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: UMLS:C0001486 (
Adenovirus
)
3,125
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Myocardial infarction is caused by insufficient coronary blood supply, which leads to myocardial damage and eventually the heart failure. Molecular mechanisms associated with the loss of cardiomyocytes during myocardial infarction (MI) and ischemia-related cardiac diseases are not yet fully understood.
Nogo-C
is an endoplasmic reticulum protein ubiquitously expressed in tissues including in the heart, however, the cardiac function of
Nogo-C
is still unknown. In the present study, we found that
Nogo-C
was upregulated in mouse hearts after MI, and hypoxic treatments also increased Nogo-C protein level in cardiomyocytes.
Adenovirus
mediated overexpression of
Nogo-C
led to cardiomyocyte apoptosis, whereas knockdown of Nogo-c by shRNA protected cardiomyocytes from hypoxia-induced cell apoptosis. Importantly,
Nogo-C
knockout mice displayed improved cardiac function, smaller infarct area, and less apoptotic cells after MI. Moreover, we found that miR-182 negatively regulated
Nogo-C
expression and was downregulated during MI, expressing miR-182 in cardiomyocytes protected hypoxia- and
Nogo-C
-mediated cell apoptosis. Our results indicate that increased cardiac
Nogo-C
expression is both sufficient and necessary for ischemia-induced cardiomyocyte apoptosis and cardiac dysfunction, suggesting that deregulation of
Nogo-C
by miRNA may be a potential therapeutic target for ischemia-related heart diseases.
...
PMID:Nogo-C regulates cardiomyocyte apoptosis during mouse myocardial infarction. 2776 37
