sMICA as novel and early predictors for acute myocardial infarction

Abstract

Background and aimsMHC class I polypeptide-related chain A (MICA) molecule is induced in response to viral infection, various types of stress, such as endoplasmic reticulum stress, and ischemia or/and reperfusion, by which MICA was shed from the cell surface into the extracellular domain, generating a soluble form (sMICA). In the present study, we designed to investigate the serum sMICA level in patients with AMI and determine whether sMICA could be an early biomarker for diagnosis of AMI.MethodsThere were 103 patients who presented with first-time AMI that was assessed after the incident. The control group consisted of 103 healthy volunteers. Serum levels of sMICA and Troponin T were detected by the specific ELISA kits.ResultsSerum levels of sMICA reach the peaks [(1.34 ± .18 and 1.72 ± .20)n/l] at 6–12 h and serum levels of cTnT reach the peaks [(1.16 ± .28 and 1.14 ± .34)n/l] at 12–24 h. Both of them were significantly higher than the healthy controls [(.168 ± .014) n/l, p = .000] for sMICA and [(.13 ± .06) n/l, p = .000] for Troponin T (cTnT). sMICA is more sensitive in the early diagnosis of AMI than cTnT. The combined ROC analysis revealed an AUC value of .78 (95 % CI .69–.83) in discriminating AMI patients from healthy controls.ConclusionsWe have detected high levels of sMICA in patients with AMI. Elevated serum sMICA may be a novel biomarker for the early detection of myocardial injury in humans.

Dynamic Monitoring of Erythrocyte Distribution Width (RDW) and Platelet Distribution Width (PDW) in Treatment of Acute Myocardial Infarction

“…Because of the acute onset of AMI and early insensitivity of therapeutic effect evaluation, it is of great importance of identifying the early response in AMI [ 24 ]. At present, serum enzyme indicators are used, including aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and its isoenzymes [ 25 ].…”

Innate (and Innate-like) Lymphoid Cells: Emerging Immune Subsets With Multiple Roles Along Transplant Life

“…94 During cellular stress, an increased proportion of HLA-E molecules may bind the heat shock protein 60 signal peptide, leading to peptide interference that would gradually uncouple CD94/NKG2A inhibitory recognition and provide a mechanism for NK cells to detect stressed cells. 95 IRI also promote MHC-I polypeptide–related sequence A (MICA) expression during acute myocardial infarction 96 or in TEC through hypoxia-inducible factor as a response to hypoxia/reoxygenation. 97 NKG2D is the receptor for the stress-inducible MICA, and its engagement activates a cytolytic response in NK cells.…”