دورية أكاديمية
The proinflammatory cytokine, interleukin-17A, augments mitochondrial function and neurite outgrowth of cultured adult sensory neurons derived from normal and diabetic rats.
| العنوان: | The proinflammatory cytokine, interleukin-17A, augments mitochondrial function and neurite outgrowth of cultured adult sensory neurons derived from normal and diabetic rats. |
|---|---|
| المؤلفون: | Habash, Tarek1,2, Saleh, Ali1, Roy Chowdhury, Subir K.1, Smith, Darrell R.1, Fernyhough, Paul1,2 pfernyhough@sbrc.ca |
| المصدر: | Experimental Neurology. Nov2015, Vol. 273, p177-189. 13p. |
| مصطلحات موضوعية: | *NERVE cell culture, *INTERLEUKIN-17, *LABORATORY rats, *SENSORY neurons, *RECEPTIVE fields (Neurology), *NEURONS, *NERVOUS system, *NEUROLOGY |
| مستخلص: | Background Diabetic neuropathy comprises dying back of nerve endings that reflects impairment in axonal plasticity and regenerative nerve growth. Metabolic changes in diabetes can lead to a dysregulation of hormonal mediators, such as cytokines, that may constrain distal nerve fiber growth. Interleukin-17 (IL-17A), a proinflammatory and neurotropic cytokine produced by T-cells, was significantly reduced in sciatic nerve of streptozotocin (STZ)-diabetic rats. Thus we studied the effect of IL-17A on the phenotype of sensory neurons derived from age matched control or type 1 diabetic rats. The aims were to determine the ability of IL-17A to enhance neurite outgrowth in cultured sensory neurons, investigate the signaling pathways activated by IL-17A, study the role of mitochondria and mechanistically link to neurite outgrowth. Results IL-17A (10 ng/ml; p < 0.05) significantly and dose-dependently increased total neurite outgrowth in cultures of adult dorsal root ganglia (DRG) sensory neurons derived from both control and streptozotocin (STZ)-diabetic rats. This enhancement was mediated by IL-17A-dependent activation of extracellular-regulated protein kinase (ERK) and phosphoinositide-3 kinase (PI-3K) signal transduction pathways. Pharmacological blockade of one of these activated pathways triggered complete inhibition of neurite outgrowth. IL-17A augmented mitochondrial bioenergetic function of sensory neurons derived from control or diabetic rats and this was also mediated via ERK or PI-3K. IL-17A-dependent elevation of bioenergetic function was associated with augmented expression of proteins of the mitochondrial electron transport system complexes. Conclusions IL-17A enhanced axonal plasticity through activation of ERK and PI-3K pathways and was associated with augmented mitochondrial bioenergetic function in sensory neurons. [ABSTRACT FROM AUTHOR] |
| قاعدة البيانات: | Academic Search Index |
| ResultId |
1 |
|---|---|
| Header |
asx Academic Search Index 110853955 1231 6 Academic Journal academicJournal 1230.79638671875 |
| PLink |
https://search.ebscohost.com/login.aspx?direct=true&site=eds-live&scope=site&db=asx&AN=110853955&custid=s6537998&authtype=sso |
| FullText |
Array
(
[Availability] => 0
)
|
| Items |
Array
(
[Name] => Title
[Label] => Title
[Group] => Ti
[Data] => The proinflammatory cytokine, interleukin-17A, augments mitochondrial function and neurite outgrowth of cultured adult sensory neurons derived from normal and diabetic rats.
)
Array ( [Name] => Author [Label] => Authors [Group] => Au [Data] => <searchLink fieldCode="AR" term="%22Habash%2C+Tarek%22">Habash, Tarek</searchLink><relatesTo>1,2</relatesTo><br /><searchLink fieldCode="AR" term="%22Saleh%2C+Ali%22">Saleh, Ali</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Roy+Chowdhury%2C+Subir+K%2E%22">Roy Chowdhury, Subir K.</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Smith%2C+Darrell+R%2E%22">Smith, Darrell R.</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Fernyhough%2C+Paul%22">Fernyhough, Paul</searchLink><relatesTo>1,2</relatesTo><i> pfernyhough@sbrc.ca</i> ) Array ( [Name] => TitleSource [Label] => Source [Group] => Src [Data] => <searchLink fieldCode="JN" term="%22Experimental+Neurology%22">Experimental Neurology</searchLink>. Nov2015, Vol. 273, p177-189. 13p. ) Array ( [Name] => Subject [Label] => Subject Terms [Group] => Su [Data] => *<searchLink fieldCode="DE" term="%22NERVE+cell+culture%22">NERVE cell culture</searchLink><br />*<searchLink fieldCode="DE" term="%22INTERLEUKIN-17%22">INTERLEUKIN-17</searchLink><br />*<searchLink fieldCode="DE" term="%22LABORATORY+rats%22">LABORATORY rats</searchLink><br />*<searchLink fieldCode="DE" term="%22SENSORY+neurons%22">SENSORY neurons</searchLink><br />*<searchLink fieldCode="DE" term="%22RECEPTIVE+fields+%28Neurology%29%22">RECEPTIVE fields (Neurology)</searchLink><br />*<searchLink fieldCode="DE" term="%22NEURONS%22">NEURONS</searchLink><br />*<searchLink fieldCode="DE" term="%22NERVOUS+system%22">NERVOUS system</searchLink><br />*<searchLink fieldCode="DE" term="%22NEUROLOGY%22">NEUROLOGY</searchLink> ) Array ( [Name] => Abstract [Label] => Abstract [Group] => Ab [Data] => Background Diabetic neuropathy comprises dying back of nerve endings that reflects impairment in axonal plasticity and regenerative nerve growth. Metabolic changes in diabetes can lead to a dysregulation of hormonal mediators, such as cytokines, that may constrain distal nerve fiber growth. Interleukin-17 (IL-17A), a proinflammatory and neurotropic cytokine produced by T-cells, was significantly reduced in sciatic nerve of streptozotocin (STZ)-diabetic rats. Thus we studied the effect of IL-17A on the phenotype of sensory neurons derived from age matched control or type 1 diabetic rats. The aims were to determine the ability of IL-17A to enhance neurite outgrowth in cultured sensory neurons, investigate the signaling pathways activated by IL-17A, study the role of mitochondria and mechanistically link to neurite outgrowth. Results IL-17A (10 ng/ml; p < 0.05) significantly and dose-dependently increased total neurite outgrowth in cultures of adult dorsal root ganglia (DRG) sensory neurons derived from both control and streptozotocin (STZ)-diabetic rats. This enhancement was mediated by IL-17A-dependent activation of extracellular-regulated protein kinase (ERK) and phosphoinositide-3 kinase (PI-3K) signal transduction pathways. Pharmacological blockade of one of these activated pathways triggered complete inhibition of neurite outgrowth. IL-17A augmented mitochondrial bioenergetic function of sensory neurons derived from control or diabetic rats and this was also mediated via ERK or PI-3K. IL-17A-dependent elevation of bioenergetic function was associated with augmented expression of proteins of the mitochondrial electron transport system complexes. Conclusions IL-17A enhanced axonal plasticity through activation of ERK and PI-3K pathways and was associated with augmented mitochondrial bioenergetic function in sensory neurons. [ABSTRACT FROM AUTHOR] ) |
| RecordInfo |
Array
(
[BibEntity] => Array
(
[Identifiers] => Array
(
[0] => Array
(
[Type] => doi
[Value] => 10.1016/j.expneurol.2015.08.016
)
)
[Languages] => Array
(
[0] => Array
(
[Code] => eng
[Text] => English
)
)
[PhysicalDescription] => Array
(
[Pagination] => Array
(
[PageCount] => 13
[StartPage] => 177
)
)
[Subjects] => Array
(
[0] => Array
(
[SubjectFull] => NERVE cell culture
[Type] => general
)
[1] => Array
(
[SubjectFull] => INTERLEUKIN-17
[Type] => general
)
[2] => Array
(
[SubjectFull] => LABORATORY rats
[Type] => general
)
[3] => Array
(
[SubjectFull] => SENSORY neurons
[Type] => general
)
[4] => Array
(
[SubjectFull] => RECEPTIVE fields (Neurology)
[Type] => general
)
[5] => Array
(
[SubjectFull] => NEURONS
[Type] => general
)
[6] => Array
(
[SubjectFull] => NERVOUS system
[Type] => general
)
[7] => Array
(
[SubjectFull] => NEUROLOGY
[Type] => general
)
)
[Titles] => Array
(
[0] => Array
(
[TitleFull] => The proinflammatory cytokine, interleukin-17A, augments mitochondrial function and neurite outgrowth of cultured adult sensory neurons derived from normal and diabetic rats.
[Type] => main
)
)
)
[BibRelationships] => Array
(
[HasContributorRelationships] => Array
(
[0] => Array
(
[PersonEntity] => Array
(
[Name] => Array
(
[NameFull] => Habash, Tarek
)
)
)
[1] => Array
(
[PersonEntity] => Array
(
[Name] => Array
(
[NameFull] => Saleh, Ali
)
)
)
[2] => Array
(
[PersonEntity] => Array
(
[Name] => Array
(
[NameFull] => Roy Chowdhury, Subir K.
)
)
)
[3] => Array
(
[PersonEntity] => Array
(
[Name] => Array
(
[NameFull] => Smith, Darrell R.
)
)
)
[4] => Array
(
[PersonEntity] => Array
(
[Name] => Array
(
[NameFull] => Fernyhough, Paul
)
)
)
)
[IsPartOfRelationships] => Array
(
[0] => Array
(
[BibEntity] => Array
(
[Dates] => Array
(
[0] => Array
(
[D] => 01
[M] => 11
[Text] => Nov2015
[Type] => published
[Y] => 2015
)
)
[Identifiers] => Array
(
[0] => Array
(
[Type] => issn-print
[Value] => 00144886
)
)
[Numbering] => Array
(
[0] => Array
(
[Type] => volume
[Value] => 273
)
)
[Titles] => Array
(
[0] => Array
(
[TitleFull] => Experimental Neurology
[Type] => main
)
)
)
)
)
)
)
|
| IllustrationInfo |