The Cross-Border Biotech Blog

Biotechnology, Health and Business in Canada, the United States and Worldwide

Friday Science Review: November 11, 2011

Genetically Modified MSCs for Acute Kidney Injury

McGill University ♦ Published in Molecular Therapy (npg), November issue

A research group has taken mesenchymal stem cells (MSCs) and enhanced them with a gene encoding erythropoietin (Epo) to show that they can be used to treat acute kidney injury (AKI). To generate a mouse model of AKI mice were injected with cisplatin, causing injury to the kidney. Epo-enhanced MSCs were then tested against unmodified MSCs for their capacity to regenerate tissue in the kidney and restore kidney function. Mice that received the Epo-enhanced MSCs exhibited improved survival and significantly better kidney function, as measured by blood levels of urea nitrogen, creatinine, and the enzymes amylase and alanine aminotransferase. Histological sections of recipient kidneys displayed less cell death and higher quantities of proliferating cells. Delivery of the Epo gene to modified MSCs causes the cells to secreate Epo protein, which is a known cytoprotective agent. This factor, in addition to the reparative effects of MSCs, produces a particularly strong regenerative effect upon transplantation.

Link Between p53 and Metabolism

York University ♦ University of Toronto ♦ Princess Margaret Hospital

Published in Molecular Cell, November 4, 2011

The tumour suppressor protein p53 has long been known to be the cell’s guardian. The protein can induce cell cycle arrest to allow for DNA repair, induce cellular senescence, or initiate signaling cascades leading to cell death if stress signals become overbearing. New findings suggest p53 is also involved in regulating metabolism on some level. A recent investigation has identified another link between p53 and metabolism, strengthening this hypothesis. Researchers found that the metabolism-regulating gene Lpin1 is partially under the control of p53. The lipin-1 protein controls the degree of fatty acid oxidation in the cell based on p53-signaling. Under normal glucose conditions, where cells can utilize glucose as a source of energy, the lipin-1 protein suppresses fatty acid oxidation. However, during times of nutritional stress lipin-1 promotes the oxidation of fatty acids to provide energy for cellular processes. In this study mouse myoblasts and human fibroblasts were cultured in conditions that induced nutritional stress. During nutrient deprivation reactive oxygen species (ROS) in the cell amass and a protein known as ATM kinase is activated, which in turn causes the activation of p53 and upregulation of Lpin1.

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