Diabetes‐induced expression of activating transcription factor 3 in mouse primary sensory neurons

Wright, Douglas E.; Ryals, Janelle M.; McCarson, Kenneth E.; Christianson, Julie A.

doi:10.1111/j.1085-9489.2004.09404.x

Cited by 34 publications

(30 citation statements)

References 52 publications

(73 reference statements)

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“…DN was also examined in C57BL/6J mice following a single high dose of STZ ( Table 2) [30,47,[55][56][57][58][59]. Similar to the majority of reports in low dose STZ-treated mice, DN was examined following diabetes duration of 1-9 weeks.…”

Section: Mouse Models Of Dnmentioning

confidence: 97%

“…Investigations of DN in this model by Wright and co-workers reveal decreased mechanical sensitivity at 8 and 9 weeks post STZtreatment with reduced IENF densities but no changes in thermal thresholds. Nerve conduction velocities were not measured ( Table 2) [30,[55][56][57]59]. Thus, while there is no doubt that the C57BL/6J mouse develops profound diabetes in response to single high dose STZ treatment, evidence of DN is again only described in short term diabetes.…”

Section: Mouse Models Of Dnmentioning

confidence: 99%

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Criteria for Creating and Assessing Mouse Models of Diabetic Neuropathy

Sullivan

Lentz²,

Roberts

et al. 2008

CDT

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Diabetic neuropathy (DN) is a serious and debilitating complication of both type 1 and type 2 diabetes. Despite intense research efforts into multiple aspects of this complication, including both vascular and neuronal metabolic derangements, the only treatment remains maintenance of euglycemia. Basic research into the mechanisms responsible for DN relies on using the most appropriate animal model. The advent of genetic manipulation has moved mouse models of human disease to the forefront. The ability to insert or delete genes affected in human patients offers unique insight into disease processes; however, mice are still not humans and difficulties remain in interpreting data derived from these animals. A number of studies have investigated and described DN in mice but it is difficult to compare these studies with each other or with human DN due to experimental differences including background strain, type of diabetes, method of induction and duration of diabetes, animal age and gender. This review describes currently used DN animal models. We followed a standardized diabetes induction protocol and designed and implemented a set of phenotyping parameters to classify the development and severity of DN. By applying standard protocols, we hope to facilitate the comparison and characterization of DN across different background strains in the hope of discovering the most human like model in which to test potential therapies. KeywordsNOD; Akita; ob/ob; db/db; outbred mice; nerve conduction velocity; intraepidermal nerve fiber density DIABETES MELLITUSThe term "diabetes mellitus" describes a number of conditions in which blood glucose is elevated including insulin dependent diabetes mellitus (IDDM) Beyond effective control of glucose levels, there are no treatments to prevent or cure DN. Numerous factors have impeded laboratory investigations aimed at the development of effective therapies, including an incomplete analysis of existing animal models that develop DN, lack of consistency among mouse models (diabetes induction and genetics) and lack of consensus concerning phenotyping methods. The AMDCC was formed by the NIH to develop new animal models of diabetes and its complications; its goal is to identify the most appropriate animal models to study the etiology, prevention and treatment of diabetic complications. The group has reported its findings comparing the effects of diabetes on cardiovascular disease [2], and nephropathy [12] in inbred mice from different genetic background strains and maintains a website containing its recommended phenotyping protocols. AMDCC investigators continue to refine genetic and dietary factors that affect the development of diabetes and its complications, potential interactions and overlap of complications within a genetic model, and common pathways that may influence treatment paradigms in human patients.In order to provide a consistent method of examining DN in diabetic mouse models, our laboratory implemented a standardized diabetes induction protocol used by the AMDCC (...

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Section: Mouse Models Of Dnmentioning

confidence: 97%

Section: Mouse Models Of Dnmentioning

confidence: 99%

Criteria for Creating and Assessing Mouse Models of Diabetic Neuropathy

Sullivan

Lentz²,

Roberts

et al. 2008

CDT

View full text Add to dashboard Cite

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“…Despite overwhelming evidence indicating that ATF3 is a stressinducible gene in a variety of tissues and acts as a transcriptional repressor, the physiological consequences of Atf3 expression are not well understood. However, it was recently reported that Atf3 is expressed in primary sensory neurons of diabetic mice [24] and ATF3 is expressed in the islets of patients with type 1 or type 2 diabetes [25,26].…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial dysfunction induces aberrant insulin signalling and glucose utilisation in murine C2C12 myotube cells

et al. 2006

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Aims/hypothesis: Mitochondrial dysfunction is considered a critical component in the development of diabetes. The aim of this study was to elucidate the molecular mechanisms involved in the development of insulin resistance and diabetes through investigation of mitochondrial retrograde signalling. Materials and methods: Mitochondrial function of C2C12 myotube cells was impaired by genetic (ethidium bromide) and metabolic (oligomycin) stress, and changes in target molecules related to insulin signalling were analysed. Results: Concomitant with reductions in mitochondrial membrane potential (ΔΨm) and ATP synthesis, production of IRS1 and solute carrier family 2 (facilitated glucose transporter), member 4 (SLC2A4, formerly known as GLUT4) were reduced. Moreover, serine phosphorylation of IRS1 increased, resulting in decreased tyrosine phosphorylation. This indicates that mitochondrial dysfunction decreases insulin-stimulated SLC2A4 translocation and glucose uptake. Mitochondrial stress activated c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK) signalling in a Ca 2+ -dependent manner, and removal of free Ca 2+ by BAPTA-AM, as well as inhibition of JNK and p38 MAPK, abrogated mitochondrial stress-induced reductions in IRS1 and SLC2A4 production. Mitochondrial dysfunction after oligomycin treatment significantly increased levels of activating transcription factor 3 (ATF3), which represses Irs1 promoter activity. Removal of the 5′ flanking region of Irs1 demonstrated that the promoter region within 191 bases from the transcription site may be involved in the transcriptional repression of Irs1 by mitochondrial stress. Conclusions/interpretation:We show distinct mitochondrial retrograde signalling, where Irs1 is downregulated through ATF3 in a Ca 2+ -, JNK-and p38 MAPK-dependent manner, and IRS1 is inactivated. Therefore, mitochondrial dysfunction causes aberrant insulin signalling and abnormal utilisation of glucose, as observed in many insulin resistance states.

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“…Thus, it is appreciated that frank nerve injury will lead to a variety of changes in the biology of the dorsal root ganglion cells of the injured axon, such as, for example, an increase in the expression of DRG activation transcription factor-3. 166 In this regard, changes in DRG activation transcription factor-3 expression have been observed not only after nerve section and compression, but after chemical stimuli (paclitaxel 135 ), in diabetes, 167 and even in some peripheral chronic inflammatory syndromes as diverse as equine laminitis. 168 It is thus reasonable to expect that many of these chronic states may lead to changes in nerve function that lead to the encoding of a nociceptive signal.…”

Section: Resultsmentioning

confidence: 99%

Behavioral Models of Pain States Evoked by Physical Injury to the Peripheral Nerve

Sorkin

Yaksh

2009

Neurotherapeutics

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Summary:Physical injury or compression of the root, dorsal root ganglion, or peripheral sensory axon leads to welldefined changes in biology and function. Behaviorally, humans report ongoing painful dysesthesias and aberrations in function, such that an otherwise innocuous stimulus will yield a pain report. These behavioral reports are believed to reflect the underlying changes in nerve function after injury, wherein increased spontaneous activity arises from the neuroma and dorsal root ganglion and spinal changes increase the response of spinal projection neurons. These pain states are distinct from those associated with tissue injury and pose particular problems in management. To provide for developing an understanding of the underlying mechanisms of these pain states and to promote development of therapeutic agents, preclinical models involving section, compression, and constriction of the peripheral nerve or compression of the dorsal root ganglion have been developed. These models give rise to behaviors, which parallel those observed in the human after nerve injury. The present review considers these models and their application.

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Diabetes‐induced expression of activating transcription factor 3 in mouse primary sensory neurons

Cited by 34 publications

References 52 publications

Criteria for Creating and Assessing Mouse Models of Diabetic Neuropathy

Criteria for Creating and Assessing Mouse Models of Diabetic Neuropathy

Mitochondrial dysfunction induces aberrant insulin signalling and glucose utilisation in murine C2C12 myotube cells

Behavioral Models of Pain States Evoked by Physical Injury to the Peripheral Nerve

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