Prolonged preservation of nerve function in diabetic neuropathy in mice by herpes simplex virus-mediated gene transfer

Chattopadhyay, Munmun; Mata, Marina; Goss, James R.; Wolfe, Darren; Huang, Shaohua; Fink, David J.

doi:10.1007/s00125-007-0702-4

Cited by 39 publications

(35 citation statements)

References 38 publications

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“…64 A prolonged expression of neurotrophin-3 in mice, achieved by herpes simplex virus (HSV)-mediated gene transfer with gene expression under the control of an HSV latency promoter, provided protection against diabetes-associated thermal hypoalgesia over a 6-month period. 50 A peroxynitrite decomposition catalyst treatment also counteracted thermal hypoalgesia in the ob/ob mouse model. 47 An ACE inhibitor (enalapril) and a hydroxymethylglutaryl-CoA reductase inhibitor (rosuvastatin) alleviated thermal sensory loss in Zucker fatty rats.…”

Section: Pathogenesis and Experimental Treatments Of Diabetes-associamentioning

confidence: 96%

Diabetic Painful and Insensate Neuropathy: Pathogenesis and Potential Treatments

2009

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Summary:Advanced peripheral diabetic neuropathy (PDN) is associated with elevated vibration and thermal perception thresholds that progress to sensory loss and degeneration of all fiber types in peripheral nerve. A considerable proportion of diabetic patients also describe abnormal sensations such as paresthesias, allodynia, hyperalgesia, and spontaneous pain. One or several manifestations of abnormal sensation and pain are described in all the diabetic rat and mouse models studied so far (i.e., streptozotocin-diabetic rats and mice, type 1 insulinopenic BB/Wor and type 2 hyperinsulinemic diabetic BBZDR/Wor rats, Zucker diabetic fatty rats, and nonobese diabetic, Akita, leptin-and leptin-receptor-deficient, and highfat diet-fed mice). Such manifestations are 1) thermal hyperalgesia, an equivalent of a clinical phenomenon described in early PDN; 2) thermal hypoalgesia, typically present in advanced PDN; 3) mechanical hyperalgesia, an equivalent of pain on pressure in early PDN; 4) mechanical hypoalgesia, an equivalent to the loss of sensitivity to mechanical noxious stimuli in advanced PDN; 5) tactile allodynia, a painful perception of a light touch; and 5) formalin-induced hyperalgesia. Rats with short-term diabetes develop painful neuropathy, whereas those with longer-term diabetes and diabetic mice typically display manifestations of both painful and insensate neuropathy, or insensate neuropathy only. Animal studies using pharmacological and genetic approaches revealed important roles of increased aldose reductase, protein kinase C, and poly(ADPribose) polymerase activities, advanced glycation end-products and their receptors, oxidative-nitrosative stress, growth factor imbalances, and C-peptide deficiency in both painful and insensate neuropathy. This review describes recent achievements in studying the pathogenesis of diabetic neuropathic pain and sensory disorders in diabetic animal models and developing potential pathogenetic treatments. Key Words: Animal models, diabetic insensate neuropathy, diabetic painful neuropathy, formalin-induced hyperalgesia, mechanical hyper-and hypoalgesia, pathogenetic treatments of diabetic neuropathic pain and sensory loss, symptomatic treatments of diabetic pain, tactile allodynia, thermal hyper-and hypoalgesia.

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Section: Pathogenesis and Experimental Treatments Of Diabetes-associamentioning

confidence: 96%

Diabetic Painful and Insensate Neuropathy: Pathogenesis and Potential Treatments

2009

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“…Herpes simplex virus-mediated gene transfer of both vascular endothelial growth factor (VEGF) (Chattopadhyay et al, 2005) and neurotrophin-3 (NT-3) (Chattopadhyay et al, 2007) have been shown to prevent reductions in proportional area of footpad skin and subcutaneous tissue occupied by PGP9.5-immunoreactive nerve fibers in STZ-diabetic mice. In the ob/ob mouse model, treatment with an aldose reducatase inhibitor prevented both onset of thermal hypoalgesia and IENF loss (Drel et al, 2006).…”

Section: Therapeutic Interventionsmentioning

confidence: 99%

Epidermal nerve fiber quantification in the assessment of diabetic neuropathy

2008

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SummaryAssessment of cutaneous innervation in skin biopsies is emerging as a valuable means of both diagnosing and staging diabetic neuropathy. Immunolabeling, using antibodies to neuronal proteins such as protein gene product 9.5, allows for the visualization and quantification of intraepidermal nerve fibers. Multiple studies have shown reductions in intraepidermal nerve fiber density in skin biopsies from patients with both type 1 and type 2 diabetes. More recent studies have focused on correlating these changes with other measures of diabetic neuropathy. A loss of epidermal innervation similar to that observed in diabetic patients has been observed in rodent models of both type 1 and type 2 diabetes and several therapeutics have been reported to prevent reductions in intraepidermal nerve fiber density in these models. This review discusses the current literature describing diabetesinduced changes in cutaneous innervation in both human and animal models of diabetic neuropathy.

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“…Recent advances and current applications of existing vectors are still focused in improving the properties of these vectors, in particular in modulating the intensity and time-course of transgene expression [52, 80]. Long-term gene expression is still difficult to achieve, although some success has been obtained in the PNS with the HSV-1 latency-active promoter 2 (LAP2) [31, 52]. Other recent studies have focused in improving target expression to specific neuronal populations [81] and, since there is considerably neuronal heterogeneity in both the PNS and CNS, it would be naive to presume that the behaviour of viral vectors will be the same for all neuronal populations in different regions of the nervous system.…”

Section: Hsv-based Vectors For Gene Therapy Of the Nervous Systemmentioning

confidence: 99%

HSV Recombinant Vectors for Gene Therapy

Manservigi

Argnani²,

Marconi³

2010

TOVJ

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The very deep knowledge acquired on the genetics and molecular biology of herpes simplex virus (HSV), has allowed the development of potential replication-competent and replication-defective vectors for several applications in human healthcare. These include delivery and expression of human genes to cells of the nervous systems, selective destruction of cancer cells, prophylaxis against infection with HSV or other infectious diseases, and targeted infection to specific tissues or organs. Replication-defective recombinant vectors are non-toxic gene transfer tools that preserve most of the neurotropic features of wild type HSV-1, particularly the ability to express genes after having established latent infections, and are thus proficient candidates for therapeutic gene transfer settings in neurons. A replication-defective HSV vector for the treatment of pain has recently entered in phase 1 clinical trial. Replication-competent (oncolytic) vectors are becoming a suitable and powerful tool to eradicate brain tumours due to their ability to replicate and spread only within the tumour mass, and have reached phase II/III clinical trials in some cases. The progress in understanding the host immune response induced by the vector is also improving the use of HSV as a vaccine vector against both HSV infection and other pathogens. This review briefly summarizes the obstacle encountered in the delivery of HSV vectors and examines the various strategies developed or proposed to overcome such challenges.

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Prolonged preservation of nerve function in diabetic neuropathy in mice by herpes simplex virus-mediated gene transfer

Cited by 39 publications

References 38 publications

Diabetic Painful and Insensate Neuropathy: Pathogenesis and Potential Treatments

Diabetic Painful and Insensate Neuropathy: Pathogenesis and Potential Treatments

Epidermal nerve fiber quantification in the assessment of diabetic neuropathy

HSV Recombinant Vectors for Gene Therapy

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