Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.6.1.3 (
ATPase
)
65,361
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Loss of platelet quality during ex vivo storage is a major concern in the transfusion medicine field and it has been known that platelet mitochondrial dysfunction is associated with storage time. In the last decade, small noncoding RNAs also known as microRNAs (miRNAs) have been reported to regulate key cellular processes through their target sequence interactions with selected mRNAs. In this study, we focused on understanding the mechanisms of platelet mitochondrial dysfunction during storage through miRNA regulation of mRNAs. RNA was isolated from day 0, day 5, and day 9 of stored human leukocyte-depleted platelets and subjected to differential miRNA and mRNA profiling. The miRNA profiling identified several miRNAs at low levels including a set of 12 different miR-548 family members (miR-548a-3p, miR-548aa, miR-548x, miR-548ac, miR-548c-3p, miR-603, miR-548aj, miR-548ae, miR-548z, miR-548u, miR-548al, and miR-570-3p). The mRNA profiling identified, among many, the mitochondrial ATP synthase subunit g (
ATP5L
) mRNA at high levels during storage. Target Scan algorithm for potential targets of miR-570-3p also identified
ATP5L
as one of its targets. We further identified two target sites for miR-570-3p in the 3' untranslated region (3'UTR) of
ATP5L
mRNA. While
ATP5L
is a subunit of F
0
ATPase
complex, its function is not established yet. Overexpression of miR-570-3p in platelets resulted in reduced levels of
ATP5L
mRNA and concomitant ATP loss. These experimental results provide first-time insights into the miRNA-mRNA interactions underlying mitochondrial dysfunction in ex vivo stored platelets and warrants further investigation.
...
PMID:miR-570 interacts with mitochondrial ATPase subunit g (ATP5L) encoding mRNA in stored platelets. 2756 Oct 77
Deficits in coordinated motor behavior and mitochondrial
complex V
activity have been observed in aged males. Testosterone supplementation can improve coordinated motor behavior in aged males. We investigated the effects of testosterone supplementation on mitochondrial
complex V
function in the substantia nigra (a brain region that regulates motor activity) in aged male rats. These rats exhibited diminished ATP levels, attenuated mitochondrial
complex V
activity, and reduced expression of 3 of the 17 mitochondrial
complex V
subunits (ATP6, ATP8 and ATP5C1) in the substantia nigra. Testosterone supplementation increased ATP levels, mitochondrial
complex V
activity, and ATP6, ATP8 and ATP5C1 expression in the substantia nigra of the rats. Conversely, orchiectomy reduced mitochondrial
complex V
activity, downregulated ATP6 and ATP8 expression, and upregulated ATP5C1, ATP5I and
ATP5L
expression in the substantia nigra. Testosterone replacement reversed those effects. Thus, testosterone enhanced mitochondrial
complex V
function in the substantia nigra of aged male rats by upregulating ATP6 and ATP8. As potential testosterone targets, these two subunits may to some degree maintain nigrostriatal dopaminergic function in aged males.
...
PMID:Testosterone enhances mitochondrial complex V function in the substantia nigra of aged male rats. 3244 51
