Transplantation proceedings
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The aim of this study was to determine whether the mobilization and recruitment of endothelial progenitor cells (EPCs) contribute to the protection of kidneys from ischemia/reperfusion (I/R) injury after ischemic preconditioning (IPC) during the late phase. ⋯ The present work suggested that IPC protected kidneys from IR injury in the later phase through enhanced mobilization and recruitment of EPCs. VEGF and SDF-1α may play important roles in this protective effect.
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We investigated gene transfer with human hepatocyte growth factor (HGF) to suppress pulmonary arterial hypertension (PAH) produced by an arteriovenous shunt in a rabbit model. The rabbit model of advanced PAH was used to show that HGF targets pulmonary arteriolar endothelial cells and inhibits disease progression. In the PAH rabbit model transfected with the HGF gene, hemodynamic abnormalities and right ventricular hypertrophy were prevented, as confirmed by invasive measurements and electrocardiographic examinations. ⋯ Western Blot and real-time reverse transcriptase-polymerase chain reaction indicated increased protein and mRNA levels of HGF and endothelial nitricoxide synthase (eNOS) in lungs after HGF transfection. Notably, exogenous HGF reduced lung expression of endothelin-1 (ET-1), which was critically involved in PAH-related pathologic changes. Our results suggested that HGF transfection suppresses PAH induced by shunt flow through enhanced expression of HGF with subsequent regulation of the concentrations of eNOS and ET-1 secreted by endothelial cells thereby promoting angiogenesis in injured lung tissue.
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MicroRNAs (miRNAs), 21-23-nucleotide noncoding RNAs, act as regulators of gene expression transcriptionally. MicroRNA-146a(miR-146a) has been demonstrated to be one of the key molecules in oncogenesis and inflammatory responses. Few data describe the expression of miR-146a in liver ischemia-reperfusion (IR) injury. The present study sought to explore the relationship of miR-146a to Toll-like receptor 4 (TLR4) signaling pathways in a rat model of warm IR injury. ⋯ miR-146a was down-regulated in the early stage of liver IR injury.
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Donor preconditioning by fenoldopam is demonstrated to improve graft function in recipients. Involvement of hypoxia-inducible factor-1alpha (HIF-1α) and heme oxygenase-1 (HO-1) in renoprotection after fenoldopam pretreatment was investigated. ⋯ Donor preconditioning by fenoldopam exerts renoprotection in grafts, at least in part, through HIF-1α activation and HO-1 expression. This provides a preference for further studies.