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ATCC pc12 cell line
Pc12 Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 4408 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pc12+cell+line/PC-12/pm42218217-53-1-8
Average 98 stars, based on 4408 article reviews

pc12 cell line - by Bioz Stars, 2026-09

98/100 stars

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Article Title: Optimizing scaffold properties for nerve regeneration: Effects of bioactive glass in 3D-printed chitosan structures.
Article Snippet: Peripheral nerve injuries remain a challenge for regenerative medicine and, when not properly healed, yield significant consequences for the patient, such as functional loss and neuropathic pain.. Despite the intrinsic repair capacity of these structures, the process is limited to mild injuries and may not result in functional recovery.. The gold standard in this field is the use of autologous grafts; however, this method has several disadvantages, including donor tissue morbidity and a low functional recovery rate.

Article Title: Potential Antioxidant and Neuroprotective Effect of Polysaccharide Isolated from Digüeñe Cyttaria espinosae
Article Snippet: .. PC12 Cells The PC12 cell line, which is derived from chromaffin cells with ectodermal lineage, was obtained from ATCC (Manassas, VA, USA) and cultured in Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 5% fetal bovine serum (FBS), 5% horse serum, and antibiotics (1% penicillin and streptomycin). ..

Article Title: Self-assembled carrier-free nanoplatforms for sequential modulation of the oxidative-inflammatory cascade in cerebral ischemia-reperfusion injury
Article Snippet: Cerebral ischemia-reperfusion injury (CIRI) poses a major challenge in managing ischemic stroke.. The excessive reactive oxygen species (ROS) and amplified inflammatory/immune responses are the pivotal factors exacerbating neuronal death after ischemic stroke, rendering the dual regulation of oxidative stress and inflammatory responses a key therapeutic target.. Here, we engineered a brain-targeted nanotherapeutic via molecular interaction-driven self-assembly, achieving high efficiency co-loading of baicalein and celastrol for synergistic oxidative stress-inflammation interception in CIRI.

CCK-8 Assay:

Article Title: Shikonin attenuates diabetic Parkinsonian neuronal injury by facilitating p53/SLC25A28-mediated iron shuttling.
Article Snippet: Diabetes significantly increases the risk of Parkinson’s disease (PD), and mitochondrial dysfunction is considered a shared pathological mechanism between diabetes and PD.. Although our previous research indicated that shikonin ameliorates hyperglycemia-driven PD progression through dual regulation of glycolysis (via inhibition of pyruvate kinase muscle isozyme 2) and mitochondrial function, its mitochondrial repair mechanism remains unclear.. Here, we demonstrate that shikonin repairs neuronal damage induced by high glucose and 6-hydroxydopamine via a PKM2-independent, p53/Solute Carrier Family 25 Member 28 (SLC25A28)-dependent mitochondrial iron shuttle.

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Article Title: Artificial expression constructs for selectively modulating gene expression in interneurons
Article Snippet: .. The PC12 cell line (available from the American Type Culture Collection, ATCC, Manassas, VA) has been shown to express a number of neuronal marker proteins in response to Neuronal Growth Factor (NGF). ..

Cell Culture:

Article Title: PKM2-driven glycolysis mediates rotenone neurotoxicity via MG-Hs in Parkinson's disease.
Article Snippet: .. The PC12 cell line was obtained from the American Type Culture Collection (ATCC), and cultured in RPMI 1640 medium (Gibco, C11875500BT) supplemented with 10% fetal bovine serum (FBS; Biochannel, BC-SE-FBS01), 50 U/mL penicillin and 50 μg/mL streptomycin (Biochannel, BC-CE-007). .. 2.2 Cell Differentiation The differentiation medium was also based on RPMI-1640 with L-glutamine, gentamicin, and amphotericin B, with 1% donor horse serum (DHS) and the addition of nerve growth factor (NGF) (Sigma-Aldrich, N2513; ) at concentrations of 100 ng/mL.

Article Title: Hypoxia, iron, and ferroptosis: a novel perspective on pheochromocytoma progression and therapy.
Article Snippet: .. The PC12 cell line (CRL-1721, ATCC) was cultured similarly. .. An iron chelator of deferoxamine (DFO), erastin, (1S, 3R)-RSL3 (RSL3), and ferrostatin-1 (Fer-1) were purchased from Cayman Chemical, Selleckchem, and Sigma-Aldrich.

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Metformin protects neuronal cells against Cd-induced apoptosis. Experimental timelines were tailored to specific assays: PC12 cells and primary neurons were pre-incubated with metformin (0–1.5 mM) for 24 h, followed by exposure to Cd (10 μM) for 4 h (for immunoblotting) or 24 h (for cell viability and apoptosis assays). ( A ) Cell viability was measured by MTS assay and expressed as a percentage relative to untreated controls. ( B ) Representative fluorescence micrographs illustrated apoptosis via DAPI staining (nuclear condensation/fragmentation, indicated by arrows, upper panels) and TUNEL (DNA strand breaks, green, lower panels). Scale bar: 20 μm. ( C , D ) Quantification of DAPI-positive apoptotic nuclei and TUNEL-positive cells from experiments shown in ( B ). ( E ) Whole-cell extracts were analyzed by immunoblot analysis with the specified antibodies. β-tubulin served as a loading control. Blots were representative of five independent experiments. ( F ) Densitometric analysis of cleaved caspase-3 and cleaved PARP bands normalized to β-tubulin was performed using NIH Image J software. Data are expressed as mean ± SEM ( n = 5). a p < 0.05 compared to control group; b p < 0.05 compared to 10 μM Cd alone group.

Journal: Cells

Article Title: Metformin Alleviates Cadmium-Induced Autophagic Flux Impairment-Dependent Apoptosis by Activating AMPK in Neuronal Cells

doi: 10.3390/cells15080739

Figure Lengend Snippet: Metformin protects neuronal cells against Cd-induced apoptosis. Experimental timelines were tailored to specific assays: PC12 cells and primary neurons were pre-incubated with metformin (0–1.5 mM) for 24 h, followed by exposure to Cd (10 μM) for 4 h (for immunoblotting) or 24 h (for cell viability and apoptosis assays). ( A ) Cell viability was measured by MTS assay and expressed as a percentage relative to untreated controls. ( B ) Representative fluorescence micrographs illustrated apoptosis via DAPI staining (nuclear condensation/fragmentation, indicated by arrows, upper panels) and TUNEL (DNA strand breaks, green, lower panels). Scale bar: 20 μm. ( C , D ) Quantification of DAPI-positive apoptotic nuclei and TUNEL-positive cells from experiments shown in ( B ). ( E ) Whole-cell extracts were analyzed by immunoblot analysis with the specified antibodies. β-tubulin served as a loading control. Blots were representative of five independent experiments. ( F ) Densitometric analysis of cleaved caspase-3 and cleaved PARP bands normalized to β-tubulin was performed using NIH Image J software. Data are expressed as mean ± SEM ( n = 5). a p < 0.05 compared to control group; b p < 0.05 compared to 10 μM Cd alone group.

Article Snippet: The rat pheochromocytoma (PC12) cell line, a widely utilized neuronal model, was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Incubation, Western Blot, MTS Assay, Fluorescence, Staining, TUNEL Assay, Control, Software

Metformin mitigates Cd-induced autophagy dysregulation in neuronal cells. PC12 cells and primary neurons, either non-infected or infected with Ad-GFP-LC3, were pre-incubated with metformin (0–1.5 mM) for 24 h, followed by exposure to Cd (10 μM) for 4 h (for Immunoblotting) or 12 h (for MDC staining and GFP-LC3 puncta analysis). ( A , B ) Following MDC labeling to visualize autophagic vacuoles, representative fluorescence micrographs ( A ) and quantitative analysis of MDC-positive vacuole fluorescence intensity ( B ) were presented. Scale bar: 20 μm. ( C , D ) Autophagosome formation was monitored via GFP-LC3 redistribution; representative images ( C ) and quantification of GFP-LC3 puncta per cell ( D ) demonstrated autophagic flux alterations. Scale bar: 2 μm. ( E ) Immunoblot analysis of autophagy-related markers was performed on whole-cell lysates using antibodies against ATG5, LC3, and p62, with β-tubulin serving as the loading control. Blots were representative of five independent experiments. ( F ) Densitometric quantification of ATG5, LC3-II, and p62 levels normalized to β-tubulin was performed using NIH Image J software. Data are expressed as mean ± SEM ( n = 5). a p < 0.05 compared to control group; b p < 0.05 compared to 10 μM Cd alone group.

Journal: Cells

Article Title: Metformin Alleviates Cadmium-Induced Autophagic Flux Impairment-Dependent Apoptosis by Activating AMPK in Neuronal Cells

doi: 10.3390/cells15080739

Figure Lengend Snippet: Metformin mitigates Cd-induced autophagy dysregulation in neuronal cells. PC12 cells and primary neurons, either non-infected or infected with Ad-GFP-LC3, were pre-incubated with metformin (0–1.5 mM) for 24 h, followed by exposure to Cd (10 μM) for 4 h (for Immunoblotting) or 12 h (for MDC staining and GFP-LC3 puncta analysis). ( A , B ) Following MDC labeling to visualize autophagic vacuoles, representative fluorescence micrographs ( A ) and quantitative analysis of MDC-positive vacuole fluorescence intensity ( B ) were presented. Scale bar: 20 μm. ( C , D ) Autophagosome formation was monitored via GFP-LC3 redistribution; representative images ( C ) and quantification of GFP-LC3 puncta per cell ( D ) demonstrated autophagic flux alterations. Scale bar: 2 μm. ( E ) Immunoblot analysis of autophagy-related markers was performed on whole-cell lysates using antibodies against ATG5, LC3, and p62, with β-tubulin serving as the loading control. Blots were representative of five independent experiments. ( F ) Densitometric quantification of ATG5, LC3-II, and p62 levels normalized to β-tubulin was performed using NIH Image J software. Data are expressed as mean ± SEM ( n = 5). a p < 0.05 compared to control group; b p < 0.05 compared to 10 μM Cd alone group.

Article Snippet: The rat pheochromocytoma (PC12) cell line, a widely utilized neuronal model, was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Infection, Incubation, Western Blot, Staining, Labeling, Fluorescence, Control, Software

Downregulation of ATG5 augments metformin’s suppression of Cd-induced autophagosome formation and apoptosis in neuronal cells. PC12 cells were transduced with lentiviral particles encoding shRNA targeting ATG5 or a non-targeting control (GFP shRNA). Following transduction, cells were optionally infected with Ad-GFP-LC3 for subsequent autophagosome visualization, then subjected to metformin pretreatment (1 mM) for 24 h and Cd (10 μM) challenge for 4 h (for immunoblotting), 12 h (for GFP-LC3 puncta analysis), or 24 h (for TUNEL staining). ( A ) Whole-cell extracts were analyzed by immunoblot analysis with the specified antibodies. β-tubulin served as a loading control. Blots were representative of five independent experiments. ( B ) Densitometric quantification of ATG5, LC3-II, and cleaved caspase-3 levels normalized to β-tubulin was performed using NIH Image J software. ( C ) Representative fluorescence micrographs depicted the distribution of GFP-LC3 puncta (green) in the cells. Scale bar: 20 μm. ( D ) Quantitative analysis of autophagosome abundance, expressed as the number of GFP-LC3 puncta per cell, reflected the net effect of ATG5 knockdown on autophagic vacuole accumulation. ( E ) Quantification of apoptotic cells was shown via TUNEL staining, visualizing nuclear DNA strand breaks. Data are expressed as mean ± SEM ( n = 5). a p < 0.05 compared to control group; b p < 0.05 compared to 10 μM Cd alone group. c p < 0.05 ATG5 shRNA group versus GFP shRNA group.

Journal: Cells

Article Title: Metformin Alleviates Cadmium-Induced Autophagic Flux Impairment-Dependent Apoptosis by Activating AMPK in Neuronal Cells

doi: 10.3390/cells15080739

Figure Lengend Snippet: Downregulation of ATG5 augments metformin’s suppression of Cd-induced autophagosome formation and apoptosis in neuronal cells. PC12 cells were transduced with lentiviral particles encoding shRNA targeting ATG5 or a non-targeting control (GFP shRNA). Following transduction, cells were optionally infected with Ad-GFP-LC3 for subsequent autophagosome visualization, then subjected to metformin pretreatment (1 mM) for 24 h and Cd (10 μM) challenge for 4 h (for immunoblotting), 12 h (for GFP-LC3 puncta analysis), or 24 h (for TUNEL staining). ( A ) Whole-cell extracts were analyzed by immunoblot analysis with the specified antibodies. β-tubulin served as a loading control. Blots were representative of five independent experiments. ( B ) Densitometric quantification of ATG5, LC3-II, and cleaved caspase-3 levels normalized to β-tubulin was performed using NIH Image J software. ( C ) Representative fluorescence micrographs depicted the distribution of GFP-LC3 puncta (green) in the cells. Scale bar: 20 μm. ( D ) Quantitative analysis of autophagosome abundance, expressed as the number of GFP-LC3 puncta per cell, reflected the net effect of ATG5 knockdown on autophagic vacuole accumulation. ( E ) Quantification of apoptotic cells was shown via TUNEL staining, visualizing nuclear DNA strand breaks. Data are expressed as mean ± SEM ( n = 5). a p < 0.05 compared to control group; b p < 0.05 compared to 10 μM Cd alone group. c p < 0.05 ATG5 shRNA group versus GFP shRNA group.

Article Snippet: The rat pheochromocytoma (PC12) cell line, a widely utilized neuronal model, was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Transduction, shRNA, Control, Infection, Western Blot, TUNEL Assay, Staining, Software, Fluorescence, Knockdown

Metformin alleviates Cd-triggered autophagic flux impairment and attenuates apoptosis resulting from autophagosome accumulation in neuronal cells. PC12 cells and primary neurons, either infected with Ad-GFP-LC3 or left uninfected, were pre-incubated with/without CQ (25 μM) for 1 h, followed by metformin (1 mM) pretreatment for 24 h, and subsequently exposed in the presence or absence of Cd (10 μM) for specified durations—4 h for immunoblot analysis, 12 h for evaluation of GFP-LC3 puncta, or 24 h for detection of DNA fragmentation via TUNEL staining. ( A ) Immunoblotting of whole-cell extracts using antibodies against ATG5, LC3, p62, cleaved caspase-3, and β-tubulin (loading control). Blots were representative of five independent experiments. ( B ) Densitometric quantification of ATG5, LC3-II, p62, and cleaved caspase-3 levels normalized to β-tubulin was performed using NIH Image J software. ( C ) Quantitative analysis of autophagosome abundance was expressed as the number of GFP-LC3 puncta per cell. ( D ) Quantification of apoptotic cells was shown via TUNEL staining, visualizing nuclear DNA strand breaks. Data are expressed as mean ± SEM ( n = 5). a p < 0.05 compared to control group; b p < 0.05 compared to 10 μM Cd alone group. c p < 0.05 compared to Cd/Metformin or Cd/CQ co-treatment group.

Journal: Cells

Article Title: Metformin Alleviates Cadmium-Induced Autophagic Flux Impairment-Dependent Apoptosis by Activating AMPK in Neuronal Cells

doi: 10.3390/cells15080739

Figure Lengend Snippet: Metformin alleviates Cd-triggered autophagic flux impairment and attenuates apoptosis resulting from autophagosome accumulation in neuronal cells. PC12 cells and primary neurons, either infected with Ad-GFP-LC3 or left uninfected, were pre-incubated with/without CQ (25 μM) for 1 h, followed by metformin (1 mM) pretreatment for 24 h, and subsequently exposed in the presence or absence of Cd (10 μM) for specified durations—4 h for immunoblot analysis, 12 h for evaluation of GFP-LC3 puncta, or 24 h for detection of DNA fragmentation via TUNEL staining. ( A ) Immunoblotting of whole-cell extracts using antibodies against ATG5, LC3, p62, cleaved caspase-3, and β-tubulin (loading control). Blots were representative of five independent experiments. ( B ) Densitometric quantification of ATG5, LC3-II, p62, and cleaved caspase-3 levels normalized to β-tubulin was performed using NIH Image J software. ( C ) Quantitative analysis of autophagosome abundance was expressed as the number of GFP-LC3 puncta per cell. ( D ) Quantification of apoptotic cells was shown via TUNEL staining, visualizing nuclear DNA strand breaks. Data are expressed as mean ± SEM ( n = 5). a p < 0.05 compared to control group; b p < 0.05 compared to 10 μM Cd alone group. c p < 0.05 compared to Cd/Metformin or Cd/CQ co-treatment group.

Article Snippet: The rat pheochromocytoma (PC12) cell line, a widely utilized neuronal model, was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Infection, Incubation, Western Blot, TUNEL Assay, Staining, Control, Software

Metformin sustains autophagic flux and attenuates Cd-elicited apoptosis through reactivation of the AMPK signaling axis. PC12 cells and primary neurons, with/without Ad-GFP-LC3 infection, were pretreated with metformin (0–1.5 mM) for 24 h, or pretreated with AICAR (2 mM, 1 h) followed by metformin (1 mM), then exposed to Cd (10 μM) for 4 h (for Immunoblotting), 12 h (for GFP-LC3 puncta analysis) or 24 h (for TUNEL staining). ( A , C ) Whole-cell extracts were analyzed by immunoblot analysis with the specified antibodies. β-tubulin served as a loading control. Blots were representative of five independent experiments. ( B , D ) Densitometric quantification of p-AMPKα, p-ACC, ATG5, LC3-II, p62, and cleaved caspase-3 levels normalized to β-tubulin was performed using NIH Image J software. ( E ) Quantitative analysis of autophagosome abundance was expressed as the number of GFP-LC3 puncta per cell. ( F ) Quantification of apoptotic cells was shown via TUNEL staining, visualizing nuclear DNA strand breaks. Data are expressed as mean ± SEM ( n = 5). a p < 0.05 compared to control group; b p < 0.05 compared to 10 μM Cd alone group. c p < 0.05 compared to Cd/Metformin or Cd/AICAR co-treatment group.

Journal: Cells

Article Title: Metformin Alleviates Cadmium-Induced Autophagic Flux Impairment-Dependent Apoptosis by Activating AMPK in Neuronal Cells

doi: 10.3390/cells15080739

Figure Lengend Snippet: Metformin sustains autophagic flux and attenuates Cd-elicited apoptosis through reactivation of the AMPK signaling axis. PC12 cells and primary neurons, with/without Ad-GFP-LC3 infection, were pretreated with metformin (0–1.5 mM) for 24 h, or pretreated with AICAR (2 mM, 1 h) followed by metformin (1 mM), then exposed to Cd (10 μM) for 4 h (for Immunoblotting), 12 h (for GFP-LC3 puncta analysis) or 24 h (for TUNEL staining). ( A , C ) Whole-cell extracts were analyzed by immunoblot analysis with the specified antibodies. β-tubulin served as a loading control. Blots were representative of five independent experiments. ( B , D ) Densitometric quantification of p-AMPKα, p-ACC, ATG5, LC3-II, p62, and cleaved caspase-3 levels normalized to β-tubulin was performed using NIH Image J software. ( E ) Quantitative analysis of autophagosome abundance was expressed as the number of GFP-LC3 puncta per cell. ( F ) Quantification of apoptotic cells was shown via TUNEL staining, visualizing nuclear DNA strand breaks. Data are expressed as mean ± SEM ( n = 5). a p < 0.05 compared to control group; b p < 0.05 compared to 10 μM Cd alone group. c p < 0.05 compared to Cd/Metformin or Cd/AICAR co-treatment group.

Article Snippet: The rat pheochromocytoma (PC12) cell line, a widely utilized neuronal model, was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Infection, Western Blot, TUNEL Assay, Staining, Control, Software

Constitutive AMPKα activation strengthens metformin’s alleviation of Cd-induced autophagic flux impairment-dependent apoptosis in neuronal cells. PC12 cells were engineered to express a constitutively active AMPKα mutant (Ad-AMPKα-ca) or GFP control (Ad-GFP), with/without subsequent Ad-GFP-LC3 or Ad-mCherry-GFP-LC3 infection for autophagic flux visualization. Cells were pretreated with/without metformin (1 mM) for 24 h, followed by exposure to Cd (10 μM) for 4 h (for immunoblotting), 12 h (for GFP-LC3 puncta and mCherry-GFP-LC3 tandem reporter assays), or 24 h (for TUNEL staining). ( A ) Whole-cell extracts were analyzed by immunoblot analysis with the specified antibodies. β-tubulin served as a loading control. Blots were representative of five independent experiments. ( B ) Densitometric quantification of p-AMPKα, p-ACC, ATG5, LC3-II, p62, and cleaved caspase-3 levels normalized to β-tubulin was performed using NIH Image J software. ( C ) Representative fluorescence micrographs depicted the distribution of GFP-LC3 puncta (green) in the cells. Scale bar: 20 μm. ( D ) Quantitative analysis of autophagosome abundance was expressed as the number of GFP-LC3 puncta per cell. ( E ) Quantification of apoptotic cells was shown via TUNEL staining, visualizing nuclear DNA strand breaks. ( F ) Representative images of tandem fluorescent mCherry-GFP-LC3 reporters: GFP signal (green) quenched in acidic lysosomal compartments, while mCherry signal (red) remains stable. Co-localized GFP + /mCherry + -LC3 (yellow in merge) puncta indicate autophagosomes that have not undergone lysosomal fusion. Scale bar: 2 μm. ( G ) Quantitative analysis of autophagic flux status was presented as the mean number of yellow (GFP + /mCherry + -LC3) puncta per cell. Data are expressed as mean ± SEM ( n = 5). a p < 0.05 compared to control group; b p < 0.05 compared to 10 μM Cd alone group. c p < 0.05 Ad-AMPKα-ca group versus Ad-GFP group.

Journal: Cells

Article Title: Metformin Alleviates Cadmium-Induced Autophagic Flux Impairment-Dependent Apoptosis by Activating AMPK in Neuronal Cells

doi: 10.3390/cells15080739

Figure Lengend Snippet: Constitutive AMPKα activation strengthens metformin’s alleviation of Cd-induced autophagic flux impairment-dependent apoptosis in neuronal cells. PC12 cells were engineered to express a constitutively active AMPKα mutant (Ad-AMPKα-ca) or GFP control (Ad-GFP), with/without subsequent Ad-GFP-LC3 or Ad-mCherry-GFP-LC3 infection for autophagic flux visualization. Cells were pretreated with/without metformin (1 mM) for 24 h, followed by exposure to Cd (10 μM) for 4 h (for immunoblotting), 12 h (for GFP-LC3 puncta and mCherry-GFP-LC3 tandem reporter assays), or 24 h (for TUNEL staining). ( A ) Whole-cell extracts were analyzed by immunoblot analysis with the specified antibodies. β-tubulin served as a loading control. Blots were representative of five independent experiments. ( B ) Densitometric quantification of p-AMPKα, p-ACC, ATG5, LC3-II, p62, and cleaved caspase-3 levels normalized to β-tubulin was performed using NIH Image J software. ( C ) Representative fluorescence micrographs depicted the distribution of GFP-LC3 puncta (green) in the cells. Scale bar: 20 μm. ( D ) Quantitative analysis of autophagosome abundance was expressed as the number of GFP-LC3 puncta per cell. ( E ) Quantification of apoptotic cells was shown via TUNEL staining, visualizing nuclear DNA strand breaks. ( F ) Representative images of tandem fluorescent mCherry-GFP-LC3 reporters: GFP signal (green) quenched in acidic lysosomal compartments, while mCherry signal (red) remains stable. Co-localized GFP + /mCherry + -LC3 (yellow in merge) puncta indicate autophagosomes that have not undergone lysosomal fusion. Scale bar: 2 μm. ( G ) Quantitative analysis of autophagic flux status was presented as the mean number of yellow (GFP + /mCherry + -LC3) puncta per cell. Data are expressed as mean ± SEM ( n = 5). a p < 0.05 compared to control group; b p < 0.05 compared to 10 μM Cd alone group. c p < 0.05 Ad-AMPKα-ca group versus Ad-GFP group.

Article Snippet: The rat pheochromocytoma (PC12) cell line, a widely utilized neuronal model, was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Activation Assay, Mutagenesis, Control, Infection, Western Blot, TUNEL Assay, Staining, Software, Fluorescence

( A and B ) The cross-talk between L- and D-Aβ42 isomers potently suppresses neurotoxicity. While individual stereoisomers are toxic to neuronal PC12 cells (A), coincubation of all-L Aβ42 with its D-isomers in a 1:1 mixture substantially rescues cell viability, with the dD/L and dSdD/L mixtures restoring viability to near-control levels (B). The 95% confidence interval of median inhibitory concentration (IC 50 ): All-L: [17.97, 22.07]; dS: [8.591, 10.47]; dD: [21.00, 27.01]; dSdD: [38.71, 59.87]. Error bars showing the SD ( n = 5, biological replicates). (** P < 0.01 and **** P < 0.0001). ( C to E ) Quantitative proteomics reveals the molecular basis for this rescue. A four-quadrant volcano plot analysis was used to specifically isolate proteins whose expression is uniquely altered by the cross-talk effect, distinguishing them from proteins affected by the individual isomers alone. ( F and G ) Identified GO and KEGG pathways for the up-regulated (F) and down-regulated (G) proteins in STEP or cross-talk group compared with L. EGF, epidermal growth factor; EGFR, epidermal growth factor receptor; GTPases, guanosine triphosphatases. ( H ) A protein-protein interaction (PPI) network for the LD group highlights a core hub of ribosomal proteins, directly implicating the restoration of protein synthesis as a key mechanism underlying the neuroprotective effect of stereochemical cross-talk.

Journal: Science Advances

Article Title: Clinically relevant stereochemistry reprograms amyloid proteome for aggregation cross-talk–conferred neuroprotection

doi: 10.1126/sciadv.aeb2729

Figure Lengend Snippet: ( A and B ) The cross-talk between L- and D-Aβ42 isomers potently suppresses neurotoxicity. While individual stereoisomers are toxic to neuronal PC12 cells (A), coincubation of all-L Aβ42 with its D-isomers in a 1:1 mixture substantially rescues cell viability, with the dD/L and dSdD/L mixtures restoring viability to near-control levels (B). The 95% confidence interval of median inhibitory concentration (IC 50 ): All-L: [17.97, 22.07]; dS: [8.591, 10.47]; dD: [21.00, 27.01]; dSdD: [38.71, 59.87]. Error bars showing the SD ( n = 5, biological replicates). (** P < 0.01 and **** P < 0.0001). ( C to E ) Quantitative proteomics reveals the molecular basis for this rescue. A four-quadrant volcano plot analysis was used to specifically isolate proteins whose expression is uniquely altered by the cross-talk effect, distinguishing them from proteins affected by the individual isomers alone. ( F and G ) Identified GO and KEGG pathways for the up-regulated (F) and down-regulated (G) proteins in STEP or cross-talk group compared with L. EGF, epidermal growth factor; EGFR, epidermal growth factor receptor; GTPases, guanosine triphosphatases. ( H ) A protein-protein interaction (PPI) network for the LD group highlights a core hub of ribosomal proteins, directly implicating the restoration of protein synthesis as a key mechanism underlying the neuroprotective effect of stereochemical cross-talk.

Article Snippet: The mouse neuroblastoma N2A cell line and rat adrenal medullary pheochromocytoma PC12 cell line were from the American Type Culture Collection (Manassas, VA).

Techniques: Control, Concentration Assay, Quantitative Proteomics, Expressing

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pc12 cell line (ATCC)

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Derivative Assay:

CCK-8 Assay:

Membrane:

Iron Assay:

Enzyme-linked Immunosorbent Assay:

Saline:

Isolation:

GSSG Assay:

Lysis:

Multiple Displacement Amplification:

Activity Assay:

Bicinchoninic Acid Protein Assay:

Bioprocessing:

Recombinant:

Marker:

Cell Culture:

Modification:

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