Review



hmc3 cell line present  (ATCC)


Bioz Verified Symbol ATCC is a verified supplier
Bioz Manufacturer Symbol ATCC manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 99
      Buy from Supplier

    Structured Review

    ATCC hmc3 cell line present
    Treatment with UA and NR promotes a significant increase in maximal and spare capacity OCR in HCM3 cells, with maximal glycolytic function increased only by UA treatment. HCM3 cells (2.2 × 10 4 cells/well) untreated (Ctr.) or treated with 10 μM UA or 3 mM NR for 1 week were incubated in appropriate medium containing 2 mM glutamine and 11 mM glucose as metabolic energy substrates for OCR measurement and 2 mM glutamine for PPR measurement. (A, B) show representative traces of oxygen consumption rates (OCR). Oligomycin (Oligo, 1 μg/mL), carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (FCCP, 200 nM each addition), and rotenone (Rot, 1 μM) plus antimycin A (AA, 1 μM) were added where indicated. Different OCR parameters were determined: (C) Maximal respiratory capacity and (D) Spare respiratory capacity. For evaluation of glycolytic function, Panels E and F represent the experimental design and raw data of OCR and extracellular acidification rate (ECAR). Glucose (10 mM), rotenone (Rot, 1 μM) plus antimycin A (AA, 1 μM), and monensin (100 μM) plus FCCP (1 μM) were added where indicated. (G) Basal glycolytic proton production (PPRglyc) and maximal glycolytic rate stimulated by rotenone plus antimycin A (H) and monensin plus FCCP (I) were calculated from OCR and ECAR. Each dot represents an independent experiment, and bars denote means (+ SEM) ( N = 4). ** P ≤ 0.01 vs. untreated cells, Ctr.; * P ≤ 0.05 vs. untreated cells, Ctr. # P ≤ 0.05 vs. NR-treated cells. (J) <t>HMC3</t> cells were treated with DMSO, 10 μM UA, or 3 mM NR for 6 days, respectively. The FCCP group was treated with 20 μM FCCP for 10 min and controlled for by using DMSO. Data was presented as mean with standard deprivation. Data were statistically tested using ordinary one-way ANOVA by Prism 10. *** P < 0.001.
    Hmc3 Cell Line Present, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 826 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hmc3+cell+line+present/pmc11631940-43-1-11?v=ATCC
    Average 99 stars, based on 826 article reviews
    hmc3 cell line present - by Bioz Stars, 2026-07
    99/100 stars

    Images

    1) Product Images from "Urolithin A and nicotinamide riboside differentially regulate innate immune defenses and metabolism in human microglial cells"

    Article Title: Urolithin A and nicotinamide riboside differentially regulate innate immune defenses and metabolism in human microglial cells

    Journal: Frontiers in Aging Neuroscience

    doi: 10.3389/fnagi.2024.1503336

    Treatment with UA and NR promotes a significant increase in maximal and spare capacity OCR in HCM3 cells, with maximal glycolytic function increased only by UA treatment. HCM3 cells (2.2 × 10 4 cells/well) untreated (Ctr.) or treated with 10 μM UA or 3 mM NR for 1 week were incubated in appropriate medium containing 2 mM glutamine and 11 mM glucose as metabolic energy substrates for OCR measurement and 2 mM glutamine for PPR measurement. (A, B) show representative traces of oxygen consumption rates (OCR). Oligomycin (Oligo, 1 μg/mL), carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (FCCP, 200 nM each addition), and rotenone (Rot, 1 μM) plus antimycin A (AA, 1 μM) were added where indicated. Different OCR parameters were determined: (C) Maximal respiratory capacity and (D) Spare respiratory capacity. For evaluation of glycolytic function, Panels E and F represent the experimental design and raw data of OCR and extracellular acidification rate (ECAR). Glucose (10 mM), rotenone (Rot, 1 μM) plus antimycin A (AA, 1 μM), and monensin (100 μM) plus FCCP (1 μM) were added where indicated. (G) Basal glycolytic proton production (PPRglyc) and maximal glycolytic rate stimulated by rotenone plus antimycin A (H) and monensin plus FCCP (I) were calculated from OCR and ECAR. Each dot represents an independent experiment, and bars denote means (+ SEM) ( N = 4). ** P ≤ 0.01 vs. untreated cells, Ctr.; * P ≤ 0.05 vs. untreated cells, Ctr. # P ≤ 0.05 vs. NR-treated cells. (J) HMC3 cells were treated with DMSO, 10 μM UA, or 3 mM NR for 6 days, respectively. The FCCP group was treated with 20 μM FCCP for 10 min and controlled for by using DMSO. Data was presented as mean with standard deprivation. Data were statistically tested using ordinary one-way ANOVA by Prism 10. *** P < 0.001.
    Figure Legend Snippet: Treatment with UA and NR promotes a significant increase in maximal and spare capacity OCR in HCM3 cells, with maximal glycolytic function increased only by UA treatment. HCM3 cells (2.2 × 10 4 cells/well) untreated (Ctr.) or treated with 10 μM UA or 3 mM NR for 1 week were incubated in appropriate medium containing 2 mM glutamine and 11 mM glucose as metabolic energy substrates for OCR measurement and 2 mM glutamine for PPR measurement. (A, B) show representative traces of oxygen consumption rates (OCR). Oligomycin (Oligo, 1 μg/mL), carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (FCCP, 200 nM each addition), and rotenone (Rot, 1 μM) plus antimycin A (AA, 1 μM) were added where indicated. Different OCR parameters were determined: (C) Maximal respiratory capacity and (D) Spare respiratory capacity. For evaluation of glycolytic function, Panels E and F represent the experimental design and raw data of OCR and extracellular acidification rate (ECAR). Glucose (10 mM), rotenone (Rot, 1 μM) plus antimycin A (AA, 1 μM), and monensin (100 μM) plus FCCP (1 μM) were added where indicated. (G) Basal glycolytic proton production (PPRglyc) and maximal glycolytic rate stimulated by rotenone plus antimycin A (H) and monensin plus FCCP (I) were calculated from OCR and ECAR. Each dot represents an independent experiment, and bars denote means (+ SEM) ( N = 4). ** P ≤ 0.01 vs. untreated cells, Ctr.; * P ≤ 0.05 vs. untreated cells, Ctr. # P ≤ 0.05 vs. NR-treated cells. (J) HMC3 cells were treated with DMSO, 10 μM UA, or 3 mM NR for 6 days, respectively. The FCCP group was treated with 20 μM FCCP for 10 min and controlled for by using DMSO. Data was presented as mean with standard deprivation. Data were statistically tested using ordinary one-way ANOVA by Prism 10. *** P < 0.001.

    Techniques Used: Incubation

    UA and NR differentially regulate transcription of several genes in microglia cells. (A) NanoString analysis was done to study neuroinflammation-related genes. Heatmap showing the directed global significance scores: orange denotes gene sets whose genes exhibit increased differential expression with the covariate, blue denotes gene sets with less differential expression. (B–E) Individual NanoString pathway scores following UA, NR, and/or DNA stimulation of HMC3 cells. (F) Venn diagram comparing the differentially expressed genes of UA vs. controls and NR vs. controls. There were ten genes that were in common, 111 UA subgroup-specific genes and 13 NR subgroup-specific genes. (G, H) Volcano plot representation of differential gene expression analysis of UA vs. controls and NR vs. controls. (I–L) Representative western blot analysis showing changed level of the TREM2, RIG-I, STING, and p21 following UA and/or NR treatment of HMC3 cells compared to control (UTR), analysed by two-way ANOVA. Each dot represents an independent experiment and bars denote means (+ SEM) ( N = 4). ** P ≤ 0.01 vs . untreated cells, Ctr.; * P ≤ 0.05 vs . untreated cells, Ctr. *** P ≤ 0.001, **** P ≤ 0.0001.
    Figure Legend Snippet: UA and NR differentially regulate transcription of several genes in microglia cells. (A) NanoString analysis was done to study neuroinflammation-related genes. Heatmap showing the directed global significance scores: orange denotes gene sets whose genes exhibit increased differential expression with the covariate, blue denotes gene sets with less differential expression. (B–E) Individual NanoString pathway scores following UA, NR, and/or DNA stimulation of HMC3 cells. (F) Venn diagram comparing the differentially expressed genes of UA vs. controls and NR vs. controls. There were ten genes that were in common, 111 UA subgroup-specific genes and 13 NR subgroup-specific genes. (G, H) Volcano plot representation of differential gene expression analysis of UA vs. controls and NR vs. controls. (I–L) Representative western blot analysis showing changed level of the TREM2, RIG-I, STING, and p21 following UA and/or NR treatment of HMC3 cells compared to control (UTR), analysed by two-way ANOVA. Each dot represents an independent experiment and bars denote means (+ SEM) ( N = 4). ** P ≤ 0.01 vs . untreated cells, Ctr.; * P ≤ 0.05 vs . untreated cells, Ctr. *** P ≤ 0.001, **** P ≤ 0.0001.

    Techniques Used: Quantitative Proteomics, Gene Expression, Western Blot, Control



    Similar Products

    hmc3 cell line present  (ATCC)
    99
    ATCC hmc3 cell line present
    Treatment with UA and NR promotes a significant increase in maximal and spare capacity OCR in HCM3 cells, with maximal glycolytic function increased only by UA treatment. HCM3 cells (2.2 × 10 4 cells/well) untreated (Ctr.) or treated with 10 μM UA or 3 mM NR for 1 week were incubated in appropriate medium containing 2 mM glutamine and 11 mM glucose as metabolic energy substrates for OCR measurement and 2 mM glutamine for PPR measurement. (A, B) show representative traces of oxygen consumption rates (OCR). Oligomycin (Oligo, 1 μg/mL), carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (FCCP, 200 nM each addition), and rotenone (Rot, 1 μM) plus antimycin A (AA, 1 μM) were added where indicated. Different OCR parameters were determined: (C) Maximal respiratory capacity and (D) Spare respiratory capacity. For evaluation of glycolytic function, Panels E and F represent the experimental design and raw data of OCR and extracellular acidification rate (ECAR). Glucose (10 mM), rotenone (Rot, 1 μM) plus antimycin A (AA, 1 μM), and monensin (100 μM) plus FCCP (1 μM) were added where indicated. (G) Basal glycolytic proton production (PPRglyc) and maximal glycolytic rate stimulated by rotenone plus antimycin A (H) and monensin plus FCCP (I) were calculated from OCR and ECAR. Each dot represents an independent experiment, and bars denote means (+ SEM) ( N = 4). ** P ≤ 0.01 vs. untreated cells, Ctr.; * P ≤ 0.05 vs. untreated cells, Ctr. # P ≤ 0.05 vs. NR-treated cells. (J) <t>HMC3</t> cells were treated with DMSO, 10 μM UA, or 3 mM NR for 6 days, respectively. The FCCP group was treated with 20 μM FCCP for 10 min and controlled for by using DMSO. Data was presented as mean with standard deprivation. Data were statistically tested using ordinary one-way ANOVA by Prism 10. *** P < 0.001.
    Hmc3 Cell Line Present, 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
    https://www.bioz.com/product/hmc3+cell+line+present/pmc11631940-43-1-11?v=ATCC
    Average 99 stars, based on 1 article reviews
    hmc3 cell line present - by Bioz Stars, 2026-07
    99/100 stars
    		  Buy from Supplier

    Image Search Results


    Treatment with UA and NR promotes a significant increase in maximal and spare capacity OCR in HCM3 cells, with maximal glycolytic function increased only by UA treatment. HCM3 cells (2.2 × 10 4 cells/well) untreated (Ctr.) or treated with 10 μM UA or 3 mM NR for 1 week were incubated in appropriate medium containing 2 mM glutamine and 11 mM glucose as metabolic energy substrates for OCR measurement and 2 mM glutamine for PPR measurement. (A, B) show representative traces of oxygen consumption rates (OCR). Oligomycin (Oligo, 1 μg/mL), carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (FCCP, 200 nM each addition), and rotenone (Rot, 1 μM) plus antimycin A (AA, 1 μM) were added where indicated. Different OCR parameters were determined: (C) Maximal respiratory capacity and (D) Spare respiratory capacity. For evaluation of glycolytic function, Panels E and F represent the experimental design and raw data of OCR and extracellular acidification rate (ECAR). Glucose (10 mM), rotenone (Rot, 1 μM) plus antimycin A (AA, 1 μM), and monensin (100 μM) plus FCCP (1 μM) were added where indicated. (G) Basal glycolytic proton production (PPRglyc) and maximal glycolytic rate stimulated by rotenone plus antimycin A (H) and monensin plus FCCP (I) were calculated from OCR and ECAR. Each dot represents an independent experiment, and bars denote means (+ SEM) ( N = 4). ** P ≤ 0.01 vs. untreated cells, Ctr.; * P ≤ 0.05 vs. untreated cells, Ctr. # P ≤ 0.05 vs. NR-treated cells. (J) HMC3 cells were treated with DMSO, 10 μM UA, or 3 mM NR for 6 days, respectively. The FCCP group was treated with 20 μM FCCP for 10 min and controlled for by using DMSO. Data was presented as mean with standard deprivation. Data were statistically tested using ordinary one-way ANOVA by Prism 10. *** P < 0.001.

    Journal: Frontiers in Aging Neuroscience

    Article Title: Urolithin A and nicotinamide riboside differentially regulate innate immune defenses and metabolism in human microglial cells

    doi: 10.3389/fnagi.2024.1503336

    Figure Lengend Snippet: Treatment with UA and NR promotes a significant increase in maximal and spare capacity OCR in HCM3 cells, with maximal glycolytic function increased only by UA treatment. HCM3 cells (2.2 × 10 4 cells/well) untreated (Ctr.) or treated with 10 μM UA or 3 mM NR for 1 week were incubated in appropriate medium containing 2 mM glutamine and 11 mM glucose as metabolic energy substrates for OCR measurement and 2 mM glutamine for PPR measurement. (A, B) show representative traces of oxygen consumption rates (OCR). Oligomycin (Oligo, 1 μg/mL), carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (FCCP, 200 nM each addition), and rotenone (Rot, 1 μM) plus antimycin A (AA, 1 μM) were added where indicated. Different OCR parameters were determined: (C) Maximal respiratory capacity and (D) Spare respiratory capacity. For evaluation of glycolytic function, Panels E and F represent the experimental design and raw data of OCR and extracellular acidification rate (ECAR). Glucose (10 mM), rotenone (Rot, 1 μM) plus antimycin A (AA, 1 μM), and monensin (100 μM) plus FCCP (1 μM) were added where indicated. (G) Basal glycolytic proton production (PPRglyc) and maximal glycolytic rate stimulated by rotenone plus antimycin A (H) and monensin plus FCCP (I) were calculated from OCR and ECAR. Each dot represents an independent experiment, and bars denote means (+ SEM) ( N = 4). ** P ≤ 0.01 vs. untreated cells, Ctr.; * P ≤ 0.05 vs. untreated cells, Ctr. # P ≤ 0.05 vs. NR-treated cells. (J) HMC3 cells were treated with DMSO, 10 μM UA, or 3 mM NR for 6 days, respectively. The FCCP group was treated with 20 μM FCCP for 10 min and controlled for by using DMSO. Data was presented as mean with standard deprivation. Data were statistically tested using ordinary one-way ANOVA by Prism 10. *** P < 0.001.

    Article Snippet: The HMC3 cell line present in this study was obtained from ATCC (CRL-3304) and was cultured in Minimum Essential Medium Eagle (Merck) containing 10% fetal bovine serum and 1% GlutaMAX (Thermo Fisher Scientific).

    Techniques: Incubation

    UA and NR differentially regulate transcription of several genes in microglia cells. (A) NanoString analysis was done to study neuroinflammation-related genes. Heatmap showing the directed global significance scores: orange denotes gene sets whose genes exhibit increased differential expression with the covariate, blue denotes gene sets with less differential expression. (B–E) Individual NanoString pathway scores following UA, NR, and/or DNA stimulation of HMC3 cells. (F) Venn diagram comparing the differentially expressed genes of UA vs. controls and NR vs. controls. There were ten genes that were in common, 111 UA subgroup-specific genes and 13 NR subgroup-specific genes. (G, H) Volcano plot representation of differential gene expression analysis of UA vs. controls and NR vs. controls. (I–L) Representative western blot analysis showing changed level of the TREM2, RIG-I, STING, and p21 following UA and/or NR treatment of HMC3 cells compared to control (UTR), analysed by two-way ANOVA. Each dot represents an independent experiment and bars denote means (+ SEM) ( N = 4). ** P ≤ 0.01 vs . untreated cells, Ctr.; * P ≤ 0.05 vs . untreated cells, Ctr. *** P ≤ 0.001, **** P ≤ 0.0001.

    Journal: Frontiers in Aging Neuroscience

    Article Title: Urolithin A and nicotinamide riboside differentially regulate innate immune defenses and metabolism in human microglial cells

    doi: 10.3389/fnagi.2024.1503336

    Figure Lengend Snippet: UA and NR differentially regulate transcription of several genes in microglia cells. (A) NanoString analysis was done to study neuroinflammation-related genes. Heatmap showing the directed global significance scores: orange denotes gene sets whose genes exhibit increased differential expression with the covariate, blue denotes gene sets with less differential expression. (B–E) Individual NanoString pathway scores following UA, NR, and/or DNA stimulation of HMC3 cells. (F) Venn diagram comparing the differentially expressed genes of UA vs. controls and NR vs. controls. There were ten genes that were in common, 111 UA subgroup-specific genes and 13 NR subgroup-specific genes. (G, H) Volcano plot representation of differential gene expression analysis of UA vs. controls and NR vs. controls. (I–L) Representative western blot analysis showing changed level of the TREM2, RIG-I, STING, and p21 following UA and/or NR treatment of HMC3 cells compared to control (UTR), analysed by two-way ANOVA. Each dot represents an independent experiment and bars denote means (+ SEM) ( N = 4). ** P ≤ 0.01 vs . untreated cells, Ctr.; * P ≤ 0.05 vs . untreated cells, Ctr. *** P ≤ 0.001, **** P ≤ 0.0001.

    Article Snippet: The HMC3 cell line present in this study was obtained from ATCC (CRL-3304) and was cultured in Minimum Essential Medium Eagle (Merck) containing 10% fetal bovine serum and 1% GlutaMAX (Thermo Fisher Scientific).

    Techniques: Quantitative Proteomics, Gene Expression, Western Blot, Control