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Predictive Value of Heat-Shock Protein Gene Expression on Severe Neonatal Hypoxic-Ischemic Encephalopathy.

Authors
  • Seo, Yu-Mi1
  • Hwang-Bo, Seok1
  • Im, Soo-Ah2
  • Kim, Myungshin3
  • Youn, Young-Ah1
  • 1 Department of Pediatrics, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea. , (North Korea)
  • 2 Department of Radiology, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea. , (North Korea)
  • 3 Department of Laboratory Medicine, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea. , (North Korea)
Type
Published Article
Journal
Diagnostics
Publisher
MDPI AG
Publication Date
Apr 13, 2022
Volume
12
Issue
4
Identifiers
DOI: 10.3390/diagnostics12040981
PMID: 35454029
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

This study aims to evaluate significant gene expression in severe hypoxic ischemic encephalopathy (HIE) in newborns, which can be used as a predictable measure for high-risk HIE infants. The study prospectively recruited 77 inborn near-term or term HIE newborns between January 2018 and December 2020. We measured six different genes within 6 h of life among the HIE infants and compared the gene levels between the mild- and severe-HIE groups. Among these, 64 HIE infants (83.1%) did not receive therapeutic hypothermia (TH) because they were categorized as mild HIE, and the 13 remaining (16.9%) infants were categorized as ≥ moderate-HIE group and received TH. More abnormal MRI findings, seizure, and use of anti-convulsant were more found in the ≥ moderate = HIE group along with longer mechanical ventilation days and hospitalization. Heat-shock protein 70 family 1 A (HSPA1A) and serpin family H member 1 (SERPINH1) genes, which encode heat-shock protein (HSP) 70 and 47, respectively, were significantly elevated in the ≥ moderate-HIE, seizure, and abnormal MRI groups. HSP 70 and 47 were significantly elevated in the severe-HIE group, possibly playing protective roles in inhibiting exacerbated neuroinflammation and maintaining a cellular homeostasis. At 18-24 months, ≥ moderate-HIE group manifested a significant language delay.

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