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The article titled "Two Coordination Polymers: Protective Activity on Nerve Injury by Increasing miR-219 and Reducing Inflammatory Response" has been retracted by the Editor-in-Chief and the Publisher of the Journal of Cluster Science. The retraction was prompted by an investigation that revealed evidence of systematic manipulation of the publication process, including citations that do not support claims made in the text, non-standard phrasing, anomalies in the figures, and discrepancies in ethics approval statements. The Editor-in-Chief no longer has confidence in the results and conclusions of the article. Some of the authors have agreed to the retraction, while others have not responded to correspondence from the Editor-in-Chief/Publisher. Springer Nature, the publisher, remains neutral regarding jurisdictional claims and institutional affiliations. [Extracted from the article]

Two novel transition metal coordination polymers (CPs) of {Cu(tdc)(Hdmea)2 (1, Hdmea = N,N-dimethylethanolamine, tdc = 2,5-thiopenedicarboxylate) and [Co3(H2O)3(tdc)3(dioxane)]·2(dioxane) (2) were prepared via the reaction of Co(NO3)2·6H2O or Cu(NO3)2·3H2O and H2tdc with or without the template reagent Hdmea. The following experiments were carried out to determine the treatment activity for compounds against nerve injury. Firstly, the real time RT-PCR was carried out to determine the miR-219 relative expression in the nerve cells. Then the activation level of the AMPK signaling pathway in the nerve cells was measured with western blot. In addition to this, the ELISA detection was also used in this research, for the inflammatory cytokines' evaluation. Finally, the inhibition of the compound 1 and compound 2 on the death of the nerve cells was determined with MTT assay. [ABSTRACT FROM AUTHOR]

Abstract Background Heparan sulfate (HS) degradation mediates pulmonary endothelial hyper-permeability and acute pulmonary edema during acute respiratory distress syndrome (ARDS). The aim of this study was to examine whether histone H4 induced HS degradation by activating heparanase (HPSE) in chlorine gas (Cl2)-induced ARDS. Methods Acute lung injury was induced by Cl2 exposure or histone H4 injection in C57BL/6 mice. Histone H4 in bronchoalveolar lavage fluid (BALF) and plasma was measured by ELISA. HS degradation was measured by immunostaining, ELISA, and flow cytometry. HPSE mRNA and protein were measured by real-time qPCR and western blot analysis, respectively, at preset timepoints. The HPSE inhibitor OGT2115 and specific siRNAs were used to study the role of HPSE during HS degradation caused by Cl2 exposure or histone H4 challenge. Blocking antibodies against TLR1, TLR2, TLR4, or TLR6 were used in vitro to investigate which signaling pathway was involved. The transcriptional regulation of HPSE was studied vis-à-vis NF-κB, which was assessed by nuclear translocation of NF-κB p65 and phosphorylation of I-κBα protein. Results Histone H4 in BALF and plasma increased evidently after Cl2 inhalation. Cl2 exposure or histone H4 challenge caused obvious acute lung injury in mice, and the pulmonary glycocalyx was degraded evidently as observed from endothelial HS staining and measurement of plasma HS fragments. Pretreatment with OGT2115, an HPSE inhibitor, relieved the acute lung injury and HS degradation caused by Cl2 exposure or histone H4 challenge. Targeted knockdown of HPSE by RNA interference (RNAi) significantly inhibited histone H4 induced HS degradation in HPMECs, as measured by immunofluorescence and flow cytometry. By inducing phosphorylation of I-κB α and nuclear translocation of NF-κB p65, histone H4 directly promoted mRNA transcription and protein expression of HPSE in a dose-dependent manner. Additionally, a blocking antibody against TLR4 markedly inhibited both activation of NF-κB and expression of HPSE induced by histone H4. Conclusions Histone H4 is a major pro-inflammatory mediator in Cl2-induced ARDS in mice, and induces HS degradation by activating HPSE via TLRs- and NF-κB-signaling pathways.