Press releases
Please quote Nature Biotechnology as the source of these items.
The April 2008 issue of Nature Biotechnology is available online.
April 2008
Renewable cell therapy for diabetes inches closer
Researchers have converted human embryonic stem (ES) cells into cells that release insulin in response to glucose and alleviate a diabetes-like condition in mice. With further research and development, this approach, reported online in Nature Biotechnology, could lead to a renewable source of cells for the treatment of diabetes.
Type 1 diabetes and some forms of type 2 diabetes involve the loss of pancreatic 'beta' cells, which regulate blood glucose (sugar) levels by releasing insulin. In previous work, Emmanuel Baetge and colleagues described a method for driving human ES cells part of the way along the developmental path of the pancreas to becoming beta cells. The resulting cells could not carry out the key function of mature beta cells, which is to release insulin in response to glucose.
In their new study, Baetge's team shows that if immature pancreatic cells derived from human ES cells are transplanted into mice, in 1-3 months they will develop into glucose-responsive, insulin-secreting cells. These in vivo-matured cells are able to regulate the blood glucose levels of mice whose own beta cells have been destroyed by a chemical treatment - an animal model that mimics some forms of diabetes. The blood glucose control achieved is of similar effectiveness to that obtained by transplanted human islets.
The principle of treating diabetes by transplantation of pancreatic beta cells (within islets) has been demonstrated using the so-called Edmonton protocol. Thus far, this therapy has relied on cells from donor pancreases. Because the supply of such cells is very limited, there is great interest in developing alternative sources of beta cells, including cells derived from human ES cells.
Pancreatic endoderm derived from human embryonic stem cells generates glucose-responsive insulin-secreting cells in vivo pp 443 - 452
Evert Kroon, Laura A Martinson, Kuniko Kadoya, Anne G Bang, Olivia G Kelly, Susan Eliazer, Holly Young, Mike Richardson, Nora G Smart, Justine Cunningham, Alan D Agulnick, Kevin A D'Amour, Melissa K Carpenter & Emmanuel E Baetge
Published online: 20 February 2008 | doi 10.1038/nbt1393
RNA Trojan horses zero in on liver cirrhosis
Using vitamin A to target the cells that cause liver cirrhosis may improve the treatment of the disease, according to research reported online this week in Nature Biotechnology.
Cirrhosis, which affects hundreds of millions of people worldwide, is a scarring response to liver damage, which is most commonly inflicted by hepatitis infection, alcohol abuse or nutritional deficiencies. It occurs when specialized liver cells called stellate cells are triggered to produce collagen, the fibrous material that toughens skin and tendons. There are no approved antifibrotic therapies, partly due to the difficulty in specifically targeting collagen-producing cells to avoid unwanted side effects on healthy tissue.
Yoshiro Niitsu and colleagues exploit two properties of liver stellate cells—their ability to take up vitamin A and to make collagen. First, they designed small interfering RNA molecules (siRNAs) that block a key protein in collagen synthesis. Then, by packaging the siRNAs in carriers coated with vitamin A, they tricked the stellate cells into letting in the inhibitor, which shut down collagen secretion.
The treatment rescued rats from cirrhosis induced by three different approaches. As relatives of liver stellate cells contribute to fibrosis in organs, such as the pancreas and kidney, this type of siRNA therapy might be extended to reverse other fibrotic conditions.
Resolution of liver cirrhosis using vitamin A–coupled liposomes to deliver siRNA against a collagen-specific chaperone pp 431 - 442
Yasushi Sato, Kazuyuki Murase, Junji Kato, Masayoshi Kobune, Tsutomu Sato, Yutaka Kawano, Rishu Takimoto, Kouichi Takada, Koji Miyanishi, Takuya Matsunaga, Tetsuji Takayama & Yoshiro Niitsu
Published online: 30 March 2008 | doi 10.1038/nbt1396