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Hyperglycemia increased extravasations of Evan’s blue and IgG and aggravated damage to TJ and BM proteins following I/R injury. Furthermore, hyperglycemia suppressed astrocyte activation and damaged astrocytic endfeet surrounding cerebral blood vessels following I/R. Hyperglycemia inhibited microglia activation and proliferation and increased neutrophil infiltration in the brain. It was concluded that hyperglycemia‑induced BBB leakage following I/R might be caused by damage to TJ and BM proteins and astrocytic endfeet. Furthermore, suppression of microglial cells and increased neutrophil infiltration to the brain may contribute to the detrimental effects of pre‑ischemic hyperglycemia on the outcome of cerebral ischemic stroke.Ror2 (receptor tyrosine kinase like orphan receptor 2) is highly expressed in various types of cancers; in the majority of these cancers, Ror2 expression is associated with more aggressive disease states. Recently, it has been reported that Ror2 is highly expressed in human papilloma virus (HPV)‑positive head and neck squamous cell cancer (HNSCC) cell lines, presumably indicating that Ror2 plays a critical role in HPV‑related cancers. However, the function of Ror2 in HPV‑positive HNSCC is currently unknown. Here, we first examined the expression levels of Ror2 in clinical specimens from patients with HPV‑negative and HPV‑positive oropharyngeal squamous cell cancer (OPSCC) via immunohistochemical analysis. We found that Ror2 was expressed in both HPV‑negative and HPV‑positive OPSCC tissues. We then confirmed that HPV‑positive HNSCC cell line, UPCISCC152 cells, express Ror2 higher than HPV‑negative cell lines as previously reported. Suppressed expression of HPV E6/7 resulted in reduced expression levels of Ror2. We also revealed that Ror2 downregulation significantly inhibited the proliferation of UPCISCC152 cells without inducing apoptosis. Moreover, Ror2 knockdown decelerated G1/S phase progression and abrogated invasive migration of UPCISCC152 cells. These results provide strong evidence that E6 and/or E7 oncoproteins regulate the progression of HPV‑positive HNSCC by upregulating Ror2 expression, suggesting that Ror2 could potentially be a novel target in HPV‑related cancers.Following the publication of this paper, it was drawn to the Editors’ attention by a concerned reader that certain of the Transwell assay data in the article (featured in Figs. 3B and 7B) were strikingly similar to data appearing in different form in other articles by different authors at different research institutes that had already been published elsewhere at the time of the present article’s submission. Furthermore, the scratch wound assay data in Fig. 7A of the above paper were strikingly similar to data published elsewhere. Owing to the fact that the contentious data in the above article had already appeared in different form in other articles prior to its submission to International Journal of Molecular Medicine, the Editor has decided that this paper should be retracted from the Journal. The authors did not reply to indicate whether or not they agreed with the retraction of the paper. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in International Journal of Molecular Medicine 42 779-788, 2018; DOI 10.3892/ijmm.2018.3660].Excessive inflammatory response and apoptosis play key roles in the pathogenic mechanisms of sepsis‑induced acute lung injury (ALI); however, the molecular pathways linked to ALI pathogenesis remain unclear. Recently, microRNAs (miRNAs/miRs) have emerged as important regulators of inflammation and apoptosis in sepsis‑induced ALI; however, the exact regulatory mechanisms of miRNAs remain poorly understood. In the present study, the gene microarray dataset GSE133733 obtained from the Gene Expression Omnibus database was analyzed and a total of 38 differentially regulated miRNAs were identified, including 17 upregulated miRNAs and 21 downregulated miRNAs, in mice with lipopolysaccharide (LPS)‑induced ALI, in comparison to the normal control mice. miR‑129 was found to be the most significant miRNA, among the identified miRNAs. The upregulation of miR‑129 markedly alleviated LPS‑induced lung injury, as indicated by the decrease in lung permeability in and the wet‑to‑dry lung weight ratio, as well as the improved survival rate of mice with ALI administered miR‑129 mimic. Moreover, the upregulation of miR‑129 reduced pulmonary inflammation and apoptosis in mice with ALI. Of note, transforming growth factor activated kinase‑1 (TAK1), a well‑known regulator of the nuclear factor‑κB (NF‑κB) pathway, was directly targeted by miR‑129 in RAW 264.7 cells. More importantly, miR‑129 upregulation impeded the LPS‑induced activation of the TAK1/NF‑κB signaling pathway, as illustrated by the suppression of the nuclear phosphorylated‑p65, p‑IκB‑α and p‑IKKβ expression levels. Collectively, the findings of the present study indicate that miR‑129 protects mice against sepsis‑induced ALI by suppressing pulmonary inflammation and apoptosis through the regulation of the TAK1/NF‑κB signaling pathway. This introduces the basis for future research concerning the application of miR‑129 and its targets for the treatment of ALI.Diabetic encephalopathy (DE) is one of the main chronic complications of diabetes, and is characterized by cognitive defects. Kartogenin MicroRNAs (miRNAs/miRs) are widely involved in the development of diabetes‑related complications. The present study evaluated the role of miR‑130b in DE and investigated its mechanisms of action. PC12 cells and hippocampal cells were exposed to a high glucose environment to induce cell injuries to mimic the in vitro model of DE. Cells were transfected with miR‑130b mimic, miR‑130b inhibitor and small interfering RNA (si)‑phosphatase and tensin homolog (PTEN) to evaluate the protective effect of the miR‑130b/PTEN axis against oxidative stress in high glucose‑stimulated cells involving Akt activity. Furthermore, the effect of agomir‑130b was also assessed on rats with DE. The expression of miR‑130b was reduced in the DE models in vivo and in vitro. The administration of miR‑130b mimic increased the viability of high glucose‑stimulated cells, prevented apoptosis, increased the activity of superoxide dismutase (SOD), decreased the malondialdehyde (MDA) content, activated Akt protein levels and inhibited the mitochondria‑mediated apoptotic pathway.