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pc12 cells (MedChemExpress)

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MedChemExpress pc12 cells
Pc12 Cells, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 209 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pc12+cells/Anisomycin/pm42364019-59-0-9
Average 97 stars, based on 209 article reviews

pc12 cells - by Bioz Stars, 2026-10

97/100 stars

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Control:

Article Title: PF4 inhibits ferroptosis-mediated intracerebral hemorrhage through modulating the CXCR3/AKT1/SLC7A11 signaling pathway
Article Snippet: PC12 cells were grown until fusion reached 70%–80%, then treated with 5 μmol/L chloroferritin hemin (Sigma-Aldrich, St. Louis, MO, USA) for 24 h. An in vitro ICH model was created. .. PC12 cells were randomly divided into eight groups: control (normal control group), Erastin (ferroptosis induction group, HY-15763, 10 μmol/L, MedChemExpress, Monmouth Junction, NJ, USA), hemin (ICH model group, HY-19424, 5 μmol/L), hemin+Z-VAD (ICH model + Caspase inhibitor treatment group, HY-16658B, 20 μM), hemin+NEC-1 (ICH model + Necrotic apoptosis inhibitor treatment group, HY-15760, 20 μM), hemin+Fer-1 (ICH model + Ferroptosis inhibitor treatment group, HY- 100579, 20 μM), hemin+Rm-PF4 (ICH model+PF4 protein treatment group, HY-P71885, 10 ng), and hemin+Rm-PF4+AMG487 (ICH model+PF4 protein+CXCR3 antagonist treatment group, HY-15319, 1 μM), followed by subsequent experiments. ..

Transfection:

Article Title: The NFATC2/Nrf2 cascade regulates spinal cord ischemia-reperfusion injury by controlling inflammation, apoptosis and oxidative stress
Article Snippet: .. The influence of OGD/R treatment or/and different transfections on the viability of PC12 cells was tested by the CCK-8 assay (MedChemExpress, Shanghai, China). ..

CCK-8 Assay:

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Activation of microglial CX3CL1-CX3CR1 signaling induces neurotoxicity in co-cultured neurons. ( A ) Schematic illustration of the 0.4-μm Transwell system used for co-culturing pre-treated microglia with neuronal cells. ( B ) Western blot analysis of PSD95 and cleaved caspase-3 (c-Casp3) expression in PC12 cells co-cultured with BV2 microglia pre-treated with increasing concentrations of recombinant CX3CL1. ( C ) CCK-8 assay assessing the viability of PC12 cells following co-culture with CX3CL1-stimulated BV2 cells. ( D , E ) Validation of CX3CR1 knockdown efficiency in BV2 cells transfected with CX3CR1 siRNA via RT-qPCR ( D ) and Western blotting ( E ). ( F – I ) Western blot analysis of PSD95 and cleaved caspase-3 (c-Casp3) expression, alongside CCK-8 cell viability assays, in PC12 cells ( F , G ) and primary hippocampal neurons ( H , I ). Both neurons were co-cultured with BV2 cells subjected to CX3CR1 siRNA transfection and graded CX3CL1 pre-stimulation. p -values were determined by one-way ANOVA followed by Tukey’s post hoc test ( C , D , G , I ).

Journal: International Journal of Molecular Sciences

Article Title: Aberrant CX3CL1-CX3CR1 Signaling Reprograms Microglial Exosome Secretion via KIFC2 to Drive Cognitive Impairment in Chronic Pain

doi: 10.3390/ijms27146304

Figure Lengend Snippet: Activation of microglial CX3CL1-CX3CR1 signaling induces neurotoxicity in co-cultured neurons. ( A ) Schematic illustration of the 0.4-μm Transwell system used for co-culturing pre-treated microglia with neuronal cells. ( B ) Western blot analysis of PSD95 and cleaved caspase-3 (c-Casp3) expression in PC12 cells co-cultured with BV2 microglia pre-treated with increasing concentrations of recombinant CX3CL1. ( C ) CCK-8 assay assessing the viability of PC12 cells following co-culture with CX3CL1-stimulated BV2 cells. ( D , E ) Validation of CX3CR1 knockdown efficiency in BV2 cells transfected with CX3CR1 siRNA via RT-qPCR ( D ) and Western blotting ( E ). ( F – I ) Western blot analysis of PSD95 and cleaved caspase-3 (c-Casp3) expression, alongside CCK-8 cell viability assays, in PC12 cells ( F , G ) and primary hippocampal neurons ( H , I ). Both neurons were co-cultured with BV2 cells subjected to CX3CR1 siRNA transfection and graded CX3CL1 pre-stimulation. p -values were determined by one-way ANOVA followed by Tukey’s post hoc test ( C , D , G , I ).

Article Snippet: PC12 cell viability was assessed using the Cell Counting Kit-8 (C0005, TargetMol, Boston, MA, USA).

Techniques: Activation Assay, Cell Culture, Western Blot, Expressing, Recombinant, CCK-8 Assay, Co-Culture Assay, Biomarker Discovery, Knockdown, Transfection, Quantitative RT-PCR

CX3CL1-CX3CR1 signaling drives profound transcriptional reprogramming in microglia. ( A – C ) Volcano plots illustrating differentially expressed genes (DEGs) in BV2 cells across three comparisons: co-culture with PC12 cells versus monoculture ( A ), CX3CL1 pre-stimulation prior to co-culture versus vehicle co-culture ( B ), and CX3CR1 siRNA transfection plus CX3CL1 pre-stimulation versus CX3CL1 pre-stimulation alone ( C ). Significant DEGs were defined by ∣log2 (fold change) ∣ > 0.585 and adjusted p < 0.05. ( D – F ) Bubble plots displaying Gene Ontology (GO) enrichment analysis of the significant DEGs identified in the respective comparisons mentioned above. Vesicle-related and specific signal transduction terms are highlighted in bold blue.

Journal: International Journal of Molecular Sciences

Article Title: Aberrant CX3CL1-CX3CR1 Signaling Reprograms Microglial Exosome Secretion via KIFC2 to Drive Cognitive Impairment in Chronic Pain

doi: 10.3390/ijms27146304

Figure Lengend Snippet: CX3CL1-CX3CR1 signaling drives profound transcriptional reprogramming in microglia. ( A – C ) Volcano plots illustrating differentially expressed genes (DEGs) in BV2 cells across three comparisons: co-culture with PC12 cells versus monoculture ( A ), CX3CL1 pre-stimulation prior to co-culture versus vehicle co-culture ( B ), and CX3CR1 siRNA transfection plus CX3CL1 pre-stimulation versus CX3CL1 pre-stimulation alone ( C ). Significant DEGs were defined by ∣log2 (fold change) ∣ > 0.585 and adjusted p < 0.05. ( D – F ) Bubble plots displaying Gene Ontology (GO) enrichment analysis of the significant DEGs identified in the respective comparisons mentioned above. Vesicle-related and specific signal transduction terms are highlighted in bold blue.

Article Snippet: PC12 cell viability was assessed using the Cell Counting Kit-8 (C0005, TargetMol, Boston, MA, USA).

Techniques: Co-Culture Assay, Transfection, Transduction

$Microglial CX3CL1-CX3CR1 activation promotes small exosome secretion via Kifc2 upregulation. ( A ) Circos plot demonstrating the functional similarities among the significant DEGs identified in the three transcriptomic comparisons: co-culture with PC12 cells versus monoculture (brick red), CX3CL1 pre-stimulation prior to co-culture versus vehicle co-culture (indigo blue), and CX3CR1 siRNA transfection plus CX3CL1 pre-stimulation versus CX3CL1 pre-stimulation alone (forest green). Purple lines connect directly shared DEGs, whereas blue lines indicate extensive functional interconnectivity among non-overlapping DEGs. ( B ) Quadrant scatter plot comparing the fold changes of DEGs between the CX3CL1 pre-stimulated vs. control group, and the CX3CR1-depleted + CX3CL1 pre-stimulated vs. CX3CL1 pre-stimulated group. ( C ) RT-qPCR quantification of Kifc2 mRNA levels in BV2 cells under monoculture, co-culture, CX3CL1 pre-stimulated co-culture, and CX3CR1-depleted + CX3CL1 pre-stimulated co-culture conditions. ( D ) RT-qPCR validation of Kifc2 knockdown efficiency in BV2 cells transfected with Kifc2 siRNA. ( E – H ) Nanoparticle tracking analysis (NTA) of BV2-derived extracellular vesicles following CX3CL1 stimulation or transfection with Cx3cr1 or Kifc2 siRNAs, displaying the absolute concentration of small exosomes (<100 nm) ( E ), total EV concentration ( F ), relative proportion of small exosomes ( G ), and overall size distribution profile ( H ). ( I ) Western blot analysis of canonical positive exosome markers (CD63 and TSG101) and the negative control marker (Calnexin) in EV fractions and whole cell lysates and purified EV fractions under control or CX3CL1-stimulated conditions. p -values were determined by one-way ANOVA followed by Tukey’s post hoc test ( C – G ).$

Journal: International Journal of Molecular Sciences

Article Title: Aberrant CX3CL1-CX3CR1 Signaling Reprograms Microglial Exosome Secretion via KIFC2 to Drive Cognitive Impairment in Chronic Pain

doi: 10.3390/ijms27146304

Figure Lengend Snippet: Microglial CX3CL1-CX3CR1 activation promotes small exosome secretion via Kifc2 upregulation. ( A ) Circos plot demonstrating the functional similarities among the significant DEGs identified in the three transcriptomic comparisons: co-culture with PC12 cells versus monoculture (brick red), CX3CL1 pre-stimulation prior to co-culture versus vehicle co-culture (indigo blue), and CX3CR1 siRNA transfection plus CX3CL1 pre-stimulation versus CX3CL1 pre-stimulation alone (forest green). Purple lines connect directly shared DEGs, whereas blue lines indicate extensive functional interconnectivity among non-overlapping DEGs. ( B ) Quadrant scatter plot comparing the fold changes of DEGs between the CX3CL1 pre-stimulated vs. control group, and the CX3CR1-depleted + CX3CL1 pre-stimulated vs. CX3CL1 pre-stimulated group. ( C ) RT-qPCR quantification of Kifc2 mRNA levels in BV2 cells under monoculture, co-culture, CX3CL1 pre-stimulated co-culture, and CX3CR1-depleted + CX3CL1 pre-stimulated co-culture conditions. ( D ) RT-qPCR validation of Kifc2 knockdown efficiency in BV2 cells transfected with Kifc2 siRNA. ( E – H ) Nanoparticle tracking analysis (NTA) of BV2-derived extracellular vesicles following CX3CL1 stimulation or transfection with Cx3cr1 or Kifc2 siRNAs, displaying the absolute concentration of small exosomes (<100 nm) ( E ), total EV concentration ( F ), relative proportion of small exosomes ( G ), and overall size distribution profile ( H ). ( I ) Western blot analysis of canonical positive exosome markers (CD63 and TSG101) and the negative control marker (Calnexin) in EV fractions and whole cell lysates and purified EV fractions under control or CX3CL1-stimulated conditions. p -values were determined by one-way ANOVA followed by Tukey’s post hoc test ( C – G ).

Article Snippet: PC12 cell viability was assessed using the Cell Counting Kit-8 (C0005, TargetMol, Boston, MA, USA).

Techniques: Activation Assay, Functional Assay, Co-Culture Assay, Transfection, Control, Quantitative RT-PCR, Biomarker Discovery, Knockdown, Derivative Assay, Concentration Assay, Western Blot, Negative Control, Marker, Purification

The microglial CX3CL1-CX3CR1 signaling activates MAPK/NF-κB pathways and triggers the secretion of IL-17-enriched exosomes. ( A – C ) KEGG pathway enrichment analysis of the significant DEGs identified in three comparisons: co-culture with PC12 cells versus monoculture ( A ), CX3CL1 pre-stimulation prior to co-culture versus vehicle co-culture ( B ), and CX3CR1 siRNA transfection plus CX3CL1 pre-stimulation versus CX3CL1 pre-stimulation alone ( C ). Specific signal transduction terms are highlighted in bold blue. ( D ) ELISA quantification of IL-17 concentrations in EVs secreted by BV2 cells subjected to CX3CL1 stimulation, CX3CR1 siRNA, or Kifc2 siRNA transfection. ( E , F ) Western blot analysis of MAPK (p38, ERK, JNK) and NF-κB (p65) phosphorylation status in BV2 cells following stimulation with 50 ng/mL CX3CL1. ( G ) Predicted and experimental NF-κB binding loci within the Kifc2 locus, cross-referenced using ReMap ChIP-seq metadata and JASPAR motif analysis. ( H ) ChIP-qPCR assay validating p-p65 binding to the Kifc2 promoter. p -values were determined by one-way ANOVA followed by Tukey’s post hoc test ( D , H ).

Journal: International Journal of Molecular Sciences

Article Title: Aberrant CX3CL1-CX3CR1 Signaling Reprograms Microglial Exosome Secretion via KIFC2 to Drive Cognitive Impairment in Chronic Pain

doi: 10.3390/ijms27146304

Figure Lengend Snippet: The microglial CX3CL1-CX3CR1 signaling activates MAPK/NF-κB pathways and triggers the secretion of IL-17-enriched exosomes. ( A – C ) KEGG pathway enrichment analysis of the significant DEGs identified in three comparisons: co-culture with PC12 cells versus monoculture ( A ), CX3CL1 pre-stimulation prior to co-culture versus vehicle co-culture ( B ), and CX3CR1 siRNA transfection plus CX3CL1 pre-stimulation versus CX3CL1 pre-stimulation alone ( C ). Specific signal transduction terms are highlighted in bold blue. ( D ) ELISA quantification of IL-17 concentrations in EVs secreted by BV2 cells subjected to CX3CL1 stimulation, CX3CR1 siRNA, or Kifc2 siRNA transfection. ( E , F ) Western blot analysis of MAPK (p38, ERK, JNK) and NF-κB (p65) phosphorylation status in BV2 cells following stimulation with 50 ng/mL CX3CL1. ( G ) Predicted and experimental NF-κB binding loci within the Kifc2 locus, cross-referenced using ReMap ChIP-seq metadata and JASPAR motif analysis. ( H ) ChIP-qPCR assay validating p-p65 binding to the Kifc2 promoter. p -values were determined by one-way ANOVA followed by Tukey’s post hoc test ( D , H ).

Article Snippet: PC12 cell viability was assessed using the Cell Counting Kit-8 (C0005, TargetMol, Boston, MA, USA).

Techniques: Co-Culture Assay, Transfection, Transduction, Enzyme-linked Immunosorbent Assay, Western Blot, Phospho-proteomics, Binding Assay, ChIP-sequencing, ChIP-qPCR

The microglial CX3CL1-CX3CR1 signaling induces neurotoxicity by promoting IL-17-enriched exosome release via the p38 MAPK-NF-κB-KIFC2 axis. ( A , B ) Western blot analysis of p38 MAPK-NF-κB phosphorylation and KIFC2 expression in BV2 cells treated with CX3CL1, in the presence of the p38 inhibitor SB203580 (20 μM) or the NF-κB inhibitor MCCK1 (2 μM). ( C – F ) NTA characterization of EVs secreted by BV2 cells treated with CX3CL1 in combination with SB203580 or MCCK1, displaying representative size distribution profiles ( C ), absolute concentration of small exosomes (<100 nm) ( D ), total EV concentration ( E ), and the relative proportion of exosomes ( F ). ( G ) ELISA quantification of IL-17 concentrations in EVs secreted by BV2 cells following the indicated inhibitor treatments. ( H ) CCK-8 assay assessing the viability of PC12 cells co-cultured with BV2 cells pre-treated with CX3CL1, SB203580, or MCCK1. ( I ) Western blot analysis of PSD95 and cleaved caspase-3 (c-Casp3) expression in PC12 cells co-cultured with similarly pre-treated BV2 cells. p -values were determined by one-way ANOVA followed by Tukey’s post hoc test ( D – H ).

Journal: International Journal of Molecular Sciences

Article Title: Aberrant CX3CL1-CX3CR1 Signaling Reprograms Microglial Exosome Secretion via KIFC2 to Drive Cognitive Impairment in Chronic Pain

doi: 10.3390/ijms27146304

Figure Lengend Snippet: The microglial CX3CL1-CX3CR1 signaling induces neurotoxicity by promoting IL-17-enriched exosome release via the p38 MAPK-NF-κB-KIFC2 axis. ( A , B ) Western blot analysis of p38 MAPK-NF-κB phosphorylation and KIFC2 expression in BV2 cells treated with CX3CL1, in the presence of the p38 inhibitor SB203580 (20 μM) or the NF-κB inhibitor MCCK1 (2 μM). ( C – F ) NTA characterization of EVs secreted by BV2 cells treated with CX3CL1 in combination with SB203580 or MCCK1, displaying representative size distribution profiles ( C ), absolute concentration of small exosomes (<100 nm) ( D ), total EV concentration ( E ), and the relative proportion of exosomes ( F ). ( G ) ELISA quantification of IL-17 concentrations in EVs secreted by BV2 cells following the indicated inhibitor treatments. ( H ) CCK-8 assay assessing the viability of PC12 cells co-cultured with BV2 cells pre-treated with CX3CL1, SB203580, or MCCK1. ( I ) Western blot analysis of PSD95 and cleaved caspase-3 (c-Casp3) expression in PC12 cells co-cultured with similarly pre-treated BV2 cells. p -values were determined by one-way ANOVA followed by Tukey’s post hoc test ( D – H ).

Article Snippet: PC12 cell viability was assessed using the Cell Counting Kit-8 (C0005, TargetMol, Boston, MA, USA).

Techniques: Western Blot, Phospho-proteomics, Expressing, Concentration Assay, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Cell Culture

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pc12 cells (MedChemExpress)

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