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Conference Paper: Role of deleted in liver cancer 2(DLC2) in diabetes-associated neuropathy

TitleRole of deleted in liver cancer 2(DLC2) in diabetes-associated neuropathy
Authors
Issue Date2016
PublisherThe University of Hong Kong.
Citation
The 2016 Neuroscience Symposium and Annual Scientific Conference of the Hong Kong Society of Neurosciences, The University of Hong Kong, Hong Kong, 18 May 2016. In Programme Book, 2016, p. 33, abstract no. P10 How to Cite?
AbstractDiabetes mellitus (DM), characterized by hyperglycemia, represents one of the main threats to human health in the 21st century. One of the major complications of diabetes is diabetic neuropathy but few effective treatment options exist for this disease. Previously we found mice deficient in DLC2, a RhoA specific GTPase-activating protein, to have increased sensitivity to thermal and inflammatory stimuli compared to wild type (DLC2+/+) in acute pain tests. Here, we hypothesize that DLC2 may also play a protective role in chronic inflammatory pain associated with diabetes. To address this, multiple low dose streptozotocin (MLDS) treatment was used to induce diabetes in DLC2-/- and DLC2+/+ mice, and nociceptive behavior were measured. Interestingly, non-diabetic and diabetic DLC2-/- mice showed more severe hyperalgesia compared to the corresponding DLC2+/+ mice. In addition, diabetic DLC2-/- mice also showed earlier onset of painful response than diabetic DLC2+/+ mice. Diabetic and non-diabetic DLC2-/- mice showed more small sensory nerve ending density in the skin. Meanwhile, the dorsal root ganglia of these mice had higher gene expression of voltage-gated sodium channel SCN11A compared to diabetic DLC2+/+ mice, while phosphorylated ERK was elevated in non-diabetic DLC2-/- mice and diabetic mice of both genotypes compared to non-diabetic DLC2+/+ mice. The DLC2-/- mice are a useful model to investigate the glucose metabolism and diabetic painful neuropathy since DLC2-/- mice display lower blood glucose level with MLDS treatment, but have more severe chronic inflammatory pain response. We also hypothesize that increased RhoA activity and pERK levels may lead to increased SCN11A transcription and activation, leading to a heightened pain response in diabetic DLC2-/-mice. This project is supported by the funding from Hong Kong GRF grant to S.K.Chung.
DescriptionConference Theme: Nature and Nurture in Brain Functions
Persistent Identifierhttp://hdl.handle.net/10722/231495

 

DC FieldValueLanguage
dc.contributor.authorFeng, R-
dc.contributor.authorTirrell, LS-
dc.contributor.authorChung, SK-
dc.date.accessioned2016-09-20T05:23:32Z-
dc.date.available2016-09-20T05:23:32Z-
dc.date.issued2016-
dc.identifier.citationThe 2016 Neuroscience Symposium and Annual Scientific Conference of the Hong Kong Society of Neurosciences, The University of Hong Kong, Hong Kong, 18 May 2016. In Programme Book, 2016, p. 33, abstract no. P10-
dc.identifier.urihttp://hdl.handle.net/10722/231495-
dc.descriptionConference Theme: Nature and Nurture in Brain Functions-
dc.description.abstractDiabetes mellitus (DM), characterized by hyperglycemia, represents one of the main threats to human health in the 21st century. One of the major complications of diabetes is diabetic neuropathy but few effective treatment options exist for this disease. Previously we found mice deficient in DLC2, a RhoA specific GTPase-activating protein, to have increased sensitivity to thermal and inflammatory stimuli compared to wild type (DLC2+/+) in acute pain tests. Here, we hypothesize that DLC2 may also play a protective role in chronic inflammatory pain associated with diabetes. To address this, multiple low dose streptozotocin (MLDS) treatment was used to induce diabetes in DLC2-/- and DLC2+/+ mice, and nociceptive behavior were measured. Interestingly, non-diabetic and diabetic DLC2-/- mice showed more severe hyperalgesia compared to the corresponding DLC2+/+ mice. In addition, diabetic DLC2-/- mice also showed earlier onset of painful response than diabetic DLC2+/+ mice. Diabetic and non-diabetic DLC2-/- mice showed more small sensory nerve ending density in the skin. Meanwhile, the dorsal root ganglia of these mice had higher gene expression of voltage-gated sodium channel SCN11A compared to diabetic DLC2+/+ mice, while phosphorylated ERK was elevated in non-diabetic DLC2-/- mice and diabetic mice of both genotypes compared to non-diabetic DLC2+/+ mice. The DLC2-/- mice are a useful model to investigate the glucose metabolism and diabetic painful neuropathy since DLC2-/- mice display lower blood glucose level with MLDS treatment, but have more severe chronic inflammatory pain response. We also hypothesize that increased RhoA activity and pERK levels may lead to increased SCN11A transcription and activation, leading to a heightened pain response in diabetic DLC2-/-mice. This project is supported by the funding from Hong Kong GRF grant to S.K.Chung.-
dc.languageeng-
dc.publisherThe University of Hong Kong.-
dc.relation.ispartofNeuroscience Symposium & Annual Scientific Conference of the Hong Kong Society of Neurosciences-
dc.titleRole of deleted in liver cancer 2(DLC2) in diabetes-associated neuropathy-
dc.typeConference_Paper-
dc.identifier.emailChung, SK: skchung@hkucc.hku.hk-
dc.identifier.authorityChung, SK=rp00381-
dc.identifier.hkuros266224-
dc.identifier.spage33, abstract no. P10-
dc.identifier.epage33, abstract no. P10-
dc.publisher.placeHong Kong-

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