News

 

March 20, 2014

"Rejuvenation of the aged muscle stem cell population restores strength to injured aged muscles"

Nature Medicine

Researchers at the Stanford University School of Medicine have pinpointed why normal aging is accompanied by a diminished ability to regain strength and mobility after muscle injury: Over time, stem cells within muscle tissues dedicated to repairing damage become less able to generate new muscle fibers and struggle to self-renew. More

Cosgrove et al. Nature Med., 20(3):255-264

 


Sept 1, 2013.
“Interleukin-6 signalling in reprogramming”
Nature Cell Biology.
Blau and colleagues show that non-dividing heterokaryons between mouse embryonic stem cells and human fibroblasts, in which human nuclei reprogram to a more embryonic state, can be used to identify signalling pathways involved in reprogramming. They delineate that IL-6 signalling and JAK-STAT target kinase Pim1 signalling are induced during this reprogramming, and that they increase the efficiency of factor-mediated reprogramming to induced pluripotent stem cell status. Read more...
References:
Brady et al, Nature Cell Biology (2013) [link] (PDF)


July 7, 2013.
New mouse model reveals a mystery of Duchenne muscular dystrophy
By Krista Conger of Inside Stanford Medicine.

NCB Children with Duchenne muscular dystrophy often die as young adults from heart and breathing complications. However, scientists have been puzzled for decades by the fact that laboratory mice bearing the same genetic mutation responsible for the disease in humans display only mild symptoms and no cardiac involvement. Now, researchers at the Stanford University School of Medicine have developed a mouse model that accurately mimics the course of the disease in humans. The study is the first to demonstrate a molecular basis for the cardiac defect that is the primary killer of people with Duchenne muscular dystrophy. Furthermore, the study provides evidence for a potential treatment to help prolong heart function. The mouse model also will allow researchers and clinicians to test a variety of therapies for the inherited condition.
“Until now, scientists had no animal model of Duchenne muscular dystrophy that manifests the symptoms of the cardiac disease that kills children and young adults with the condition,” said Helen Blau, PhD, the Donald E. and Delia B. Baxter Professor at Stanford and director of the Baxter Laboratory for Stem Cell Biology. “This has been a conundrum for three decades. We found that mice with moderately shortened telomeres and the Duchenne mutation exhibit profound cardiac defects and die at a young age, just like human patients.” Read more...
References:
Mourkioti et al, Nature Cell Biology (2013) [link] (PDF)

News article from Nature [link]
News article from Stanford School of Medicine Scope Blog [link]

Oct 1, 2012.
“(Re)Programming Director.”
The Scientist.
Profile of Dr. Helen Blau.

Helen Blau was born in London and holds dual citizenship in the United States and the U.K. But she spent most of her childhood in Europe. “I loved that my family traveled so much,” says Blau, who attended summer schools in the Swiss Alps and lived with French and Austrian families. “The experience made me adventurous, encouraged me to take risks, and exposed me to different languages and cultures—all of which shaped my development.” Read more...

Aug 31, 2012.
“Helen Blau: She thinks like a cell”
Circulation Research
Profile of Dr. Helen Blau.

Professor Helen Blau, Director of the Baxter Laboratory for Stem Cell Biology at Stanford University in California, has spent her career studying cells and probing their plasticity. She does this in order to answer the fundamental questions that drive her research: how do cells develop from pluripotency to differentiated states, how do they maintain their identities, and can reprogramming alter those identities?” (PDF)


May 30, 2012.
“Redefining differentiation: Reshaping our ends.”
Nature Cell Biology.
Profile of Dr. Helen Blau.

“There's a divinity that shapes our ends; rough hew them how we will,” wrote Shakespeare in Hamlet. But is anatomy indeed destiny? As an assistant professor at Stanford University in the 1980s, and after years of growing cells in culture and staring at them under the microscope, I could not believe that once cells differentiated, their fate was sealed forever. Why was differentiation 'one way'? I still remember my excitement when our heterokaryon experiments, in which human differentiated cells were fused with mouse muscle myotubes, demonstrated that the 'terminally' differentiated state of human cells could be altered. The revelation of cell fate plasticity was thrilling. If understood mechanistically, this plasticity might be enlisted for new medical applications. That was the turning point in my career. Read more...

Mar 25, 2011.
“Blau awarded the Seventh Annual AACR-Irving Weinstein Foundation Distinguished Lectureship”
American Association for Cancer Research.

Helen M. Blau, Ph.D., will be awarded the Seventh Annual AACR-Irving Weinstein Foundation Distinguished Lectureship. She is the Donald E. and Delia B. Baxter professor and director of the Baxter Laboratory for Stem Cell Biology in the microbiology and immunology department, at the Stanford Institute for Stem Cell Biology and Regenerative Medicine at the Stanford University School of Medicine. Read more...

August 4, 2010.
Newts' ability to regenerate tissue replicated in mouse cells by scientists
By Krista Conger of Inside Stanford Medicine.

WSJ Tissue regeneration a la salamanders and newts seems like it should be the stuff of science fiction. But it happens routinely. Why can’t we mammals just re-grow a limb or churn out a few new heart muscle cells as needed? New research suggests there might be a very good reason: Restricting our cells’ ability to pop in and out of the cell cycle at will — a prerequisite for the cell division necessary to make new tissue — reduces the chances that they’ll run amok and form potentially deadly cancers. Now scientists at the Stanford University School of Medicine have taken a big step toward being able to confer this regenerative capacity on mammalian muscle cells; they accomplished this feat in experiments with laboratory mice in which they blocked the expression of just two tumor-suppressing proteins. The finding may move us closer to future regenerative therapies in humans — surprisingly, by sending us shimmying back down the evolutionary tree. Read more...
References:
Pajcini et al, Cell Stem Cell (2010) [link] (PDF)
News article from The Wall Street Journal (PDF)
News article from The New York Times (PDF)
News article from Stanford School of Medicine Scope Blog Read more...