Arch Med Sci
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We recently reported that a series of brief hind limb ischemia and reperfusion (IR) at the beginning of renal ischemia (remote per-conditioning - RPEC) significantly attenuated the ischemia/reperfusion-induced acute kidney injury. In the present study, we investigated whether the nitric oxide synthase (NOS) pathway is involved in the RPEC protection of the rat ischemic kidneys. ⋯ These findings suggest that the protective effects of RPEC on renal IR injury are closely dependent on the nitric oxide production after the reperfusion and both eNOS and iNOS are involved in this protection.
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Our study was conducted to prove that miR-509-5p improved the proliferative and invasive abilities of papillary thyroid carcinoma (PTC) cells through inhibiting SFRP1 expression. ⋯ MiR-509-5p improved the proliferative, migrating and invasive abilities of PTC cells through inhibiting SFRP1 expression.
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Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest malignancies. However, the molecular mechanisms underlying PDAC are still not completely understood. Circular RNAs (circRNAs) are a unique class of RNA formed by special loop splicing. More and more researchers have paid attention to circRNAs. ⋯ Our study identified differentially expressed circRNAs in PDAC, suggesting that circRNAs may also act as biomarkers for PDAC. Additional investigations of function and up-stream regulation of differentially expressed circRNA in PDAC are still needed.
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Urotensin II (UII) is an important vasoactive peptide involved in the pathogenesis of atherosclerosis. Monocytes/macrophages play important roles in every step of atherosclerosis. Although UII has a chemoattractant effect on monocytes, it is unclear whether UII regulates inflammatory responses in macrophages. The present study sought to explore whether UII can promote leukotriene B4 (LTB4) production by macrophages. ⋯ Urotensin II may promote 5-lipoxygenase expression and LTB4 release in RAW264.7 macrophages via UT-ROS-Akt pathways. These results indicate that UII may participate in macrophage activation and suggest a potential new mechanism underlying atherosclerosis.
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For some cancers bone is the preferred site for metastasis and involves a cascade involving transition of epithelial cells to mesenchymal cells and subsequent intravasation to the blood and lymph vessels, and finally hematogenous dissemination to perivascular niches of the bone marrow sinusoids. It has been shown that protein kinase C can aid metastasis to bone. Hence, pharmacological inhibition of protein kinase C (PKC) activity is thought of as a potential therapeutic option in bone metastatic lesions. The objective of the current study was to investigate how PKCs exert their effect on bone cancer metastasis and to test the efficacy of pharmacological inhibition of PKC on bone metastasis. ⋯ Our results indicate that PKC potentiates tumor metastasis to the bone by potentiating translation increase and can be putatively inhibited by pharmacological inhibition.