ArticleMolecular neurobiology2018
MiR-29c/PRKCI Regulates Axonal Growth of Dorsal Root Ganglia Neurons Under Hyperglycemia.
Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Innovative strategies for diabetic peripheral neuropathy: From clinical management to emerging bioengineering solutions.Bioactive materials · 2026Review
- MiR-210-3p is upregulated in diabetic peripheral neuropathy and may be involved in the progression of the disease by targeting brain-derived neurotrophic factor.Journal of diabetes investigation · 2026Article
- Clinical Importance of miRNA in Diabetic Neuropathy: Pathophysiology, Diagnosis, and Therapeutic Potential.Current diabetes reviews · 2026Review
- Extracellular vesicle-derived MicroRNAs as potential therapies for spinal cord and peripheral nerve injuries.RNA biology · 2025Review
- miR-29c-3p downregulation accelerates spinal cord injury progression by targeting BRD4.Journal of orthopaedic surgery and research · 2025Article
- Exploring the role of miRNA in diabetic neuropathy: from diagnostics to therapeutics.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Transcriptome analysis of microRNAs, circRNAs, and mRNAs in the dorsal root ganglia of paclitaxel-induced mice with neuropathic pain.Frontiers in molecular neuroscience · 2022Article
- A Rare Variation in the 3' Untranslated Region of the Presenilin 2 Gene Is Linked to Alzheimer's Disease.Molecular neurobiology · 2021Article
- Small extracellular vesicles ameliorate peripheral neuropathy and enhance chemotherapy of oxaliplatin on ovarian cancer.Journal of extracellular vesicles · 2021Article
- What Is in the Field for Genetics and Epigenetics of Diabetic Neuropathy: The Role of MicroRNAs.Journal of diabetes research · 2021Review
- Upregulation of miR-133a-3p in the Sciatic Nerve Contributes to Neuropathic Pain Development.Molecular neurobiology · 2020Article
- Emerging Roles of microRNAs as Biomarkers and Therapeutic Targets for Diabetic Neuropathy.Frontiers in neurology · 2020Review
- Single-Cell RNA-seq Reveals Profound Alterations in Mechanosensitive Dorsal Root Ganglion Neurons with Vitamin E Deficiency.iScience · 2019Article
- MiR-34a Regulates Axonal Growth of Dorsal Root Ganglia Neurons by Targeting FOXP2 and VAT1 in Postnatal and Adult Mouse.Molecular neurobiology · 2018Article
- Circulating microRNAs as biomarkers for diabetic neuropathy: A novel approach.World journal of experimental medicine · 2018Review
- Exosomes derived from high-glucose-stimulated Schwann cells promote development of diabetic peripheral neuropathy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- TNFα and IL-1β modify the miRNA cargo of astrocyte shed extracellular vesicles to regulate neurotrophic signaling in neurons.Cell death & disease · 2018Article
- MicroRNA and Microvascular Complications of Diabetes.International journal of endocrinology · 2018Review
- Microfluidics of Small-Population Neurons Allows for a Precise Quantification of the Peripheral Axonal Growth State.Frontiers in cellular neuroscience · 2018Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Diabetes initially induces distal axonal damage of peripheral nerves, but molecular mechanisms that mediate axonal injury are not fully understood. MircoRNAs (miRNAs) regulate axonal growth. We found that diabetic db/db mice exhibited substantial upregulation of miR-29c in dorsal root ganglia (DRG) neurons, sciatic nerve, and foot pad tissues. Bioinformatic analysis revealed PRKCI, a gene that encodes a member of the protein kinase C (PKC) iota, as a putative target for miR-29c. Western blot analysis showed that diabetic mice exhibited a considerable reduction of PRKCI protein levels in sciatic nerve tissues and DRG neurons. Using dual-luciferase assay, we found that co-transfection of a plasmid containing miR-29c binding site at 3' UTR of PRKCI gene and miR-29c mimics effectively reduced luminescence activity, which was abolished when miR-29c seed sequences at 3' UTR of PRKCI gene were mutated. In vitro, high glucose substantially upregulated and reduced miR-29c and PRKCI protein levels, respectively, in DRG neurons, which were associated with significant reduction of axonal growth. Knockdown of endogenous miR-29c in DRG neurons by siRNAs overcame reduced PRKCI protein and axonal growth under high glucose condition. Moreover, knockdown of PRKCI in DRG neurons by siRNAs under regular glucose condition considerably inhibited axonal growth. Together, these findings suggest that miR-29c is a negative regulator of axonal growth of DRG neurons by targeting PRKCI under hyperglycemia.
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