ArticleFrontiers in neuroscience2014
Increased peripherin in sympathetic axons innervating plantar metatarsal arteries in STZ-induced type I diabetic rats.
Article in Frontiers in neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 4 citations in OpenAlex.
- Modeling Diabetic Neuropathy: Injury Biomarkers for Early Detection Through Neuronal and Glial In Vitro Models.International journal of molecular sciences · 2026Review
- Article
- Cell and molecular profiles in peripheral nerves shift toward inflammatory phenotypes in diabetic peripheral neuropathy.The Journal of clinical investigation · 2025Article
- A New Way for Beta Cell Neogenesis: Transdifferentiation from Alpha Cells Induced by Glucagon-Like Peptide 1.Journal of diabetes research · 2019Article
- Organ of Corti explants direct tonotopically graded morphology of spiral ganglion neurons in vitro.The Journal of comparative neurology · 2016Article
- Side-to-Side Jejunoileal Bypass Induces Better Glucose-Lowering Effect than End-to-Side Jejunoileal Bypass on Nonobese Diabetic Rats.Obesity surgery · 2015Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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Abstract
A common characteristic of axonopathy is the abnormal accumulation of cytoskeletal proteins. We recently reported that streptozotocin (STZ)-induced type 1 diabetes produced a change in the morphology of sympathetic nerve fibers supplying rat plantar metatarsal arteries (PMAs). Here we investigated whether these morphological changes are associated with axonal accumulation of the type III intermediate filament peripherin and the microtubule protein β-tubulin III, as both are implicated in axonal remodeling. PMAs from hyperglycemic STZ-treated rats receiving a low dose of insulin (STZ-LI) were compared with those from normoglycemic STZ-treated rats receiving a high dose of insulin (STZ-HI) and vehicle-treated controls. Western blotting revealed an increase in protein expression level for peripherin in PMAs from STZ-LI rats but no change in that for β-tubulin III. In addition, there was an increase in the number of peripherin immunoreactive nerve fibers in the perivascular nerve plexus of PMAs from STZ-LI rats. Co-labeling for peripherin and neuropeptide Y (a marker for sympathetic axons) revealed that peripherin immunoreactivity increased in sympathetic axons. None of these changes were detected in PMAs from STZ-HI rats, indicating that increased peripherin in sympathetic axons of STZ-LI rats is likely due to hyperglycemia and provides a marker of diabetes-induced nerve damage.
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