microRNA-107 protects against inflammation and endoplasmic reticulum stress of vascular endothelial cells via KRT1-dependent Notch signaling pathway in a mouse model of coronary atherosclerosis.

Coronary atherosclerosis is a long-term, sustained, and evolving inflammatory disease manifested with the remodeling of the coronary arteries. The purpose of this study is to explore the potential role of microRNA-107 (miR-107) in vascular endothelial cells (VECs) in coronary atherosclerosis by regulating the KRT1 gene and the Notch signaling pathway. A mouse model of coronary atherosclerosis was established. The relationship between miR-107 and KRT1 was analyzed and verified by dual-luciferase reporter assay. The functional role of miR-107 in coronary atherosclerosis was determined using ectopic expression and depletion. Blood lipid levels and atherosclerotic index (AI) were measured in atherosclerotic mice. Expression pattern of miR-107, KRT1, Notch signaling pathway, inflammatory/anti-inflammatory factors, and endoplasmic reticulum (ER) stress-related genes was evaluated by means of reverse transcription quantitative polymerase chain reaction, western blot analysis, and enzyme-linked immunosorbent assay. Meanwhile, cell-cycle distribution and cell apoptosis in VECs were assessed by flow cytometry. Atherosclerotic mice exhibited higher blood lipid levels, AI, apoptotic index, and KRT1-positive expression as well as inhibited Notch signaling pathway when compared with normal mice. The miR-107 was revealed to bind to KRT1; miR-107 upregulation or KRT1 silencing resulted in reductions in blood lipid levels and AI, inhibition in cell apoptosis, inflammation, and ER stress. Restored miR-107 or downregulated KRT1 activated the Notch signaling pathway. These results supported the notion that miR-107-targeted KRT1 inhibition activated the Notch pathway, thereby, protecting against the coronary atherosclerosis. Findings in this study might provide a novel biomarker for the coronary atherosclerosis treatment.

MicroRNA-9-5p promotes angiogenesis but inhibits apoptosis and inflammation of high glucose-induced injury in human umbilical vascular endothelial cells by targeting CXCR4.

High glucose (HG) has the potential to cause vascular endothelial cell injury, while microRNAs (miRNAs) play a key role in treating endothelial cell injury. CXC chemokine receptor-4 (CXCR4) is reported to be expressed in vascular endothelial cells. Hence, this study investigated role of miR-9-5p in the angiogenesis and apoptosis of HG-induced human umbilical vascular endothelial cells (HUVECs) injury. Dual luciferase reporter gene assay verified that miR-9-5p targeted CXCR4. RT-qPCR and western blot analysis revealed that miR-9-5p was down-regulated, meanwhile CXCR4 was up-regulated in the HG-induced HUVECs. HUVECs were cultured in 30 mmol/L HG in vitro, and then transfected with miR-9-5p mimic or CXCR4 siRNA to identify the effect of miR-9-5p on cell activity, angiogenesis, apoptosis, and inflammation of HG-induced HUVECs. The results suggested that overexpression of miR-9-5p or silencing of CXCR4 in HG-induced HUVECs increased cell proliferation and tubule length, while decreasing the apoptosis rate and the expression of inflammatory factors. Furthermore, miR-9-5p inhibited the phosphorylation of extracellular regulated protein kinases (ERK), protein kinase B (AKT), and Mammalian Target of Rapamycin (mTOR) proteins via downregulation of CXCR4. Therefore, overexpression of miR-9-5p suppressed the mitogen-activated protein kinase (MAPK)/ERK and the PI3K/AKT/mTOR pathway by inhibiting CXCR4, thereby reducing HG-induced injury in HUVECs.

[Study on serological blood group conversion rule and clinical blood transfusion in allogeneic hematopoietic stem cell transplantation].

OBJECTIVE: To explore the conversion rule of serological blood group and blood group substance after successful allogeneic hematopoietic stem cell transplantation, and to provide theory for clinical special blood type identification and blood transfusion. METHODS: The growth cycle of recipient WBC and RBC, RBC chimera, blood group antibody production and remaining in full transition were observed. Conversion rule of blood group substance, contradiction between cells typing and sera typing were detected by saline medium tube method and microcolumn gel method after stem cells transplantation. RESULTS: The average time of engraftment in 21 recipients was about 18.6 days, RBC growth cycle in 8 major blood type incompatibility was 56.6 days, 25.9 days in 9 minor blood type incompatibility, 67 days in 4 bidirectional blood type incompatibility (P < 0.01). The ratio of RBC chimeric growth was 1:9, gradually converse to donor's blood group. Residue of recipient anti-A(B) was left after conditioning regimen, disappeared after full transformation, and recipient anti-A(B) was converse to donor's blood type in major blood type incompatibility. 5 A blood type recipient donated by O blood type blood generated anti-B instead of anti-A, 3 B blood type recipient generated only anti-A instead of B in minor blood type incompatibility, and 1 AB blood type recipient donated by A did not generate anti-B. Among 4 bidirectional blood type incompatibility, 2 B blood type recipient donated by A blood type blood did not generate anti-B, 2 A recipient by B could not produce anti-A. Recipient blood group substance helped original ABO blood type substance remain unchanged. CONCLUSION: Among patient with allogeneic hematopoietic stem cell transplantation, recipient's ABO and RBC blood type can be converse to donor's, but there is significant difference between patients of serological blood group and of normal people (P < 0.01). Recipient blood group substance helps original ABO blood type substance remain unchanged (P > 0.01).