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Different Profile of mRNA Expression in Sinoatrial Node from Streptozotocin-Induced Diabetic Rat
- Source :
- PLoS ONE, Vol 11, Iss 4, p e0153934 (2016), Ferdous, Z, Qureshi, M A, Jayaprakash, P, Parekh, K, John, A, Oz, M, Raza, H, Dobrzynski, H, Adrian, T E & Howarth, F C 2016, ' Different profile of mRNA expression in sinoatrial node from streptozotocin-induced diabetic rat ', PLoS ONE, vol. 11, no. 4, e0153934 . https://doi.org/10.1371/journal.pone.0153934, PLoS ONE
- Publication Year :
- 2016
- Publisher :
- Public Library of Science (PLoS), 2016.
-
Abstract
- Background Experiments in isolated perfused heart have shown that heart rate is lower and sinoatrial node (SAN) action potential duration is longer in streptozotocin (STZ)–induced diabetic rat compared to controls. In sino-atrial preparations the pacemaker cycle length and sino-atrial conduction time are prolonged in STZ heart. To further clarify the molecular basis of electrical disturbances in the diabetic heart the profile of mRNA encoding a wide variety of proteins associated with the generation and transmission of electrical activity has been evaluated in the SAN of STZ-induced diabetic rat heart. Methodology/Principal Findings Heart rate was measured in isolated perfused heart with an extracellular suction electrode. Expression of mRNA encoding a variety of intercellular proteins, intracellular Ca2+-transport and regulatory proteins, cell membrane transport proteins and calcium, sodium and potassium channel proteins were measured in SAN and right atrial (RA) biopsies using real-time reverse transcription polymerase chain reaction techniques. Heart rate was lower in STZ (203±7 bpm) compared to control (239±11 bpm) rat. Among many differences in the profile of mRNA there are some worthy of particular emphasis. Expression of genes encoding some proteins were significantly downregulated in STZ-SAN: calcium channel, Cacng4 (7-fold); potassium channel, Kcnd2 whilst genes encoding some other proteins were significantly upregulated in STZ-SAN: gap junction, Gjc1; cell membrane transport, Slc8a1, Trpc1, Trpc6 (4-fold); intracellular Ca2+-transport, Ryr3; calcium channel Cacna1g, Cacna1h, Cacnb3; potassium channels, Kcnj5, Kcnk3 and natriuretic peptides, Nppa (5-fold) and Nppb (7-fold). Conclusions/Significance Collectively, this study has demonstrated differences in the profile of mRNA encoding a variety of proteins that are associated with the generation, conduction and regulation of electrical signals in the SAN of STZ-induced diabetic rat heart. Data from this study will provide a basis for a substantial range of future studies to investigate whether these changes in mRNA translate into changes in electrophysiological function.
- Subjects :
- Voltage-Gated Ion Channels
Male
0301 basic medicine
Potassium Channels
Physiology
Action Potentials
lcsh:Medicine
Voltage-Gated Sodium Channels
030204 cardiovascular system & hematology
Biochemistry
Ion Channels
Sodium Channels
Endocrinology
0302 clinical medicine
Heart Rate
Medicine and Health Sciences
lcsh:Science
Sinoatrial Node
Medicine(all)
Voltage-Gated Calcium Channels
Multidisciplinary
Voltage-dependent calcium channel
Agricultural and Biological Sciences(all)
Chemistry
Physics
Voltage-Gated Potassium Channels
Heart
Voltage-gated potassium channel
Potassium channel
Electrophysiology
medicine.anatomical_structure
Physical Sciences
Anatomy
Ion Channel Gating
Research Article
medicine.medical_specialty
Endocrine Disorders
Biophysics
Neurophysiology
Membrane Potential
Diabetes Mellitus, Experimental
03 medical and health sciences
Internal medicine
Diabetes Mellitus
medicine
Animals
RNA, Messenger
Rats, Wistar
Voltage-gated ion channel
Sinoatrial node
Biochemistry, Genetics and Molecular Biology(all)
Sodium channel
Calcium channel
lcsh:R
Biology and Life Sciences
Proteins
Membrane transport
Rats
030104 developmental biology
Metabolic Disorders
Cardiovascular Anatomy
lcsh:Q
Calcium Channels
Transcriptome
Neuroscience
Subjects
Details
- Language :
- English
- ISSN :
- 19326203
- Volume :
- 11
- Issue :
- 4
- Database :
- OpenAIRE
- Journal :
- PLoS ONE
- Accession number :
- edsair.doi.dedup.....0b540ecddc208c30f6f066b418cdc6fa