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Conference Paper: Development of diabetic retinopathy and worsened outcomes after ischemic stroke in a transgenic mouse model of Type 1diabetes

TitleDevelopment of diabetic retinopathy and worsened outcomes after ischemic stroke in a transgenic mouse model of Type 1diabetes
Authors
KeywordsMedical sciences
Endocrinology medical sciences
Gastroenterology medical sciences
Nurses and nursing
Issue Date2015
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/DME
Citation
The 2015 Diabetes UK Professional Conference, London, UK., 11-13 March 2015. In Diabetic Medicine, 2015, v. 32 suppl. S1, p. 31, abstract P4 How to Cite?
AbstractAIMS: Patients with Type 1 diabetes are more prone to develop retinopathy and display a more severe post-ischaemic outcome. We aim (i) to study the progressive effect of hyperglycaemia on retinal function and (ii) to investigate the potential mechanisms in the exacerbation in these patients after stroke. METHODS: Retinal functions of Ins2Akita/+ mice, a transgenic mouse model of Type 1 diabetes, were assessed using electroretinography (n=10–13). Two hour middle cerebral artery occlusion was induced in Ins2Akita/+ mice followed by 2h of reperfusion (n=10–12). Protein expressions in ipsilateral brains were detected by western blot analysis (n=4–7). RESULTS: (i) In electroretinography assessment, Ins2Akita/+ mice displayed diminished amplitude in b-wave at 20 weeks old (448 +/- 13uV vs 350 +/- 21uV, p < 0.001) and in a-wave (-181 +/- 7uV vs -126 +/- 11uV, p < 0.001) and ΣOPs (218 +/- 14uV vs 146 +/- 9uV, p < 0.001) at 36 weeks old. (ii) After reperfusion, Ins2Akita/+ mice exhibited increased mortality (0% vs 20%, p < 0.05), neurological deficits (1.7 +/- 0.5 vs 2.3 +/- 1.0, p < 0.05), infarct size (18.9% +/- 4.2% vs 34.9% +/- 4.1%, p < 0.05) and haemorrhage (0.07% +/- 0.07% vs 0.42% +/- 0.15%, p < 0.05). Decreased ZO-1 (0.6 +/- 0.1 vs 0.2 +/- 0.1, p < 0.01) but elevated VEGF (3.7 +/- 2.2 vs 11.5 +/- 3.8, p < 0.001) and pErk (12.5 +/- 7.9 vs 48.2 +/- 15.1, p < 0.001) protein expressions were observed in the post-ischaemic Ins2Akita/+ brain. CONCLUSIONS: Ins2Akita/+ mice showed hyperglycaemia-associated visual dysfunction and worsened outcomes after ischaemia, which were comparable to clinical studies. Ins2Akita/+ mice could therefore be used for studying the pathogenesis of early diabetic retinopathy. Vulnerable blood vessel integrity and pronounced inflammatory response may account for the post-ischaemia exacerbation, suggesting that VEGF and pErk are the potential therapeutic targets for diabetic subjects upon stroke.
DescriptionPoster Abstracts - Basic and clinical science posters: basic science of diabetes complications: no.P4
This free journal suppl. entitled: Special Issue: Abstracts of the Diabetes UK Professional Conference 2015, ExCeL London, 11–13 March 2015
Persistent Identifierhttp://hdl.handle.net/10722/218603
ISSN
2015 Impact Factor: 3.152
2015 SCImago Journal Rankings: 1.654

 

DC FieldValueLanguage
dc.contributor.authorLai, AKW-
dc.contributor.authorLo, AC-
dc.date.accessioned2015-09-18T06:47:59Z-
dc.date.available2015-09-18T06:47:59Z-
dc.date.issued2015-
dc.identifier.citationThe 2015 Diabetes UK Professional Conference, London, UK., 11-13 March 2015. In Diabetic Medicine, 2015, v. 32 suppl. S1, p. 31, abstract P4-
dc.identifier.issn0742-3071-
dc.identifier.urihttp://hdl.handle.net/10722/218603-
dc.descriptionPoster Abstracts - Basic and clinical science posters: basic science of diabetes complications: no.P4-
dc.descriptionThis free journal suppl. entitled: Special Issue: Abstracts of the Diabetes UK Professional Conference 2015, ExCeL London, 11–13 March 2015-
dc.description.abstractAIMS: Patients with Type 1 diabetes are more prone to develop retinopathy and display a more severe post-ischaemic outcome. We aim (i) to study the progressive effect of hyperglycaemia on retinal function and (ii) to investigate the potential mechanisms in the exacerbation in these patients after stroke. METHODS: Retinal functions of Ins2Akita/+ mice, a transgenic mouse model of Type 1 diabetes, were assessed using electroretinography (n=10–13). Two hour middle cerebral artery occlusion was induced in Ins2Akita/+ mice followed by 2h of reperfusion (n=10–12). Protein expressions in ipsilateral brains were detected by western blot analysis (n=4–7). RESULTS: (i) In electroretinography assessment, Ins2Akita/+ mice displayed diminished amplitude in b-wave at 20 weeks old (448 +/- 13uV vs 350 +/- 21uV, p < 0.001) and in a-wave (-181 +/- 7uV vs -126 +/- 11uV, p < 0.001) and ΣOPs (218 +/- 14uV vs 146 +/- 9uV, p < 0.001) at 36 weeks old. (ii) After reperfusion, Ins2Akita/+ mice exhibited increased mortality (0% vs 20%, p < 0.05), neurological deficits (1.7 +/- 0.5 vs 2.3 +/- 1.0, p < 0.05), infarct size (18.9% +/- 4.2% vs 34.9% +/- 4.1%, p < 0.05) and haemorrhage (0.07% +/- 0.07% vs 0.42% +/- 0.15%, p < 0.05). Decreased ZO-1 (0.6 +/- 0.1 vs 0.2 +/- 0.1, p < 0.01) but elevated VEGF (3.7 +/- 2.2 vs 11.5 +/- 3.8, p < 0.001) and pErk (12.5 +/- 7.9 vs 48.2 +/- 15.1, p < 0.001) protein expressions were observed in the post-ischaemic Ins2Akita/+ brain. CONCLUSIONS: Ins2Akita/+ mice showed hyperglycaemia-associated visual dysfunction and worsened outcomes after ischaemia, which were comparable to clinical studies. Ins2Akita/+ mice could therefore be used for studying the pathogenesis of early diabetic retinopathy. Vulnerable blood vessel integrity and pronounced inflammatory response may account for the post-ischaemia exacerbation, suggesting that VEGF and pErk are the potential therapeutic targets for diabetic subjects upon stroke.-
dc.languageeng-
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/DME-
dc.relation.ispartofDiabetic Medicine-
dc.rightsThe definitive version is available at www.blackwell-synergy.com-
dc.subjectMedical sciences-
dc.subjectEndocrinology medical sciences-
dc.subjectGastroenterology medical sciences-
dc.subjectNurses and nursing-
dc.titleDevelopment of diabetic retinopathy and worsened outcomes after ischemic stroke in a transgenic mouse model of Type 1diabetes-
dc.typeConference_Paper-
dc.identifier.emailLo, AC: amylo@hku.hk-
dc.identifier.authorityLo, AC=rp00425-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1111/dme.12668-
dc.identifier.hkuros251438-
dc.identifier.volume32-
dc.identifier.issuesuppl. S1-
dc.identifier.spage31, abstract P4-
dc.identifier.epage31, abstract P4-
dc.publisher.placeUnited Kingdom-

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