Inhibition of miR-143-3p alleviates myocardial ischemia reperfusion injury via limiting mitochondria-mediated apoptosis.

MicroRNA (miR)-143-3p is a potential regulatory molecule in myocardial ischemia/reperfusion injury (MI/RI), wherein its expression and pathological effects remains controversial. Thus, a mouse MI/RI and cell hypoxia/reoxygenation (H/R) models were built for clarifying the miR-143-3p's role in MI/RI. Following myocardial ischemia for 30 min, mice underwent reperfusion for 3, 6, 12 and 24 h. It was found miR-143-3p increased in the ischemic heart tissue over time after reperfusion. Cardiomyocytes transfected with miR-143-3p were more susceptible to apoptosis. Mechanistically, miR-143-3p targeted B cell lymphoma 2 (bcl-2). And miR-143-3p inhibition reduced cardiomyocytes apoptosis upon H/R, whereas it was reversed by a specific bcl-2 inhibitor ABT-737. Of note, miR-143-3p inhibition upregulated bcl-2 with better mitochondrial membrane potential (Δψm), reduced cytoplasmic cytochrome c (cyto-c) and caspase proteins, and minimized infarction area in mice upon I/R. Collectively, inhibition of miR-143-3p might alleviate MI/RI via targeting bcl-2 to limit mitochondria-mediated apoptosis. To our knowledge, this study further clarifies the miR-143-3p's pathological role in the early stages of MI/RI, and inhibiting miR-143-3p could be an effective treatment for ischemic myocardial disease.

Nucleation ability of thermally reduced graphene oxide for polylactide: role of size and structural integrity.

Following our previous work on graphene oxide-induced polylactide (PLA) crystallization [Macromolecules 2010, 43, 5000-5008], in the current work, we further revealed the role of size and structural integrity of thermally reduced graphene oxide (RGO) in PLA crystallization. RGO nanoplatelets with different architectures were obtained via bath and probe ultrasound (RGOw and RGOp). The average size of RGO decreased substantially with ultrasound intensity and time, where the generation of RGO edges constituted the translocation of functional group sites from in-plane to edges. The formation of sp(3)-configuration dominated in RGOw, whereas the partial recovery of sp(2)-configuration occurred in RGOp, giving rise to either the escalation of sp(3)/sp(2) ratio for RGOw or retrogradation of that for RGOp. Isothermal crystallization kinetics of PLA nanocomposites containing RGOw and RGOp was determined by in situ synchrotron wide-angle X-ray diffraction. The induction period and overall crystallization rate of PLA/RGOw nanocomposites were strengthened with diminishing platelet size because of more nucleation sites encouraged by redistribution of functional groups. However, the adverse situation was found in PLA/RGOp nanocomposites. The observed phenomenon was ascribed to the disruption of the internal structure, i.e., the C═C sp(2) π-bond network, which deteriorated the CH-π interaction between PLA and RGO. These results conclusively suggested that the size and structural integrity of RGO had a concerted effort to determine the final nucleation ability of RGO dispersed by ultrasound.

Graphene Oxide Nanosheet Induced Intrachain Conformational Ordering in a Semicrystalline Polymer.

The physical origin of graphene oxide nanosheet (GONS)-driven polymer crystallization was studied from the perspective of intrachain conformational ordering. Time-resolved Fourier-transform infrared spectroscopy indicated that both conformational ordering and crystallization of isotactic polypropylene (iPP) were obviously accelerated by the presence of GONSs, indicating their efficient nucleation activity for iPP crystallization. Furthermore, the ordering of long helical segments occurred prior to the crystallization of iPP, as revealed by two-dimensional correlation infrared analysis. Compared to pure bulk system, the presence of GONSs was in favor of the formation of long ordering segments, especially at the early stage, accompanied by considerable enhancement of the crystallization kinetics. GONS-driven iPP crystallization was suggested to be attributed to this GONS-induced intrachain conformational ordering.