Format

Send to

Choose Destination
Biotechnol Lett. 2019 Jan;41(1):59-68. doi: 10.1007/s10529-018-2614-4. Epub 2018 Oct 11.

COX6B1 relieves hypoxia/reoxygenation injury of neonatal rat cardiomyocytes by regulating mitochondrial function.

Author information

1
Department of Cardiovascular Surgery, The Second Affiliated Hospital of Xi'an Jiaotong University, No.157 West 5 Road, Xi'an, 710004, Shaanxi Province, China.
2
Department of Anesthesiology, The Second Affiliated Hospital of Xi'an Jiaotong University, No.157 West 5 Road, Xi'an, 710004, Shaanxi Province, China.
3
Department of Cardiovascular Surgery, The Second Affiliated Hospital of Xi'an Jiaotong University, No.157 West 5 Road, Xi'an, 710004, Shaanxi Province, China. feip_peifx@163.com.

Abstract

OBJECTIVE:

Mitochondrial dysfunction plays a pivotal role in various pathophysiological processes of heart. Cytochrome oxidase subunit 6B1 (COX6B1) is a subunit of cytochrome oxidase.

METHODS:

Cardiomyocytes were isolated from neonatal SD rats (within 24 h of birth) by repeating digestion of collagenase and trypsin. COX6B1 over-expression and hypoxia/reoxygenation was conducted on neonatal rat cardiomyocytes. Cell viability, apoptosis rates, mitochondria membrane potential and mitochondrial permeabilization transition pores (mPTPs) were then determined respectively by Cell performing Counting Kit-8 (CCK-8), Annexin-V/PI assay, JC-1 assay, mPTP assay. The expression of cyto C and apoptosis-related factors were detected by RT-Qpcr and Western blot.

RESULTS:

Hypoxia/reoxygenation increased apoptosis and mPTP levels, and decreased mitochondria membrane potential in I/R and I/R + EV groups. COX6B1 over-expression increased mitochondria cyto C, pro-caspase-3, pro-caspase-9 and bcl-2, while it decreased cytosol cyto C, cleaved-caspase-3, cleaved-caspase-9 and bax compared to I/R + EV group.

CONCLUSION:

COX6B1 protected cardiomyocytes from hypoxia/reoxygenation injury by reducing ROS production and cell apoptosis, during which reduction of the release of cytochrome C from mitochondria to cytosol was involved. Our study demonstrated that COX6B1 may be an candidate target gene in preventing hypoxia/reoxygenation injury of cardiomyocytes.

KEYWORDS:

COX6B1; Cardiomyocytes; Hypoxia/reoxygenation injury; Mitochondria

PMID:
30311029
PMCID:
PMC6313357
DOI:
10.1007/s10529-018-2614-4
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Springer Icon for PubMed Central
Loading ...
Support Center