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Long noncoding RNA H19 promotes leukocyte inflammation in ischaemic stroke by targeting the miR-29b/C1QTNF6 axis
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  • Guangwen Li,
  • Xiaoqing Ma,
  • Haiping Zhao,
  • Junfen Fan,
  • Tianwei Liu,
  • Yumin Luo,
  • Yunliang Guo
Guangwen Li
The Affiliated Hospital of Qingdao University
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Xiaoqing Ma
Qingdao University
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Haiping Zhao
Xuanwu Hospital Capital Medical University
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Junfen Fan
Xuanwu Hospital Capital Medical University
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Tianwei Liu
The Affiliated Hospital of Qingdao University
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Yumin Luo
Xuanwu Hospital Capital Medical University

Corresponding Author:[email protected]

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Yunliang Guo
The Affiliated Hospital of Qingdao University
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Abstract

Background and Purpose Inflammatory processes induced by leukocytes are crucially involved in the pathophysiology of acute ischemic stroke. This study aimed to elucidate the inflammatory mechanism of long non-coding RNA (lncRNA) H19-mediated regulation of C1QTNF6 by sponging miR-29b in leukocytes during ischemic stroke. Experimental Approach H19 and miR-29b expression in leukocytes of patients with ischemic stroke and middle cerebral artery occlusion rats was measured through real-time PCR. Moreover, we performed in vivo and in vitro experiments to determine the impact of H19 and miR-29b on C1QTNF6 expression in leukocytes after ischemic injury. Key Results There was H19 and C1QTNF6 upregulation, as well as miR-29b downregulation, in neutrophils of patients with stroke. Moreover, miR-29b could bind C1QTNF6 mRNA to repress its expression while H19 could sponge miR-29b to maintain C1QTNF6 expression. Moreover, C1QTNF6 overexpression promoted the release of IL-1β and TNF-α in leukocytes and further exacerbates blood-brain barrier disruption. Conclusion and Implications Our findings confirm the inflammation-modulatory effect of the H19/miR-29b/C1QTNF6 axis on cerebral ischemic injury.