Abstract:
:Histamine is a widely distributed biogenic amine involved in the regulation of an array of biological processes. Serum histamine level is markedly elevated in the early stages of acute myocardial infarction, whereas the role it plays remains unclear. Histidine decarboxylase (HDC) is the unique enzyme responsible for histamine production, and cardiac injury is significantly aggravated in HDC knockout mice (HDC-/-), in which histamine is deficient. We also observed that autophagy was highly activated in cardiomyocytes of HDC-/- mice post acute myocardial infarction (AMI), which was abolished by compensation of exogenous histamine. The in vivo and in vitro results showed that acting through histamine 1 receptor, histamine increased miR-206 and miR-216b, which worked in concert to target to Atg13, resulting in the reduction of autophagy activation under hypoxia and AMI condition. Further study revealed that Atg13 interacted with FADD to promote the activation of caspase-8 and cell apoptosis. Taken together, these data unveil a novel intracellular signaling pathway involved in histamine regulating myocardial autophagy and apoptosis under hypoxia and AMI condition, which might help to more comprehensively evaluate the usage of histamine receptor antagonists and to develop new therapeutic targets for myocardial infarction.
journal_name
Cell Death Disjournal_title
Cell death & diseaseauthors
Ding S,Abudupataer M,Zhou Z,Chen J,Li H,Xu L,Zhang W,Zhang S,Zou Y,Hong T,Wang TC,Yang X,Ge Jdoi
10.1038/s41419-018-0723-6subject
Has Abstractpub_date
2018-06-07 00:00:00pages
694issue
6issn
2041-4889pii
10.1038/s41419-018-0723-6journal_volume
9pub_type
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