miRNA signature of unfolded protein response in H9c2 rat cardiomyoblasts

Hdl Handle:
http://hdl.handle.net/10147/332048
Title:
miRNA signature of unfolded protein response in H9c2 rat cardiomyoblasts
Authors:
Read, Danielle E; Gupta, Ananya; Ladilov, Yury; Samali, Afshin; Gupta, Sanjeev
Citation:
Read DE, Gupta A, Ladilov Y et al. Cell & Bioscience. 2014 Sep 19;4(1):56
Issue Date:
19-Sep-2014
URI:
http://dx.doi.org/10.1186/2045-3701-4-56; http://hdl.handle.net/10147/332048
Abstract:
Abstract Background Glucose and oxygen deprivation during ischemia is known to affect the homeostasis of the endoplasmic reticulum (ER) in ways predicted to activate the unfolded protein response (UPR). Activation of UPR signalling due to ER stress is associated with the development of myocardial infarction (MI). MicroRNAs (miRNAs) are key regulators of cardiovascular development and deregulation of miRNA expression is involved in the onset of many cardiovascular diseases. However, little is known about the mechanisms regulating the miRNA expression in the cardiovascular system during disease development and progression. Here we performed genome-wide miRNA expression profiling in rat cardiomyoblasts to identify the miRNAs deregulated during UPR, a crucial component of ischemia. Results We found that expression of 86 microRNAs changed significantly during conditions of UPR in H9c2 cardiomyoblasts. We found that miRNAs with known function in cardiomyoblasts biology (miR-206, miR-24, miR-125b, miR-133b) were significantly deregulated during the conditions of UPR in H9c2 cells. The expression of miR-7a was upregulated by UPR and simulated in vitro ischemia in cardiomyoblasts. Further, ectopic expression of miR-7a provides resistance against UPR-mediated apoptosis in cardiomyoblasts. The ample overlap of miRNA expression signature between our analysis and different models of cardiac dysfunction further confirms the role of UPR in cardiovascular diseases. Conclusions This study demonstrates the role of UPR in deregulating the expression of miRNAs in MI. Our results provide novel insights about the molecular mechanisms of deregulated miRNA expression during the heart disease pathogenesis.
Item Type:
Article
Language:
en
Keywords:
GENETICS; CORONARY HEART DISEASE

Full metadata record

DC FieldValue Language
dc.contributor.authorRead, Danielle Een_GB
dc.contributor.authorGupta, Ananyaen_GB
dc.contributor.authorLadilov, Yuryen_GB
dc.contributor.authorSamali, Afshinen_GB
dc.contributor.authorGupta, Sanjeeven_GB
dc.date.accessioned2014-10-02T11:17:52Z-
dc.date.available2014-10-02T11:17:52Z-
dc.date.issued2014-09-19-
dc.identifier.citationRead DE, Gupta A, Ladilov Y et al. Cell & Bioscience. 2014 Sep 19;4(1):56en_GB
dc.identifier.urihttp://dx.doi.org/10.1186/2045-3701-4-56-
dc.identifier.urihttp://hdl.handle.net/10147/332048-
dc.description.abstractAbstract Background Glucose and oxygen deprivation during ischemia is known to affect the homeostasis of the endoplasmic reticulum (ER) in ways predicted to activate the unfolded protein response (UPR). Activation of UPR signalling due to ER stress is associated with the development of myocardial infarction (MI). MicroRNAs (miRNAs) are key regulators of cardiovascular development and deregulation of miRNA expression is involved in the onset of many cardiovascular diseases. However, little is known about the mechanisms regulating the miRNA expression in the cardiovascular system during disease development and progression. Here we performed genome-wide miRNA expression profiling in rat cardiomyoblasts to identify the miRNAs deregulated during UPR, a crucial component of ischemia. Results We found that expression of 86 microRNAs changed significantly during conditions of UPR in H9c2 cardiomyoblasts. We found that miRNAs with known function in cardiomyoblasts biology (miR-206, miR-24, miR-125b, miR-133b) were significantly deregulated during the conditions of UPR in H9c2 cells. The expression of miR-7a was upregulated by UPR and simulated in vitro ischemia in cardiomyoblasts. Further, ectopic expression of miR-7a provides resistance against UPR-mediated apoptosis in cardiomyoblasts. The ample overlap of miRNA expression signature between our analysis and different models of cardiac dysfunction further confirms the role of UPR in cardiovascular diseases. Conclusions This study demonstrates the role of UPR in deregulating the expression of miRNAs in MI. Our results provide novel insights about the molecular mechanisms of deregulated miRNA expression during the heart disease pathogenesis.-
dc.language.isoenen
dc.subjectGENETICSen_GB
dc.subjectCORONARY HEART DISEASEen_GB
dc.titlemiRNA signature of unfolded protein response in H9c2 rat cardiomyoblastsen_GB
dc.typeArticleen
dc.language.rfc3066en-
dc.rights.holderDanielle E Read et al.; licensee BioMed Central Ltd.-
dc.description.statusPeer Reviewed-
dc.date.updated2014-10-02T11:03:00Z-
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