplot of DAMPs module scores in epithelial cells stratified by ferroptosis state (Ferro_High vs Ferro_Low). (I) Dot plot visualizing the expression profiles of DAMPs-associated genes in epithelial cells, stratified by their ferroptosis states. Dot diameter corresponds to the proportion of cells expressing the target gene, while the color gradient indicates the average expression intensity. (J) Boxplots delineating the variations in T-cell activation scores among the three defined ferroptosis subgroups (Ferro_High, Ferro_Med, and Ferro_Low). (K) Dot plot displaying the expression dynamics of T-cell-related markers across different ferroptosis cohorts. The cellular fraction expressing each gene is represented by dot size, with the mean expression level denoted by color scaling. (L) Boxplot showing cytotoxicity scores in T cells across ferroptosis groups.

    Article Snippet: Human renal tubular epithelial cell line (HK-2) and rat renal tubular epithelial cell line (NRK52E) were purchased from Procell Life Science & Technology Co., Ltd. (Wuhan, China).

    Techniques: Single Cell, Activation Assay, Expressing, Marker

    The therapeutic effects of MSCs in CKD. A Images of H&E staining (scale bar = 100 μm), Masson staining (scale bar = 100 μm), and TEM observation (scale bar = 2 μm) of renal tissue from the Control group, CKD group, and Treatment group, as well as bar charts of the tubular damage score and degree of renal interstitial fibrosis. (B-D) HK-2 cells were treated with TGF-β1 and MSCs: Western blotting detection of fibronectin, α- SMA, Col3a1, Col1a1, Col1a2, E-cadherin. * p < 0.05, ** p < 0.01, *** p < 0.001

    Journal: European Journal of Medical Research

    Article Title: Mechanism of ultrasound-guided renal parenchymal injection of MSCs for the treatment of chronic kidney disease: down-regulated SGK1 promotes M2 macrophage polarization

    doi: 10.1186/s40001-025-03724-8

    Figure Lengend Snippet: The therapeutic effects of MSCs in CKD. A Images of H&E staining (scale bar = 100 μm), Masson staining (scale bar = 100 μm), and TEM observation (scale bar = 2 μm) of renal tissue from the Control group, CKD group, and Treatment group, as well as bar charts of the tubular damage score and degree of renal interstitial fibrosis. (B-D) HK-2 cells were treated with TGF-β1 and MSCs: Western blotting detection of fibronectin, α- SMA, Col3a1, Col1a1, Col1a2, E-cadherin. * p < 0.05, ** p < 0.01, *** p < 0.001

    Article Snippet: Human umbilical cord MSCs (MEISEN, CTCC-159-HUM), human acute monocytic leukemia cell line THP-1 (MEISEN, CTCC-001-0044) and human renal tubular epithelial cell line HK-2 cells (ATCC, CRL-2190) were cultured in DMEM (Gibco, 11,965–092) with 10% fetal bovine serum (FBS; Gibco, 10,099–141) and 1% penicillin–streptomycin (Gibco, 15,140-122).

    Techniques: Staining, Control, Western Blot

    Bioinformatics analysis and Western blot confirm that SGK1 is a downstream target gene for MSCs in the treatment of renal fibrosis. A Correlation analysis revealed the values of 9 samples. B Volcano plot showing the DEGs in the CKD models relative to the controls, with red dots representing significantly upregulated genes and blue dots indicating downregulated genes. C , D GO enrichment analysis of these DEGs was performed to identify enriched molecular functions, biological processes, and cellular components. E Heatmap showing the DEGs asscociated with immune modulation. F Western blotting detection of the protein levels of SGK1, LTB4R2, SH2D1B, and MAP3K6 in rat renal tissues from the Control group, CKD group, and Treatment group. G Western blotting detection of the protein levels of SGK1, LTB4R2, SH2D1B, and MAP3K6 in HK-2 cells treated with TGF-β1 and MSCs. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Journal: European Journal of Medical Research

    Article Title: Mechanism of ultrasound-guided renal parenchymal injection of MSCs for the treatment of chronic kidney disease: down-regulated SGK1 promotes M2 macrophage polarization

    doi: 10.1186/s40001-025-03724-8

    Figure Lengend Snippet: Bioinformatics analysis and Western blot confirm that SGK1 is a downstream target gene for MSCs in the treatment of renal fibrosis. A Correlation analysis revealed the values of 9 samples. B Volcano plot showing the DEGs in the CKD models relative to the controls, with red dots representing significantly upregulated genes and blue dots indicating downregulated genes. C , D GO enrichment analysis of these DEGs was performed to identify enriched molecular functions, biological processes, and cellular components. E Heatmap showing the DEGs asscociated with immune modulation. F Western blotting detection of the protein levels of SGK1, LTB4R2, SH2D1B, and MAP3K6 in rat renal tissues from the Control group, CKD group, and Treatment group. G Western blotting detection of the protein levels of SGK1, LTB4R2, SH2D1B, and MAP3K6 in HK-2 cells treated with TGF-β1 and MSCs. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Article Snippet: Human umbilical cord MSCs (MEISEN, CTCC-159-HUM), human acute monocytic leukemia cell line THP-1 (MEISEN, CTCC-001-0044) and human renal tubular epithelial cell line HK-2 cells (ATCC, CRL-2190) were cultured in DMEM (Gibco, 11,965–092) with 10% fetal bovine serum (FBS; Gibco, 10,099–141) and 1% penicillin–streptomycin (Gibco, 15,140-122).

    Techniques: Western Blot, Control

    MSCs downregulated SGK1 and inactivated the NF-κB signaling pathway. A Top 20 pathways between the controls and CKD models enriched by KEGG. B Enrichment analysis of circular KEGG pathway. C , D Macrophages co-cultured with MSCs (Co-culture) or nothing (Control), and the SGK1 expression level was detected using western blotting and cell immunofluorescence techniques. E , F HK-2 cells were divided into four groups: Model (treated with 10 ng/mL TGF-β1 for 12 h), Co-culture (treated with 10 ng/mL TGF-β1 and MSCs for 12 h), Co-culture + OE-NC (transfected with blank overexpression vectors and treated with 10 ng/mL TGF-β1 and MSCs for 12 h), Co-culture + OE-SGK1 (transfected with SGK1 overexpression vectors and treated with 10 ng/mL TGF-β1 and MSCs for 12 h): The protein levels of SGK1 and NF-κB (phospho S536) detected by western blotting assay. ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Journal: European Journal of Medical Research

    Article Title: Mechanism of ultrasound-guided renal parenchymal injection of MSCs for the treatment of chronic kidney disease: down-regulated SGK1 promotes M2 macrophage polarization

    doi: 10.1186/s40001-025-03724-8

    Figure Lengend Snippet: MSCs downregulated SGK1 and inactivated the NF-κB signaling pathway. A Top 20 pathways between the controls and CKD models enriched by KEGG. B Enrichment analysis of circular KEGG pathway. C , D Macrophages co-cultured with MSCs (Co-culture) or nothing (Control), and the SGK1 expression level was detected using western blotting and cell immunofluorescence techniques. E , F HK-2 cells were divided into four groups: Model (treated with 10 ng/mL TGF-β1 for 12 h), Co-culture (treated with 10 ng/mL TGF-β1 and MSCs for 12 h), Co-culture + OE-NC (transfected with blank overexpression vectors and treated with 10 ng/mL TGF-β1 and MSCs for 12 h), Co-culture + OE-SGK1 (transfected with SGK1 overexpression vectors and treated with 10 ng/mL TGF-β1 and MSCs for 12 h): The protein levels of SGK1 and NF-κB (phospho S536) detected by western blotting assay. ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Article Snippet: Human umbilical cord MSCs (MEISEN, CTCC-159-HUM), human acute monocytic leukemia cell line THP-1 (MEISEN, CTCC-001-0044) and human renal tubular epithelial cell line HK-2 cells (ATCC, CRL-2190) were cultured in DMEM (Gibco, 11,965–092) with 10% fetal bovine serum (FBS; Gibco, 10,099–141) and 1% penicillin–streptomycin (Gibco, 15,140-122).

    Techniques: Cell Culture, Co-Culture Assay, Control, Expressing, Western Blot, Immunofluorescence, Transfection, Over Expression

    MSCs suppress macrophage M2 polarization and fibrosis in HK-2 cells by inhibiting the SGK1-NF-κB axis. (A-B) Macrophages or SGK1-overexpressing macrophages were co-cultured with MSCs in the presence or absence of the NF-κB inhibitor BAY 11-7085. A Western blot analysis of NF-κB (phospho S536) and SGK1 expression in macrophages. B Flow cytometry analysis of the proportions of CD86 + CD11b + (M1) and CD206 + CD11b + (M2) macrophages. C Supernatants from the aforementioned macrophages were co-cultured with a TGF-β-induced HK-2 cell model. Western blot was used to detect expression of the fibrosis markers α-SMA, fibronectin, and Col3a1. ns p > 0.05, ** p < 0.01,*** p < 0.001, and **** p < 0.0001

    Journal: European Journal of Medical Research

    Article Title: Mechanism of ultrasound-guided renal parenchymal injection of MSCs for the treatment of chronic kidney disease: down-regulated SGK1 promotes M2 macrophage polarization

    doi: 10.1186/s40001-025-03724-8

    Figure Lengend Snippet: MSCs suppress macrophage M2 polarization and fibrosis in HK-2 cells by inhibiting the SGK1-NF-κB axis. (A-B) Macrophages or SGK1-overexpressing macrophages were co-cultured with MSCs in the presence or absence of the NF-κB inhibitor BAY 11-7085. A Western blot analysis of NF-κB (phospho S536) and SGK1 expression in macrophages. B Flow cytometry analysis of the proportions of CD86 + CD11b + (M1) and CD206 + CD11b + (M2) macrophages. C Supernatants from the aforementioned macrophages were co-cultured with a TGF-β-induced HK-2 cell model. Western blot was used to detect expression of the fibrosis markers α-SMA, fibronectin, and Col3a1. ns p > 0.05, ** p < 0.01,*** p < 0.001, and **** p < 0.0001

    Article Snippet: Human umbilical cord MSCs (MEISEN, CTCC-159-HUM), human acute monocytic leukemia cell line THP-1 (MEISEN, CTCC-001-0044) and human renal tubular epithelial cell line HK-2 cells (ATCC, CRL-2190) were cultured in DMEM (Gibco, 11,965–092) with 10% fetal bovine serum (FBS; Gibco, 10,099–141) and 1% penicillin–streptomycin (Gibco, 15,140-122).

    Techniques: Cell Culture, Western Blot, Expressing, Flow Cytometry