BACKGROUND:Many scholars have experimental y confirmed the obvious effect of mesenchymal stem cells to repair radiation injury. OBJECTIVE:To preliminarily investigate the mechanism of human umbilical cord mesenchymal stem cells promoting the healing of combined radiation-wound skin injury and whether they possess tumorigenicity in vitro. METHODS:Fifteen Sprague-Dawley rats were randomly divided into three groups, five rats in each group. The right buttock of rats (2.5 cm×2.0 cm) was irradiated with 40 Gyβ-rays produced by a linear accelerator, in which a round wound with a diameter of 1.5 cm was made. After 12 hours of modeling, human umbilical cord mesenchymal stem cells at three concentrations (5.0×106, 1.0×107 and 2.0×107 ) were injected through tail vein of rats, and luciferin (20 mg/kg) was injected intraperitoneal y. celldistribution in vivo was traced using IVIS in vivo imaging system. The ability of human umbilical cord mesenchymal stem cells to form colonies was observed using the colony formation assay with soft agar. RESULTS AND CONCLUSION:Human umbilical cord mesenchymal stem cells injected through tail vein of rats were mostly gathered in the lungs. cells were accumulated in the injured site of rats injected with 2.0×10 7 human umbilical cord mesenchymal stem cells;however, the fluorescence signal was not observed in the injured site of rats injected with 5.0×106 and 1.0×107 human umbilical cord mesenchymal stem cells. The other results indicated human umbilical cord mesenchymal stem cells of low dose, medium dose and high dose had no colony formation on soft agar, but the tumor cells had a great ability to form colony. These findings indicate that human umbilical cord mesenchymal stem cells promote healing combined radiation-wound skin injury by local migration and exhibit no tumorigenicity in vitro in a short period.

Ischemia-reperfusion injury (IRI) is a common pathophysiological phenomenon, secondary to multiple pathological processes, such as organ transplantation, acute kidney injury and myocardial infarction. IRI may significantly aggravate the severity of diseases and increase the fatality of patients. Aseptic inflammation is one of the critical mechanisms of IRI. Damage-associated molecular pattern (DAMP) is a pivotal substance, which mediates aseptic inflammation. After released into extracellular space, it could effectively activate the immune system, and initiate and maintain the inflammatory responses by binding with pattern recognition receptor (PRR). Neutrophil extracellular trap (NET) is a DNA-based network structure released by neutrophils during the process of inflammatory responses, which contains histones and multiple granular proteins. Recent studies have demonstrated that DAMP and NET may aggravate IRI via aseptic inflammation. In this article, relevant studies of DAMP, NET and their relationship in IRI were reviewed, which was of great significance for understanding the pathophysiological mechanism of IRI and studying the corresponding prevention and treatment strategies.

Matrix metalloproteinase (MMP) is a large class of proteases which can cut or reshape extracellular matrix (ECM) and cell surface proteins. The activity of MMP is regulated by a variety of cytokines, including tissue inhibitor of metalloprotease (TIMP), signal transduction molecules and cell adhesion molecules. The latest research shows that MMP has a role in the pathophysiology process of many acute and chronic kidney diseases. In this article, the classification, expression and distribution in the kidney of MMP and its role in injury related renal transplantation was reviewed.

Kidney is a highly vascularized organ and peritubular capillary network constitutes the critical component of its microvascular system. Peritubular capillaries, as the main vessels for blood supply in renal tubules and renal interstitium, involve in important physiological processes in renal tubules such as energy metabolism, substance secretion and reabsorption. In recent years, it has been demonstrated that ischemia-reperfusion injury, rejection and renal fibrosis during kidney transplantation would result in compromised structural integrity and decreased number in peritubular capillaries, thus leading to interstitial fibrosis in renal allograft, which would seriously affect the long-term stability of renal function in the renal allograft. Therefore, we reviewed the structure and function of peritubular capillary, peritubular capillary and ischemia-reperfusion injury, rejection and renal allograft fibrosis, focusing on the mechanism for peritubular capillary injury in kidney transplantation and the specific changes manifested, with the aim of providing a reference for preventing and treating perioperative complications in kidney transplantation and improving the long-term prognosis of grafts.

The review focused upon the molecular mechanisms underlying ischemia reperfusion injury leading to interstitial fibrosis in transplanted kidneys, the roles of vascular dysfunction, epithelial cells, and pericytes in this process, the construction of different animal experimental models and their effects and recent novel approaches for the prevention and treatment of this process.