Immortalized Mouse Schwann Cells (IMS32)
Cat.No.: CSC-I9219L
Species: Mus musculus
Source: Brain
Morphology: Spindle-shaped
Culture Properties: Adherent
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Note: Never can cells be kept at -20 °C.
IMS32, also known as Immortalized Mouse Schwann cells clone 32, is a spontaneously immortalized cell line established from peripheral nerves and dorsal root ganglia of adult ICR mice at 4-6 weeks of age. Unlike primary Schwann cells-which have a finite lifespan and undergo phenotypic drift with serial passaging-IMS32 arose spontaneously from long‑term primary cultures and displays high proliferative activity while retaining the defining biological features of mature Schwann cells.
IMS32 exhibits the characteristic spindle‑shaped morphology of Schwann cells and expresses canonical glial markers, including S100, glial fibrillary acidic protein (GFAP), and the p75 low‑affinity neurotrophin receptor, as well as a variety of neurotrophic factors. Conditioned medium from IMS32 cultures promotes neurite outgrowth in PC12 cells and primary mouse dorsal root ganglion neurons, providing functional evidence of their neurotrophic secretome.
The primary advantage of IMS32 is its status as one of the best‑characterized and most widely used immortalized Schwann cell models available. It overcomes the experimental bottlenecks associated with primary Schwann cell isolation, including low yield, donor‑to‑donor variability, and rapid senescence in culture. IMS32 cells retain metabolic responsiveness to hyperglycemic and hyperlipidemic conditions, making them particularly valuable for investigating diabetic peripheral neuropathy-including polyol pathway hyperactivity, protein glycation, oxidative stress, and neurotrophic deficits-as well as for exploring the mechanisms underlying peripheral nerve regeneration and the development of novel neurological therapeutics.
Imeglimin Improves Hyperglycemia and Hypoglycemia-Induced Cell Death and Mitochondrial Dysfunction in Immortalized Adult Mouse Schwann IMS32 Cells
Imeglimin, a novel oral antidiabetic drug, enhances glucose-stimulated insulin secretion, improves insulin sensitivity, and reduces mitochondrial reactive oxygen species (ROS) generation. Diabetic neuropathy is driven by oxidative stress caused by hyperglycemia, with mitochondrial ROS overproduction playing a central role. Hypoglycemia also contributes to oxidative stress. This study evaluates the effects of imeglimin on Schwann cells under high- and low-glucose conditions.
We used IMS32 cells, an immortalized mouse Schwann cell line, to investigate cell survival and mitochondrial function under normal, high-, and low-glucose conditions. Assessments included mitochondrial oxidative stress, cytochrome c release, mitochondrial membrane potential, oxygen consumption rate (OCR), Complex I activity, and ATP synthesis.
High- and low-glucose conditions caused cell death, elevated mitochondrial ROS, triggered cytochrome c release, disrupted mitochondrial membrane potential, and increased OCR and Complex I activity, while suppressing ATP synthesis. Imeglimin treatment mitigated cell death, reduced oxidative stress, restored mitochondrial membrane potential, normalized OCR and Complex I activity, and improved ATP synthesis under both glucose conditions.
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