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Long non-coding RNA MALAT1 functions as a mediator in cardioprotective effects of fentanyl in myocardial ischemia-reperfusion injury
- Source :
- Cell Biology International. 41:62-70
- Publication Year :
- 2016
- Publisher :
- Wiley, 2016.
-
Abstract
- Long non-coding (lncRNA) MALAT1 can be increased by hypoxia or ischemic limbs. Also, downregulation of MALAT1 contributes to reduction of cardiomyocyte apoptosis. However, the functional involvement of MALAT1 in myocardial ischemia-reperfusion (I/R) injury has not been defined. This study investigated the functional involvement of lncRNA-MALAT1 in cardioprotective effects of fentanyl. HL-1, a cardiac muscle cell line from the AT-1 mouse atrial cardiomyocyte tumor lineage was pre-treated with fentanyl and generated cell model of hypoxia-reoxygenation (H/R). Relative expression of MALAT1, miR-145, and Bnip3 mRNA in cells was determined by quantitative real-time PCR. Cardiomyocyte H/R injury was indicated by lactate dehydrogenase (LDH) release and cell apoptosis. The results showed that fentanyl abrogates expression of responsive gene for H/R and induces downregulation of MALAT1 and Bnip3 and upregulation of miR-145. We found that miR-145/Bnip3 pathway was negatively regulated by MALAT1 in H/R-HL-1 cell with or without fentanyl treatment. Moreover, both MALAT1 overexpression and miR-145 knockdown reverse cardioprotective effects of fentanyl, as indicated by increase in LDH release and cell apoptosis. The reversal effect of MALAT1 for fentanyl is confirmed in cardiac ischemia/reperfusion (I/R) mice. In summary, lncRNA-MALAT1 is sensitive to H/R injury and abrogates cardioprotective effects of Fentanyl by negatively regulating miR-145/Bnip3 pathway.
- Subjects :
- 0301 basic medicine
Gene knockdown
Cell
Cell Biology
General Medicine
Pharmacology
Hypoxia (medical)
medicine.disease
03 medical and health sciences
chemistry.chemical_compound
030104 developmental biology
medicine.anatomical_structure
Downregulation and upregulation
chemistry
Apoptosis
Lactate dehydrogenase
medicine
medicine.symptom
Reperfusion injury
Cardiac muscle cell
Subjects
Details
- ISSN :
- 10656995
- Volume :
- 41
- Database :
- OpenAIRE
- Journal :
- Cell Biology International
- Accession number :
- edsair.doi...........59778bd0697d4f703ba8b807e5516e2b