Platelet-rich Plasma Induces M2 Macrophage Polarization via Regulating AMPK Singling Pathway / 中国实验血液学杂志

OBJECTIVE@#To investigate the role of platelet-rich plasma (PRP) in inducing the M2 macrophage polarization via regulating AMPK singling pathway.@*METHODS@#The expressions of M1 marker CD11c and M2 marker CD206 in macrophages of blank control group, LPS group, LPS+PRP group, and LPS+PRP+Compound C group were detected by flow cytometry. Western blot was used to observe the effects of PRP on the expression of AMPK-mTOR signaling pathway-related proteins at different times (12 h, 18 h and 24 h) after LPS treatment. RNA interference technology was used to silence the expression of AMPK in macrophages, and the expression of TGF-β protein was subsequently examined by Western blot.@*RESULTS@#LPS significantly reduced the expression of CD206 and increased the expression of CD11c (P <0.05). After the addition of PRP, the expression of CD206 was significantly increased (P <0.05), while the expression of CD11c was significantly decreased (P <0.05). Compared with LPS group, PRP treatment significantly increased the expressions of p-AMPK and p-ULK1 proteins at 12 h, 18 h and 24 h, while significantly decreased the expression of p-mTOR protein (P <0.05). After the addition of AMPK inhibitor Compound C, the expression of CD206 was significantly reduced (P <0.05) and the expression of CD11c was significantly increased compared with LPS+PRP group (P <0.05). After silencing the expression of AMPK in macrophages, the promotion effect of PRP on TGF-β was significantly reduced (P <0.05).@*CONCLUSION@#PRP can stimulate the transformation of macrophages to M2 type via AMPK signalling pathway.

MicroRNA expression profile and pathogenetic initial study in essential hypertension / 中华心血管病杂志

<p><b>OBJECTIVE</b>To study the differential microRNAs expression between patients with essential hypertension and healthy controls.</p><p><b>METHODS</b>Whole blood from 15 hypertensive patients and 5 controls healthies were separated into plasma at 3000 rpm for 10 minutes. MicroRNAs were harvested using kit, and stored at -80°C. MicroRNAs profiling were performed using Exiqon microRCURY(TM) LNA microRNAs array, and were quantitative RT-PCR for the differential microRNAs expression. In addition, we used a set of plasma samples from 24 hypertensive patients and 22 healthy donors to independently validate the expression of these signature microRNAs.</p><p><b>RESULTS</b>MicroRNAs expression profile was found to be differentially in the essential hypertensive patients compared with the healthy donors. Of 1700 microRNAs detected on the microarray, 46 microRNAs were found to be differentially expressed in the essential hypertensive patient, 27 microRNAs were collected in Sanger microRNAs data-bank, the function of remaining 19 microRNAs were unknown. In the 27 microRNAs, 9 microRNAs were up-regulated in the hypertension patient samples, while 18 known microRNAs were down-regulated. MiR-296-5p (Fold change 0.47, P = 0.013) and miR-133b (Fold change 0.57, P = 0.033) were consistently down-regulated in the patient plasma, whereas let-7e (Fold change 1.62, P = 0.009) and hcmv-miR-UL112 (Fold change 2.72, P = 0.004), one human cytomegalovirus encoded microRNAs, were up-regulated in the patient samples. The microRNAs expression was independently validated using another sample. We showed that MHC class I polypeptide-related chain B (MHC class I polypeptide-related chain B, MICB) and Interferon regulatory factor 1 (Interferon regulatory factor 1, IRF1) were functional targets of hcmv-miR-UL112 by fluorescent reporter assays.</p><p><b>CONCLUSIONS</b>The hypertensive patients have distinct microRNAs expression Profile. Hcmv-miR-UL112 may have important implications toward pathogenesis of essential hypertension.</p>