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Retracted : CXCL16 protects against oxygen and glucose deprivation‐induced injury in human microvascular endothelial cells‐1: Potential role in ischemic stroke
Author(s) -
Wang Min,
Liu Ruiting
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.28616
Subject(s) - apoptosis , viability assay , cxcl16 , protein kinase b , pi3k/akt/mtor pathway , creb , microbiology and biotechnology , endothelial stem cell , chemistry , biology , cancer research , chemokine , receptor , chemokine receptor , biochemistry , in vitro , transcription factor , gene
Aim To explore the protective effect of chemokine ligand 16 (CXCL16) against cell damage induced by oxygen‐glucose deprivation (OGD) in human microvascular endothelial cells‐1 (HMEC‐1) and its possible mechanism. Methods Cell Counting Kit‐8 (CCK‐8) assay and flow cytometry were performed to determine cell viability and apoptosis of HMEC‐1, respectively. qRT‐PCR analysis was applied to display the expression of CXCL16 and miR‐424. Western blot analysis was used to detect the expression of apoptosis‐related proteins, CXCL16, cAMP/PKA/CREB, and PI3K–AKT–GSK3β pathway‐related proteins. Results OGD significantly inhibited cell viability and promoted apoptosis. CXCL16 overexpression decreased the proliferation inhibition and apoptosis of HMEC‐1 induced by OGD. Furthermore, we found that CXCL16 was a target of miR‐424 and was downregulated by miR‐424. The further study showed that overexpression of miR‐424 significantly increased proliferation inhibition and apoptosis of HMEC‐1 induced by OGD. In addition, we also found that miR‐424 was downregulated by PMS2L2. In the subsequence experiment, overexpression of PMS2L2 significantly decreased the proliferation inhibition and apoptosis of HMEC‐1 induced by OGD, which suggested that PMS2L2 decreased cell damage of HMEC‐1 induced by OGD. Simultaneously, CXCL16 treatment markedly increased the phosphorylation of PKA/CREB and PI3K–AKT–GSK3β and these signal pathways were blocked by signal inhibitors. Conclusion Our study first demonstrates that oxygen‐glucose deprivation (OGD)‐induced human microvascular endothelial cells‐1 (HMEC‐1) cell injury was alleviated by CXCL16 targeted by miR‐424 which further targeted by PMS2L2. This process might also be regulated by activating PKA/CREB and PI3K–AKT–GSK3β pathways.