ArticleDiabetologia2015
Bone marrow-derived TNF-α causes diabetic neuropathy in mice.
Article in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Association Between Tumor Necrosis Factor-α and Diabetic Peripheral Neuropathy in Patients with Type 2 Diabetes: a Meta-Analysis.Molecular neurobiology · 2017Pooled it
- Oxidative-Inflammatory Crosstalk and Multi-Target Natural Agents: Decoding Diabetic Vascular Complications.Current issues in molecular biology · 2025Review
- Expression of proinflammatory cytokines and proinsulin by bone marrow-derived cells for fracture healing in long-term diabetic mice.BMC musculoskeletal disorders · 2023Article
- Complete remission of diabetes with a transient HDAC inhibitor and insulin in streptozotocin mice.Communications biology · 2023Article
- Neuronal-Hematopoietic Cell Fusion in Diabetic Neuropathy.Stem cells translational medicine · 2023Article
- Bone marrow-derived vasculogenesis leads to scarless regeneration in deep wounds with periosteal defects.Scientific reports · 2022Article
- The effect of tropisetron on peripheral diabetic neuropathy: possible protective actions against inflammation and apoptosis.Cell stress & chaperones · 2022Article
- Hematopoietic Progenitors and the Bone Marrow Niche Shape the Inflammatory Response and Contribute to Chronic Disease.International journal of molecular sciences · 2022Review
- Balance Analysis of Peripheral Neuropathy in Type 2 Diabetes Mellitus Based on Logistic Regression Equation.Scanning · 2022Article
- Malfunctioning CD106-positive, short-term hematopoietic stem cells trigger diabetic neuropathy in mice by cell fusion.Communications biology · 2021Article
- Prospects for the application of transcranial magnetic stimulation in diabetic neuropathy.Neural regeneration research · 2021Review
- When Good Guys Turn Bad: Bone Marrow's and Hematopoietic Stem Cells' Role in the Pathobiology of Diabetic Complications.International journal of molecular sciences · 2020Review
- Therapeutic effects of moxibustion simultaneously targeting Nrf2 and NF-κB in diabetic peripheral neuropathy.Applied biochemistry and biotechnology · 2019Article
- Transcriptional networks of progressive diabetic peripheral neuropathy in the db/db mouse model of type 2 diabetes: An inflammatory story.Experimental neurology · 2018Article
- Ablation of a small subpopulation of diabetes-specific bone marrow-derived cells in mice protects against diabetic neuropathy.American journal of physiology. Endocrinology and metabolism · 2016Article
- Proinsulin-producing, hyperglycemia-induced adipose tissue macrophages underlie insulin resistance in high fat-fed diabetic mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Tang-Tong-Fang Confers Protection against Experimental Diabetic Peripheral Neuropathy by Reducing Inflammation.Evidence-based complementary and alternative medicine : eCAM · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
aims/hypothesisDysregulation of biochemical pathways in response to hyperglycaemia in cells intrinsic to the nervous system (Schwann cells, neurons, vasa nervorum) are thought to underlie diabetic peripheral neuropathy (DPN). TNF-α is a known aetiological factor; Tnf-knockout mice are protected against DPN. We hypothesised that TNF-α produced by a small but specific bone marrow (BM) subpopulation marked by proinsulin production (proinsulin-producing BM-derived cells, PI-BMDCs) is essential for DPN development.
methodsWe produced mice deficient in TNF-α, globally in BM and selectively in PI-BMDCs only, by gene targeting and BM transplantation, and induced diabetes by streptozotocin. Motor and sensory nerve conduction velocities were used to gauge nerve dysfunction. Immunocytochemistry, fluorescence in situ hybridisation (FISH) and PCR analysis of dorsal root ganglia (DRG) were employed to monitor outcome.
resultsWe found that loss of TNF-α in BM only protected mice from DPN. We developed a strategy to delete TNF-α specifically in PI-BMDCs, and found that PI-BMDC-specific loss of TNF-α protected against DPN as robustly as loss of total BM TNF-α. Selective loss of PI-BMDC-derived TNF-α downregulated TUNEL-positive DRG neurons. FISH revealed PI-BMDC-neuron fusion cells in the DRG in mice with DPN; fusion cells were undetectable in non-diabetic mice or diabetic mice that had lost TNF-α expression selectively in the PI-BMDC subpopulation. CONCLUSIONS/
interpretationBMDC-specific TNF-α is essential for DPN development; its selective removal from a small PI-BMDC subpopulation protects against DPN. The pathogenicity of PI-BMDC-derived TNF-α may have important therapeutic implications.
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Registered trials
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