Trash talking and creating a stem cell community

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Imilce Rodriguez-Fernandez likes to talk trash. No, really, she does. In her case it’s cellular trash, the kind that builds up in our cells and has to be removed to ensure the cells don’t become sick.

Imilce was one of several stem cell researchers who took part in a couple of public events over the weekend, on either side of San Francisco Bay, that served to span both a geographical and generational divide and create a common sense of community.

The first event was at the Buck Institute for Research on Aging in Marin County, near San Francisco. It was titled “Stem Cell Celebration” and that’s pretty much what it was. It featured some extraordinary young scientists from the Buck talking about the work they are doing in uncovering some of the connections between aging and chronic diseases, and coming up with solutions to stop or even reverse some of those changes.

One of those scientists was Imilce. She explained that just as it is important for people to get rid of their trash so they can have a clean, healthy home, so it is important for our cells to do the same. Cells that fail to get rid of their protein trash become sick, unhealthy and ultimately stop working.

Imilce is exploring the cellular janitorial services our bodies have developed to deal with trash, and trying to find ways to enhance them so they are more effective, particularly as we age and those janitorial services aren’t as efficient as they were in our youth.

Unlocking the secrets of premature aging

Chris Wiley, another postdoctoral researcher at the Buck, showed that some medications that are used to treat HIV may be life-saving on one level, preventing the onset of full-blown AIDS, but that those benefits come with a cost, namely premature aging. Chris said the impact of aging doesn’t just affect one cell or one part of the body, but ripples out affecting other cells and other parts of the body. By studying the impact those medications have on our bodies he’s hoping to find ways to maintain the benefits of those drugs, but get rid of the downside.

Creating a Community

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Across the Bay, the U.C. Berkeley Student Society for Stem Cell Research held it’s 4th annual conference and the theme was “Culturing a Stem Cell Community.”

The list of speakers was a Who’s Who of CIRM-funded scientists from U.C. Davis’ Jan Nolta and Paul Knoepfler, to U.C. Irvine’s Henry Klassen and U.C. Berkeley’s David Schaffer. The talks ranged from progress in fighting blindness, to how advances in stem cell gene editing are cause for celebration, and concern.

What struck me most about both meetings was the age divide. At the Buck those presenting were young scientists, millennials; the audience was considerably older, baby boomers. At UC Berkeley it was the reverse; the presenters were experienced scientists of the baby boom generation, and the audience were keen young students representing the next generation of scientists.

Bridging the divide

But regardless of the age differences there was a shared sense of involvement, a feeling that regardless of which side of the audience we are on we all have something in common, we are all part of the stem cell community.

All communities have a story, something that helps bind them together and gives them a sense of common purpose. For the stem cell community there is not one single story, there are many. But while those stories all start from a different place, they end up with a common theme; inspiration, determination and hope.

 

A time to kill, a time to heal: cells linked to aging also help heal wounds

Senescent cells, so called because of the role they play in the aging process, have acquired a bit of a bad reputation.

Yet new research from the Buck Institute suggests that these cells may not be so bad after all.

Buck Institute faculty Judith Campisi and Postdoc Marco Demaria. [Credit: The Buck Institute]

Buck Institute Professor Judith Campisi and Postdoc Marco Demaria. [Credit: The Buck Institute]

Reporting in today’s issue of Developmental Cell, Buck Institute scientists have found that, while senescent cells do indeed contribute to cellular aging and age-related diseases, they also play an important role in healing wounds. Furthermore, the team has identified the specific molecule in senescent cells that does the healing—pointing to a new therapy that could harness the good aspects of senescent cells, while flushing out the bad.

As we age, so do our cells. During cellular senescence, cells begin to lose their ability to grow and divide. The number of so-called senescent cells accumulates over time, releasing molecules thought to contribute to aging and age-related diseases such as arthritis and some forms of cancer.

But experiments led by Buck Institute Professor Judith Campisi and postdoctoral fellow Marco Demaria revealed that following a skin wound, cells that produce collagen and that line the blood vessels become senescent, and lose the ability to divide. Instead, they accelerate wound healing by secreting a growth factor called PDGF-AA. And once the wound was healed, the cells lost their senescence and shifted back into their normal state.

Because cellular senescence has long been linked to aging and age-related diseases, some research has been focused on finding ways to flush out senescent cells entirely. But the findings by the Buck Institute team throw a wrench in that idea, by revealing that these cells do in fact serve an important purpose.

According to Campisi, there is still a lot to learn:

“It is essential that we understand the full impact of senescence. The possibility of eliminating senescent cells holds great promise and is one of the most exciting avenues currently being explored in efforts to extend healthspan. This study shows that we can likely harness the positive aspects of senescence to ensure that future treatments truly do no harm.”