Lesion induced Cell Modeling Service

Creative Biolabs stands at the forefront of lesion-induced cellular model development, utilizing advanced cell culture techniques and sophisticated molecular tools to provide robust support for neurodegenerative disease research. Our models empower researchers to accurately simulate disease progression, evaluate drug efficacy, and accelerate the development of therapeutic strategies

Unlocking Insights with Lesion-induced Cellular Models

• Our lesion-induced cellular models involve the precise creation of cellular damage within cultured systems, enabling the study of disease progression, repair mechanisms, and therapeutic responses.
• We simulate critical pathological conditions, including neuroinflammation, excitotoxicity, and neurotoxicity, by applying specific proteins or chemical compounds meticulously selected to replicate key disease features.
• We offer customizable model designs and experimental protocols to meet very specific research needs.

Available Lesion-induced Models at Creative Biolabs

Below, we detail our expertise in modeling key neurological disorders, including induction methods, available cells, and cutting-edge detection strategies. These models enable the evaluation of potential therapeutics and customization of assays for specific research needs.

Alzheimer's Disease (AD): Mimicking Aβ and Tau Pathology

• Induction methods:
  
  • Aβ1-42 exposure: Neurons are exposed to Aβ1-42, inducing neurotoxicity, synaptic dysfunction, and tau hyperphosphorylation.
  • Tau Seed Incubation: Recombinant tau proteins, including wild-type and disease-associated mutants (e.g., P301L), are introduced to cells to initiate tau seeding and aggregation.
• Available cells: Primary cortical/hippocampal neurons, SH-SY5Y cell line, HT22 cell line, iPSC-derived neurons.
• Assays: Toxic Amyloid-beta Peptide 1-42 Exposure Assay, Tau Uptake & Seeding Assay

Fig.1 Vitamin A mitigates Aβ1-42-induced neurotoxicity in vitro.¹

Parkinson's Disease (PD): Modeling Dopaminergic Neuron Degeneration

• Induction Methods:
  
  • 6-OHDA: 6-hydroxydopamine (6-OHDA) is applied to induce selective dopaminergic neuron degeneration via oxidative stress. We optimize 6-OHDA concentrations and exposure times to generate reproducible lesions.
  • MPP+: 1-methyl-4-phenylpyridinium (MPP+) is used to inhibit mitochondrial complex I, leading to mitochondrial dysfunction and oxidative stress. We monitor mitochondrial respiration and oxidative stress markers to validate the model.
  • Rotenone: Rotenone induces α-synuclein aggregation and mitochondrial dysfunction. We utilize precisely measured rotenone concentrations and durations of exposure for optimal effect.
• Available cells: Primary cortical/hippocampal/mesencephalic neurons, SH-SY5Y cell line, iPSC-derived neurons.
• Assays: Cell Viability Assay, α-Synuclein Aggregation Analysis, Neuronal Mitophagy Detection Assay

Amyotrophic Lateral Sclerosis (ALS): Modeling Motor Neuron Lesions

• Induction Methods:
  
  • Sodium arsenite: Acute sodium arsenite exposure triggers stress granule (SG) formation and TDP-43 recruitment in TDP-43-overexpressing cells.
  • L-glutamate: L-glutamate induces excitotoxicity and neuronal cell death, mimicking the glutamate-mediated neurodegeneration observed in ALS.
• Available cells: Primary cortical neurons, NSC-34 cell line, SH-SY5Y cell line, TDP-43 overexpress cell line, iPSC-derived neurons.
• Assays: TDP-43 Aggregation Assay, Neurotoxicity Assay

Epilepsy: Modeling Neuronal Hyperexcitability and Seizure Pathways

• Induction Methods:
  
  • Kainic Acid/4-AP Exposure: This method activates glutamate receptors, generating synchronized neuronal firing within hippocampal or cortical cultures, thus replicating a temporal lobe epilepsy condition.
  • Low-Mg²⁺ or High-K⁺ Medium: This procedure interrupts ion homeostasis to produce spontaneous epileptiform activity inside of neuronal networks.
• Available cells: Primary hippocampal/cortical neurons, iPSC-derived glutamatergic/GABAergic neurons, Ion channel overexpression cell line
• Assays: Microelectrode Array (MEA) Assay, Calcium Imaging Assay

Multiple Sclerosis (MS): Simulating Demyelination and Neuroinflammation

• Induction Methods:
  
  • Lysophosphatidylcholine (LPC) or Cuprizone Exposure: This method introduces oligodendrocyte apoptosis and demyelination in co-cultures comprised of neurons and oligodendrocytes.
  • Cytokine Cocktails: IL-1β, TNF-α, and IFN-γ treatment, which activates microglia and astrocytes, replicating neuroinflammatory microenvironments.
• Available Cells: Primary neuron-oligodendrocyte co-cultures, iPSC-derived oligodendrocytes and microglia, Human astrocyte-microglia co-culture systems
• Assays: Cytokine Release Assay, LPS induced Neuroinflammation Assay, Myelination, Demyelination & Remyelination Assay

Contact us to leverage our lesion-induced in vitro expertise for your neurological drug discovery pipeline. Let us transform your research challenges into actionable breakthroughs.

Reference

1. Amin, Faiz Ul et al. "Vanillic acid attenuates Aβ1-42-induced oxidative stress and cognitive impairment in mice." Sci Rep. 2017;7:40753. Distributed under Open Access License CC BY 4.0 without modification.