Development & Aging

Lab finds a creative way to support their PI

by Heather Buschman, Ph.D. on April 5, 2013 at 5:19 am | 0 Comments

Malene Hansen, Ph.D., assistant professor in our Del E. Webb Center for Neuroscience, Aging, and Stem Cell Research and native of Denmark, gave a faculty promotion seminar last week. It was her chance to show off her science and service to a committee that will evaluate her for promotion to associate professor. Check out her lab members in attendance. They’re showing their support with Danish flag scarves! Best of luck to Hansen and her team.

Unraveling the molecular roots of Down syndrome

by Heather Buschman, Ph.D. on March 24, 2013 at 11:00 am | 29 Comments

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Neurons from a normal mouse (left) are longer and fuller than neurons from a mouse lacking SNX27 (right).

Researchers discover that the extra chromosome inherited in Down syndrome impairs learning and memory because it leads to low levels of SNX27 protein in the brain.

What is it about the extra chromosome inherited in Down syndrome—chromosome 21—that alters brain and body development? Researchers have new evidence that points to a protein called sorting nexin 27, or SNX27. SNX27 production is inhibited by a molecule encoded on chromosome 21. The study, published March 24 in Nature Medicine, shows that SNX27 is reduced in human Down syndrome brains. The extra copy of chromosome 21 means a person with Down syndrome produces less SNX27 protein, which in turn disrupts brain function. What’s more, the researchers showed that restoring SNX27 in Down syndrome mice improves cognitive function and behavior.

“Junk DNA” drives embryonic development

by Heather Buschman, Ph.D. on December 3, 2012 at 6:04 am | 0 Comments

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Differentiating mouse embryonic stem cells (green = mesoderm progenitor cells, red = endoderm progenitor cells). The microRNAs identified in this study block endoderm formation, while enhancing mesoderm formation.

An embryo is an amazing thing. From just one initial cell, an entire living, breathing body emerges, full of working cells and organs. It comes as no surprise that embryonic development is a very carefully orchestrated process—everything has to fall into the right place at the right time. Developmental and cell biologists study this very thing, unraveling the molecular cues that determine how we become human.

“One of the first, and arguably most important, steps in development is the allocation of cells into three germ layers—ectoderm, mesoderm, and endoderm—that give rise to all tissues and organs in the body,” explains Mark Mercola, Ph.D., professor and director of Sanford-Burnham’s Muscle Development and Regeneration Program in the Sanford Children’s Health Research Center.

In a study published November 14 in the journal Genes & Development, Mercola and his team, including postdoctoral researcher Alexandre Colas, Ph.D., and Wesley McKeithan, discovered that microRNAs play an important role in this cell- and germ layer-directing process during development.

Sanford-Burnham research projects selected to go to space

by Communications Staff on November 29, 2012 at 6:30 am | 1 comment

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The International Space Station, as seen from the departing Space Shuttle Discovery in 2009 (Image courtesy of NASA)

Space Florida to send two experiments from Sanford-Burnham Medical Research Institute to the International Space Station

We’re excited to announce today that two of our research teams have won Space Florida’s International Space Station (ISS) Research Competition. Eight teams were selected from a pool of international applicants to send experiments to space in late 2013. The competition was initiated by Space Florida, the state’s spaceport and aerospace authority, and NanoRacks, LLC. Sanford-Burnham’s research will fly as payloads to the ISS aboard a SpaceX Falcon 9 launch vehicle and research will be conducted on board the U.S. National Lab at the ISS.

Here’s what the two teams are hoping to accomplish:

California’s stem cell agency boosts heart disease research at Sanford-Burnham

by Heather Buschman, Ph.D. on September 12, 2012 at 6:29 am | 0 Comments

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Huei-Sheng Vincent Chen, Ph.D.

The California Institute for Regenerative Medicine (CIRM) has awarded a $1.58 million grant to Huei-Sheng Vincent Chen, Ph.D., associate professor at Sanford-Burnham. Chen’s proposal was one of 28 new projects funded as part of CIRM’s Basic Biology IV awards program, which supports basic research aimed at increasing our understanding of stem cells and how to work with them. This new funding will allow Chen and his team to develop personalized models of inherited heart conditions using stem cells derived from patients’ own skin cells. They will also use these models to develop new therapies.

“Most heart conditions that cause sudden death in young people—those under age 35—are caused by inherited genetic mutations. But doctors have a hard time treating these types of heart conditions because not much is known about how genetic mutations cause them and because they’re usually diagnosed late in the disease process,” Chen said. “At the moment, the only way to treat these inherited heart diseases is to implant a heart-shocking device to prevent sudden death. More frequently, however, no therapy is available to slow the disease’s progression.”

New heart failure trigger could change the way cardiovascular drugs are made

by Heather Buschman, Ph.D. on July 18, 2012 at 10:01 am | 1 comment

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APJ’s yin-yang role in cardiac function: the receptor APJ serves a dual function in heart health, depending on how it’s activated. While APJ enhances heart health upon binding the hormone apelin (green), APJ can also trigger heart enlargement and failure when it senses certain mechanical changes (red).

In their quest to treat cardiovascular disease, researchers and pharmaceutical companies have long been interested in developing new medicines that activate a heart protein called APJ. But researchers at Sanford-Burnham Medical Research Institute and the Stanford University School of Medicine have now uncovered a second, previously unknown, function for APJ—it senses mechanical changes when the heart is in danger and sets the body on a course toward heart failure. This means that activating APJ could actually be harmful in some cases—potentially eye-opening information for some heart drug makers. The study appears July 18 in Nature.

“Just finding a molecule that activates APJ is not enough. What’s important to heart failure is not if this receptor is ‘on’ or ‘off,’ but the way it’s activated,” said Pilar Ruiz-Lozano, Ph.D., who led the study. Ruiz-Lozano, formerly assistant professor at Sanford-Burnham, is now associate professor of pediatrics in the Stanford University School of Medicine and adjunct faculty member at Sanford-Burnham.

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Recycling fat to live longer?

by Heather Buschman, Ph.D. on September 6, 2011 at 9:00 am | 0 Comments

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Germline-less C. elegans nematodes with an autophagy marker shown in green. (Image courtesy of the Hansen lab)

Aging is generally accepted as a universal fact of life, but how do humans and other organisms age at the molecular level?

At Sanford-Burnham, a team led by Dr. Malene Hansen uses a type of worm called Caenorhabditis elegans to work out the molecular underpinnings of the aging process. Recently, they found that two cellular processes—lipid metabolism and autophagy—work together to influence worms’ lifespan. Autophagy, a major mechanism cells use to digest and recycle their own contents, has become the subject of intense scientific scrutiny over the past few years, particularly since the process (or its malfunction) has been implicated in many human diseases, including cancer and Alzheimer’s disease. (See Autophagy 101.)

The Hansen group’s latest study, published online September 8 in Current Biology, provides a more detailed understanding of the roles autophagy and lipid metabolism play in aging.

“The particular worm model we used in this study is known to live longer than normal worms, but we didn’t completely understand why,” said Dr. Hansen, assistant professor in Sanford-Burnham’s Del E. Webb Center for Neuroscience, Aging, and Stem Cell Research and senior author of the study. “Our results suggest that increased autophagy has an anti-aging effect, possibly by promoting the activity of a fat-digesting enzyme. In other words, it seems that recycling fat is a good thing—at least for worms.”

Marching to the same beat

by Ana Miletic Sedy on August 4, 2011 at 11:23 am | 0 Comments

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heart muscle in a fruit fly (image courtesy of the Bodmer lab)

Heart disease is the leading cause of death in the United States, accounting for more than 25 percent of all deaths each year. While many factors work together to contribute to heart disease—including environment, lifestyle, and genetics—we only have control over the first two. To address the third factor (genetics), researchers at Sanford-Burnham recently turned to fruit flies.

Fly and human genes are so closely related that the sequences of newly discovered human genes, including many that contribute to disease, can often be matched up with fly counterparts. Since fruit flies are relatively easy to work with (they’re small, breed quickly, and don’t require a lot of maintenance), they often give scientists clues to the functions of human genes and helps them develop drugs that target them.

As Dr. Rolf Bodmer, director of Sanford-Burnham’s Development and Aging Program, explains in the Journal of Cell Biology, “We use fruit flies to learn about the fundamental genetic mechanisms that are important for the development and function of the heart.”

Dr. Bodmer himself discovered early in his career that flies lacking Tinman, a protein that regulates the expression of other genes, fail to develop heart tissue during embryonic development. If Tinman is removed later during fly development, the flies’ hearts don’t function properly.

Now researchers in Dr. Bodmer’s lab, led by postdoctoral researcher Dr. Li Qian, uncovered a genetic network that controls heart development and function in fruit flies and mice, with additional clues that it might also play a role in human heart health.

“Eye of newt” reverses a long-held scientific dogma

by Heather Buschman, Ph.D. on July 12, 2011 at 8:57 am | 0 Comments

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Japanese fire belly newt (Cynops pyrrhogaster)

For nearly 250 years, generations of scientists believed that the older an animal gets, the less able it is to regenerate and replace damaged or diseased tissue. (Even Charles Darwin weighed in.) Everyone assumed that, as animals age, cellular resources become exhausted, DNA repair mechanisms break down, healing takes longer and tumors develop. As of today, however, that’s no longer the doctrine. It still might be harder and harder for humans to repair wounds and heal as we age, but it turns out that the humble newt is another story.

When injured, newts can regenerate limbs, tails or eyes right back to factory standards. Humans can only do that at the very tip of the finger and only under very limited circumstances. And according to a new study published today in the journal Nature Communications, old newts can do it just as well as young newts. The study focused on the newt’s optical lens, which can be removed entirely and, after the incision heals, completely regenerate in a single day. The study’s lead author, Dr. Goro Eguchi, began breeding newts and collecting lenses 16 years ago. Throughout the years since, lenses were removed 18 times from the same animals. By the time of the last tissue collection, they were at least 30 years old (very old, for a newt).

Vitamin A for the heart

by Heather Buschman, Ph.D. on January 26, 2011 at 4:16 pm | 2 Comments

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Dr. Thomas Brade, post-doctoral researcher in the Duester lab, studies retinoic acid and development.

Vitamin A is supposed to be really good for you – improving your vision, complexion and even pre-natal health. But what does it do, exactly?

“That’s actually not very well known,” says Dr. Gregg Duester, professor in Sanford-Burnham’s Development and Aging program. “For example, even though it’s been clear for 100 years that vitamin A is required for proper embryonic development, only now are we getting to the molecular details of what it does.”

Researchers in Dr. Duester’s lab study retinoic acid, an active form of vitamin A. They are especially interested in understanding how retinoic acid tells the right body parts to form in the right places at the right time in a developing embryo. Recently, while comparing limb buds (the precursors of arms and legs) in mice with – and without – the ability to generate retinoic acid from vitamin A, they decided to check out the differences in their hearts, too. As it turns out, the ventricles (the part of the heart that pumps blood out to the rest of the body) in retinoic acid-deficient mouse embryos, were thinner than those in their normal counterparts.

Top Stories - Development & Aging

Lab finds a creative way to support their PI

Unraveling the molecular roots of Down syndrome

“Junk DNA” drives embryonic development

Sanford-Burnham research projects selected to go to space

California’s stem cell agency boosts heart disease research at Sanford-Burnham

New heart failure trigger could change the way cardiovascular drugs are made

Recycling fat to live longer?

Marching to the same beat

“Eye of newt” reverses a long-held scientific dogma

Vitamin A for the heart

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