Neurovascular control and neurogenic inflammation in diabetes

Schaper, Nicolaas C.; Huijberts, M. S. P.; Pickwell, Kristy M.

doi:10.1002/dmrr.862

Cited by 46 publications

(29 citation statements)

References 42 publications

(54 reference statements)

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“…These cell type are well-known in the literature to express NGF in a variety of conditions (54). These findings could be the results of two potential mechanisms: (1) Increased levels of peripheral NGF from the dermal cells could be taken up by Trk A-positive nerve fibers in the skin and delivered in a retrograde manner to DRG neurons (14); (2) NGF secreted by peripheral nerve endings could trigger neurogenic inflammation by attracting inflammatory mediators, including mast cells and macrophages (55). We speculate that this retrograde transport of peripherally produced NGF could contribute to PDN by maintaining increased neuropeptide expression and mechanical allodynia while the NGF gene expression diminished in the DRG.…”

Section: Discussionmentioning

confidence: 99%

Nerve Growth Factor Mediates Mechanical Allodynia in a Mouse Model of Type 2 Diabetes

Cheng

Dauch

Hayes

et al. 2009

Journal of Neuropathology and Experimental Neurology

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We reported previously that the C57BLKS db/db (db/db) mouse develops the neuropathy of type 2 diabetes. In the current study, we demonstrate that the db/db mouse develops transient mechanical allodynia at the early stage of diabetes. We hypothesize that nerve growth factor (NGF) mediates the development of mechanical allodynia in the db/db mouse. NGF, substance P (SP), and calcitonin gene related peptide (CGRP) gene expression was upregulated in the dorsal root ganglion (DRG) of db/db mice prior or during the period of mechanical allodynia. In parallel, there were increased numbers of small- to medium-sized NGF-immunopositive DRG neurons in db/db mice in comparison with the control db+ mice. These neurons also expressed SP, suggesting that they mediated nociception. The NGF expression in the hind paw skin was also increased in a variety of dermal cells and nerve fibers, suggesting the contribution of a peripheral source of NGF to mechanical allodynia. This upregulation of NGF coincided with enhanced tropomyosin-related kinase (Trk) A receptor phosphorylation in DRG. Finally, an antibody against NGF significantly inhibited mechanical allodynia and the numbers of SP-positive DRG neurons in db/db mice. The current findings provide evidence that inhibition of NGF action is a potential strategy for treating painful diabetic neuropathy.

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Section: Discussionmentioning

confidence: 99%

Nerve Growth Factor Mediates Mechanical Allodynia in a Mouse Model of Type 2 Diabetes

Cheng

Dauch

Hayes

et al. 2009

Journal of Neuropathology and Experimental Neurology

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“…Apart from the loss of pain perception, which is a key factor in the development of neuropathic foot ulcers, loss of autonomic function and small fibre neuropathy can result in impaired neurogenic control of local microcirculatory blood flow, impaired fluid homeostasis, diminished energy metabolism, oxygen delivery, and inflammatory responses. These processes could render the feet of diabetic patients with neuropathy more susceptible to tissue damage and infection [9]. …”

Section: Introductionmentioning

confidence: 99%

Adenosine receptor agonists for promotion of dermal wound healing

Valls¹,

Cronstein²,

Montesinos³

2009

Biochemical Pharmacology

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Wound healing is a dynamic and complex process that involves a well coordinated, highly regulated series of events including inflammation, tissue formation, revascularization and tissue remodeling. However, this orderly sequence is impaired in certain pathophysiological conditions such as diabetes mellitus, venous insufficiency, chronic glucocorticoid use, aging and malnutrition. Together with proper wound care, promotion of the healing process is the primary objective in the management of chronic poorly healing wounds. Recent studies have demonstrated that A 2A adenosine receptor agonists promote wound healing in normal and diabetic animals and one such agonist, Sonedenoson, is currently being evaluated as a prospective new therapy of diabetic foot ulcers. We will review the mechanisms by which adenosine receptor activation affects the function of the cells and tissues that participate in wound healing, emphasizing the potential beneficial impact of adenosine receptor agonists in diabetic impaired healing.

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“…Since this somewhat inventive surgical application was first considered 4 years ago, published papers have documented the physiological changes which accompany denervation in DSPN and give some basis for this aggressive approach. 21,22 Schaper et al 22 have summarized this work and suggest that:…”

Section: Discussionmentioning

confidence: 99%

Early stage diabetic Charcot Foot syndrome may respond to nerve decompression

2009

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Diabetic Charcot Foot syndrome has been postulated to require a triggering event to initiate its puzzling inflammatory process, characterized by bony resorption, pathologic fractures, soft tissue ligamentous failure, and destruction of foot architecture. Two cases are presented where multiple lower extremity nerve decompression was performed early in the Charcot process. Resolution of clinical signs and radiographic abnormalities rapidly followed. The observation that these events were temporally concurrent suggests that nerve entrapment might reasonably be investigated as one of the postulated triggering events for the Charcot Foot in diabetes. (c) 2009 Wiley-Liss, Inc. Microsurgery 2009.

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Neurovascular control and neurogenic inflammation in diabetes

Cited by 46 publications

References 42 publications

Nerve Growth Factor Mediates Mechanical Allodynia in a Mouse Model of Type 2 Diabetes

Nerve Growth Factor Mediates Mechanical Allodynia in a Mouse Model of Type 2 Diabetes

Adenosine receptor agonists for promotion of dermal wound healing

Early stage diabetic Charcot Foot syndrome may respond to nerve decompression

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