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MiR-335 regulates e...
MiR-335 regulates exocytotic proteins and affects glucose-stimulated insulin secretion through decreased Ca2+-dependent exocytosis in beta cells
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- Salunkhe, V.A. (författare)
- Lund University,Lunds universitet,Diabetes - öcellsexocytos,Forskargrupper vid Lunds universitet,Diabetes - Islet Cell Exocytosis,Lund University Research Groups
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- Ofori, J. (författare)
- Lund University,Lunds universitet,Diabetes - öcellsexocytos,Forskargrupper vid Lunds universitet,Diabetes - Islet Cell Exocytosis,Lund University Research Groups
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- Gandasi, N.R. (författare)
- Uppsala University
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- Salö, S.A. (författare)
- Roskilde University,Lund University
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- Wendt, A. (författare)
- Lund University,Lunds universitet,Diabetes - öcellsexocytos,Forskargrupper vid Lunds universitet,Diabetes - Islet Cell Exocytosis,Lund University Research Groups
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- Barg, S. (författare)
- Uppsala University
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- Esguerra, J.L.S. (författare)
- Lund University,Lunds universitet,Diabetes - öcellsexocytos,Forskargrupper vid Lunds universitet,Diabetes - Islet Cell Exocytosis,Lund University Research Groups
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- Eliasson, L. (författare)
- Lund University,Lunds universitet,Diabetes - öcellsexocytos,Forskargrupper vid Lunds universitet,Diabetes - Islet Cell Exocytosis,Lund University Research Groups
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(creator_code:org_t)
- 2015-08-12
- 2015
- Engelska 1 s.
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Ingår i: Diabetologia. - : Springer Science and Business Media LLC. - 1432-0428 .- 0012-186X. ; 58:Suppl. 1, s. 128-128
- Relaterad länk:
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http://dx.doi.org/10...
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https://link.springe...
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https://lup.lub.lu.s...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- Background and aims: Ca2+-induced exocytosis is essential for insulin to be secreted from beta-cells, and in islets from type-2 diabetic (T2D) donors the expression of several genes coding for exocytotic proteins is reduced. Largely this phenomenon cannot be explained by polymorphism; rather it is likely due to epigenetic factors like microRNAs (miRNAs). Indeed, previous studies have identified a number of miRNAs with differential expression in the islets from T2D donors and the Goto- Kakizaki (GK) rat. One of the upregulatedmiRNAs in the GK rat is miR- 335, predicted to target several exocytotic genes amongst those Stxbp1 is a validated target. Here we aim to investigate whether miR-335 regulates the expression of exocytotic genes and affects insulin secretion and exocytosis in beta-cells. Materials and methods: Insulin secretion was measured by radio immuno assay. Exocytosis and docking of insulin granules was studied by capacitance measurements using the patch-clamp technique and by TIRF microscopy. Rat miR-335 was overexpressed using chemicallymodified mature microRNA mimic in INS-1 832/13 beta-cells by transfection. Gene knockdown was performed with RNAi. Protein and mRNA levels were analysed with Western Blot and RT-qPCR, respectively. Results: Overexpression of miR-335 (OE335) in INS-1 832/13 cells reduced insulin secretion at 16.7 mM glucose compared to control cells (SCR) (n=3; p
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Endokrinologi och diabetes (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Endocrinology and Diabetes (hsv//eng)
Nyckelord
- glucose
- protein
- insulin
- microRNA
- synaptotagmin
- nitrogen 15
- messenger RNA
- insulin release
- exocytosis
- European
- diabetes mellitus
- gene
- microscopy
- donor
- membrane
- Goto Kakizaki rat
- rat
- genetic transfection
- patch clamp technique
- immunoassay
- gene silencing
- pancreas islet beta cell
- density
- electric potential
- Western blotting
- adaptation
- cell function
- telecommunication
Publikations- och innehållstyp
- kon (ämneskategori)
- ref (ämneskategori)
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