161: Dr. Jennifer Elisseeff - The Future of Tissue Regeneration

In this episode, we are joined by Dr. Jennifer Elisseeff to discuss the evolving field of tissue engineering and its applications in regenerative medicine.

She explains the shift from using stem cells to focusing on immune cells for tissue repair, the challenges of regenerating cartilage, and the importance of vascularity in tissue health.

The discussion also covers the impact of aging on tissue repair, the role of senescent cells, and the future of personalized medicine in tissue engineering.

Dr. Elisseeff emphasizes the need for innovative approaches and the integration of immunotherapies to enhance tissue repair processes.

Learn more about Dr. Jennifer Elisseeff:

https://www.bme.jhu.edu/people/faculty/jennifer-h-elisseeff/

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Transcript

Disclaimer: This transcript was generated by AI and may not be 100% accurate. If you notice any errors or corrections, please email us at phil@longevityroadmap.com.

    The immune system is potentially the regulator of the tissue structure, and there are immunotherapies out there, right? So it opens up a whole new therapeutic window.

Welcome everybody. This is Buck Joffrey with Longevity Roadmap, uh, today. Uh, really interesting show. You can talk to Dr. Jennifer Elisseeff. Uh, she's a professor over at Johns Hopkins, and specifically we go into the idea of tissue engineering. Um, you know, we talk about longevity and health span on this show, but you know, I mean there's just also sort of physical.

We are in tears as we get older. You know, a good example of that for me was that, uh, you know, and, and we're gonna talk about this more in, in upcoming shows, but, uh, I had, uh, bilateral, uh, labral tears in my hips along with like a, you know, my back has been an absolute mess, uh, since I was 15 years old. But, um, I had the chance of, uh, going down to Columbia and getting stem cells, uh, myself.

Pretty remarkable results, especially in my hips where, you know, I was feeling it literally every day. And now I, you know, I, I don't feel anything. But that's one part of tissue engineering. Um, so in this show, what we're gonna really focus in on is some of the, um, you know, basics of what exactly is going on, uh, in tissue engineering.

Uh, we talk a little bit about, you know, the types of materials that are being used, uh, the immune system's role. The role of aging and, uh, and sometimes, uh, how senescent cells might not be as bad as you think when it comes to regeneration. Anyway, fascinating show. Hope you enjoy it, and we'll have that interview right after these messages.

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Welcome back to the show, everyone. Today my guest on Longevity Roadmap is, uh, Dr.

Jennifer Elisseeff. She's the Morton Goldberg professor at Johns Hopkins University and Director of the Translational Tissue Engineering Center. She's trained as both an engineer and a biomedical scientist, and she's a pioneer in injectable materials and regenerative therapies. Thanks for being on, uh, Dr.

Elisseeff.

My pleasure.

So I wanted to just kind of give people sort of a broad perspective on what exactly tissue engineering and is, and, you know, how does it fit into sort of the large, larger field of regenerative medicine right now.

Well, first of all, I think the definition has changed over time. So 25 years ago when I started, tissue engineering was defined as, um, using a scaffold of some kind.

And we would build synthetic scaffolds and combine them with cells and signals. And in particular we had interest in stem cells and use that to rebuild it tissue. Nowadays, I think of it as just trying to engineer the structure of tissues in the body. And you can imagine with aging that changes, right?

And And can we use those approaches to make the aged tissue behave and look and act younger?

Yeah. So I guess what are some of the most important right now, these days? Real world examples already in use.

Already in use. Um, I, I would say we're still a little bit more in the fundamental side. I think anytime we're trying to repair tissues, that's an element of tissue engineering.

So, um, whether you have a muscle injury that you're working to repair or a cartilage injury in your knee. Those are all examples of, um, sort of repair processes we're trying to accelerate. We're also interested in how different tissue talk to each other in the body, um, and how that can be used to help engineer systems.

So when you're, when you're developing a regenerative therapy, um, what are the endpoints that you're looking at to determine whether something successful? Is it, you know, integration, durability, restoring function? How, how do you, how do you look at it?

That's a great question because initially we thought we had to duplicate the tissue exactly.

To get it back working, but you don't always have to duplicate the original function or the shape of the tissue to actually get performance and get what, what you need. I mean, ideally that would be the case, but if you're running a clinical trial or essentially trying to get. People back into whatever exercise routine or just daily life, um, you know, you don't necessarily have to replicate the original structure.

Yeah. And, and what are some of those materials that you actually are working with? I mean, you mentioned stem cells and, but above and beyond that, um, I'm sure there's other technologies, other, um, other materials that you're using. Can you give us a sense of like how those, uh, what, what some of those are?

Sure. Well, first I I, I'd like to describe how we've actually shifted from. Stem cells to actually immune cells. So we spent all this work trying to see how we could use materials in Apple to modulate stem cells. But after some clinical testing and careful evaluation that, hey, actually we think the immune system is potentially the regulator of the tissue structure.

And there are immunotherapies out there, right? So it opens up a whole new therapeutic window, and that's particularly important for aging, where you have this inflammation that might be blocking, um, tissue repair. So we've been looking at biological scaffolds that are derived from the structures of tissues and are giving a signal to the immune system to say, Hey, come here and, um, create an environment that's gonna rebuild the tissue.

Can you give us an example, just kind of like a theoretical, just just so people have a framework to kind of think of what you're doing. When you talk about scaffolds and you're talking about, um, immune cells, like just in the big picture kind of can sort of give us a framework to think about.

Yeah, so, um, so the biological scaffolds that we're using looks like, look like powders or sheets, and they're derived from, um, the normal proteins of Purdue Glycans that are in our tissues normally.

Um, and when I think of immune cells, there are a couple important players here. So T cells, um, we've been quite interested in, um, as sort of regulators of the immune environment. So you may have heard of T cells and immunotherapies for cancer, um, and T-cell and autoimmune disease, but T-cell also contribute to tissue repair and help modulate things like macrophages, which are really the boots on the ground with cleaning up the tissue and damaged and helping to direct repair processes and even contributing to things like new blood vessel formation and.

The whole vasculature is something that's obviously important for the tissue health, and I think something that, um, can be a really interesting target in aging tissues.

So in such a, um, sort of a system, say you're trying to, let's just, let's just say for example, I, I'm, I would imagine a lot of this is orthopedic in nature, correct?

Yeah. We tend to do a lot with the muscle and the joint.

Yeah.

Yeah.

So you have a joint. You're trying to regenerate, you know, cartilage or something like that. Where does the tissue that you're going to, um, use actually come from?

Um, so we've looked at, um, actually, um, powders and matrices, uh, biological scaffolds derived from, um, pig tissues.

Um, and these are processed in a way to give signals to. Tissue environment in the case of cartilage. One thing that's interesting, so cartilage is, um, the sort of slippery tissue that allows your joints to move smoothly and ideally painlessly, right? But there's another tissue that's next to that, the synovium, um, that.

It gives a lot of signals and is where some of immune cells can be, and the cross top between those two can be important. So, um, you know, you don't always need to target the cartilage directly to help regrow it. You can target surrounding tissues, um, to help regrow.

So in that scenario too, like you also were talking about immune cells.

Would those immune cells come from the pig or would they be potentially autologous or

they're your own cells? So we're very interested in using your own body to help repair, whether it's leveraging your own stem cells or, um, you know, leveraging your own immune cells to help direct the local tissue repair.

And there's a beautiful work, um, a number of years ago by Ben Cosgrove and Helen Blau. We think of aging and loss of stem cells or stem cell dysfunction. They took stem cells out and put them in sort of a healthy culture environment and, and they sort of perked up, right? The, the stem cell cells were okay.

They were just in an environment that was not to repair. And, and, you know, as we started getting into the immune system, I was struck, um, by, by, um, um. Newscast on NPR and um, it was Tom Hanks talking about visiting veterans facilities. And he met two veterans that had both lost, um, a limb and one was in rehab for three weeks and the other three years.

And the only difference was that one had an infection. So we think of the immune system as being important and fighting off infections, but it also contributes to repair, but it can't do the them both at the same time. So if you're revved up to fight an infection, it's uh, it's harder to repair, right? So, and obviously you don't wanna have an infection, right?

And that's gonna be important. Or, you know, survival and being healthy. But how do we modulate that? Okay, actually now it's time to repair, safe to repair and leverage that normal pathway of repair from the immune system.

Yeah, and, and, and it's interesting. You, you know, it, it's like as a, as a guy who, I mean, I, I've done some, uh, reconstructive surgery using skin grafts and that kind of thing.

Um, you know, one of the big issues of course is, is vascularity. I mean, you, you can put all the tissue you want in, but if it, if you don't have blood vessels to actually supply it with blood and make those appropriate connections, uh, it's gonna die anyway. Right. So, ta talk about that challenge and, and what are some of the things that you do to improve that potentially?

Well, um, what's, um, interesting, I, I'll, I'll tell, um, I actually two stories. Um, one is you gradually develop more fibrosis in tissues with aging. I think one of the contributor to that is the reduced, um. Capacity or reduced function of your smaller vessels, the ones that you described feeding those tissues.

And I think this is one of the reasons if we combine sort of exercise performance with longevity, that interval training means so much more as you age, right? So you're, you're training those small blood vessels to, um, stay healthy. Um, but I, I wanna tell another story that we have, um, that we're really excited about, just how the body talks to each other.

And the importance of, um, blood vessels. Um, we've been looking at how different types of tissue wounds impact things like tumor growth and response to these, you know, new immunotherapies to try to understand why do some people respond well and others not Well, if we give a muscle wound, it actually increases tumor growth and decreases response to immunotherapies.

Um, but if we put a cartilage injury in arthritis. We actually see decreased tumor growth and increased response to immunotherapy. And it's the blood vessels that are doing that. So you know, you have the same sort of phenotype of your T cells, but those blood vessels and activation also of those blood vessels in the tumor and enhance the response and efficacy.

And that really comes from factors in the blood. From that arthritis and, and we see this translate actually to patients too. So just the complexity of all the different,

it's interesting because I would think almost increased vascularity to a tumor would actually make the tumor grow faster.

Right. Well, so it's, it's, the blood vessels are more stable.

So, um, without that, um, um, arthritic environment, you have these little blood vessels trying to come out right to, but they're sort of dysfunctional and they're not bringing the immune cells in there. So we have these more stable, larger blood vessels in the tumor. Where then, okay, the T cells and immune cells can get in that tumor and start fighting.

So, you know, and that, that's sort of an interesting concept because when I think about that, I'm thinking, wow, is lack of appropriate vascularity, you know, in inability to get good blood flow behind potential tumor growth in general. Is that, is that the insinuation potentially. Um, not that it, not that it's the sole factor, but it a big contributor.

Yeah.

Um, yeah, it's complicated. You've got the metabolic function of the cancer cells, right, that are growing actively. Um, also something that we see in, um, tumors, that's generally something you don't want is that same fibrosis that I mentioned. Accumulates with aging just more broadly, and that fibrosis, um, also impacts blood vessel development.

Um, and we see that we've actually been studying, um, fibrosis and blood vessels in two scenarios. One actually in the capsule that forms around breast implants. It's, um, a nice model system to, to study that. And also in fibroids, um, very common, um, benign tumor and in these spaces where we get lots of fibrosis.

You have this thick matrix with no blood vessels, but then adjacent to it you've got these big malformed blood vessels. So, so that whole balance of tissue structure, I think is sort of what I think of tissue engineering today. So how can we, um, think about recreating that normal tissue structure where you have appropriate vasculature?

Minimal fibrosis, you don't want that fibrosis, um, to impact, you know, whether it's your muscle function or your liver, or even scar in the skin. Right? Uh, so, so how can we either, you know, with materials or even with other types of therapies, modulate that tissue structure?

Yeah. You've mentioned aging a few times now.

Um. Can, can you talk about the components of aging that change the body over time that makes this increasingly challenging? Of course, you've mentioned increases among fibrosis. What, what other factors really come into the aging process? Because again, now you're talking about regeneration, you know, apart from athletes and, you know, athletic injuries and stuff like that.

A lot of this is. Probably related to age related degeneration of joints and tissues.

Yeah, so, so you know, there's so many different facets of aging to study, but the, what we're very interested in is the tissue repair part. So when we put that biological scaffold in a young muscle environment, you know, we get a nice repair process.

If we put it in an old environment, it just doesn't work as well. And I think of, you know, even if you are an athlete, right, the recovery time increases, right? So the repair process is delayed. And, and I sort of joke sometimes and think of, um, aging as a chronic non-healing wound, right?

Yeah.

So it's like specific injury.

I, I feel that one personally actually. So I'm a big non-healing wound.

So, so some of the same processes that we see in sort of a chronic non-healing wound are what we see in aging, so that chronic inflammation and, and the chronic senescence, right? So we've been interested in what senescence does, um, and what it is in, in the body and how it might help or hurt in various scenarios.

Um, so as we've studied, uh, tissue repair in an aging environment, so the muscle balloon, for example. We find that we can recover some of that response to that pro regenerative scaffold by combining it with an immunotherapy, for example, that dampens the negative inflammation because you actually need inflammation for tissue repair.

Right? But it's timing and the kind of inflammation that's important. And that's, that's what we're trying to. Tease out and study now.

So you mentioned senescent cells. Uh, we talked about senescent cells on the show a bunch of times where basically you've got these zombie cells, uh, that aren't really up to any good and they're kind of sitting around secreting, inflammatory, uh, cytokines around them, basically, you know, making it problematic for all the cells around them as well.

So, uh, talk a little bit specifically, if you would, on how they interfere with repair.

Well, uh, I, I'd like to first step, I'm, I'm not the biggest fan of zombie cell terminology. Okay. Alright. Well, our paper on those in the ca in the context of arthritis came out around Halloween, number of years ago. Ah, there we go.

There is connecting with Halloween and so that's a little bit hub of zombie cell started. So just like the immune system, I said it's, you know, you need the immune system to repair tissues, um, senescent cells. You actually need. In the early tissue repair process, and they actually help with building the new blood vessels.

So, so I think that,

how, how so? Yeah.

So, um, you know, that, um, arthritis tumor example I gave that's dependent on senescence around the blood vessels, um, helping to stabilize and promote their regener, um, you know, the blood, blood vessel formation. So if you delete senescent cells. Early in the wound healing process, um, you're gonna delay your repair, right?

So I, I think of it more as a parallel with inflammation, right? Um, they're signaling cells contributing to the environment and sometimes you need them, but if they stick around too long. Or the, you know, the wrong type of ones, the wrong type of inflammation, the wrong type of senescent cell sticks around too long.

That's when you have a problem. And you know, we see a lot of senescent cells in that capsule around breast implants and fibroids. So I think. There's senescence associated with that fibrosis, which obviously is what we don't want, and that's chronic, just like that inflammation. Um, but then you have some that are actually part of the normal inflammatory wound healing, um, cascade.

So, um, I think there is physiological senescence. Um, but again, going back to the aging as a chronic non-healing wound example works really well.

Yeah, totally. Um. They do, do they also, so with with scent cells, there's a dam, there's a balance. There is what you're saying, where you kind of need them. But I mean, to a certain extent, aren't they also potentially gonna interfere with repair or not so much?

Exactly. So it's the timing of them. The type of nce. So we've been looking at different types of senescence, um,

different stuff. Yeah, talk about that, that, that would be useful because we're, we're so programmed right now in this space to think of senescence cells as nothing good, you know?

Yeah. Yes, yes. Um, I, I might be fighting a little uphill battle there.

So, so one of the big challenges, they'd been studied in the dish for so long in vitro. Right, but then seeing what they are in vivo like and actual tissues is, um, a lot more challenging. And so using new computational approaches and new tools, we can start predicting which cells are senescent in tissues.

And what we found is, um, multiple cell types can be senescent. So, um, an endothelial cell or the cell that surrounds the blood vessel called a parasite, they can become senescent. And that's actually important for new blood vessel formation. Um, but it can also be related to autoimmunity, right? Where you get inflammation and those blood vessels are inflamed.

So, um, again, it can be good or bad. The Fibroblastic senescence. Um. These are like the, the cells that make extracellular matrix. So, um, the bulk protein molecules that make up your tissues. And, um, you need that a little bit at the beginning, right? But if they stick around chronically, um, that's not good. So again, it's the type and the timing, uh, just like the immune.

Do you, uh, when, when we've been talking about primarily, at least I've been thinking about it, things in, in terms of, you know, joints and muscles and maybe skin, but are, are, are there other applications, um, that, that you guys are actively looking at? Others are looking at that, that we might not think about?

Well, inflammation and senescence can impact, um, every organ, right? So people are looking at a neurodegeneration, they're looking at it in liver fibrosis, cardiac fibrosis, arthrosclerosis, um, connections with diabetes. Um, pretty much anything where the tissues. Don't have the right structure and, and content.

Right. So again, the tissue engineering part, so you know, it doesn't

have even, how about organs? How about organs? Uh, well you talked about, you talked about cardiac fibrosis, I guess, so, you know, that, that kind of thing.

Cardiac, liver, lung fibrosis, um, pretty much any fibrotic and

inflammatory, any fibrotic.

Yeah. Yeah, yeah, yeah. Especially the, I mean, fibrotic lung disease is another big one, right? Um,

yes.

Yeah, absolutely. Um. From, um, you know, you mentioned that, that, that I guess initially had asked you, you know, what's, what are we using right now? And, you know, how's going? And, and it, it sounded like this is stuff that's really a little bit, maybe further out, but what areas of tissue engineering do you think are sort of, uh, closest to having a meaningful impact, uh, on our health in the next decade or so?

Yeah, so I think, um, these biological scaffolds, um, they are being injected into the joint to help tissue repair. They're being injected into soft tissue defects, um, that might occur from surgery or things like lumpectomy also for cosmetic applications. Um, those are, um. I think the scaffolds that we see today a little bit, but um, you know, there's some regulation things about them, some regulatory aspects that I think they could really grow a lot more in the future.

Um, I think immunotherapies are gonna expand, right? So cancer immunology really, you know, created this massive new field, right, of understanding how the immune system. Can be targeted. Um, and now that's moving to autoimmunity too. So autoimmune research has looked a lot at, um, um, targeting the immune system.

And I think we're just scratching the surface of how we can use immunotherapies to promote tissue repair. And, you know, some of these are on the market today for other applications, um, and how we combine those, see, this is where I think. There's so much that can be relatively easily done, right? If there's the will, um, and the final is of combining immunotherapies with pro regenerative scaffolds, right?

As I mentioned, with aging, you have that increased inflammation that's blocking repair. So let's put in something to promote, repair, and also block, um, that inflammation that's, you know, inhibiting that repair process that wants to happen.

We, we've sort of talked around stem cells, and I guess this kind of gets to, um, the regulatory challenges as well.

Um, you know, anecdotally, I, you know, I actually went down to Columbia, this, uh, company called Bio Accelerator, which is an American company and had some things done there with pretty miraculous results. I have bilateral labral tears in my hips that, that I'd feel every single day, and I don't feel it at all anymore.

Um. Can you talk a little bit, maybe just in general about stem cell use and you know, what your thoughts on that are? I know we've talked about, uh, uh, immune cells, but, but let, let's drill down a little bit more on stem cells and I guess some of the limitations.

Well, you might be unhappy with my responses or some cells.

Yeah. So, um, yeah, there was, um, a lot of work in the joint space on injecting chondrocytes. Right. But it was always a little suspicious that you injected so many cells. It didn't seem like that many of them survived, but there were some potential benefits, but it was super expensive.

Yeah.

And then, um, you see these other trials where I remember seeing a slide at a, at a meeting where I was listing.

2000 trials of stem cells for heart applications. Right. Um, and, you know, minimal to no effects. And the next slide is, oh, here was, here's what we need to do to change that. And I'm thinking, what other drug in history would we keep trying, right? But here, um, I think there's another beautiful study that compared, um, actually injecting dead stem cells with live stem cells.

So I think the presence of dead cells, even. Injecting, those are giving the same signals that these decellularized tissues are giving. They're saying there's tissue damage here, right? There's tissue damage and come help repair. Right? And so how much of that is stem cell? I mean, there's definitely certain elements of a stem cell that's gonna help, but I think learning what that is.

We can, you know, make it an easier therapy so you don't have to manage of like, delivering a live cell is really hard.

I think that's accurate. I mean, even the, I think people who are doing stem cells, um, you know, even, even when I was down in Columbia, the idea was not we're gonna put the stem cells in you and those stem cells are gonna turn into tissue, but rather that there's this entire milieu.

That comes around, uh, the stem cells themselves and, you know, we, we, we hear about exosomes and things like that, but whatever that, whatever that, you know, stuff that comes along with the tissues tends to somehow trigger again, the immune system, uh, to, you know, come in and, and repair more than it would otherwise is kind of the, I think the concept there.

Yes. Absolutely. And, and these tissues like tendons and cartilage and ligaments, you know, they don't have great vasculature, if any at all. And, and so helping to bring in those elements of repair in an area where, you know, you don't have that blood vessel or the way to bring in those nutrients is, is important.

And you know, I think in our arthritis tumor example. When we damage that cartilage, it's screaming signals of, you know, throat vessels I need to repair, but the tissue's inhibiting it 'cause it doesn't normally have that. So, um, it's, it's similar to actually your cornea, right? Um, there's some similarity in your cartilage and your cornea, right?

You don't have the vasculature and then when you really damage it, you get scar formation instead. So, um, I, you know, how much of it is that balance of blood vessels, um, or not? The other interesting thing with stem cells as people are trying to use them for cardiac applications is a lot of them end up in the spleen.

Right? And your spleen is an immunological organ, essentially. Right? So how much of it is signaling to the spleen that's, Hey, we, you know, we need to regenerate things in the body.

What's the hardest part right now about bringing any of these things to from the lab into the real world?

I would say taking different approaches.

There are a lot of barriers to doing that, right? If you're doing the same old thing, I think there's a little bit of a path that's worn down, but I think we need really different out of the box approaches, right? Um, and, and even the concept of immunotherapies and t-cell for regeneration is new and different, right?

So, so there are a lot of barriers, not just regulatory, which of course is always a lot of work, but just the way people think. And also, um, understanding the variety in people, right? So, um, you know, we see this around us. Aging happens at different rates and different people, right? And our history of infections, our history of all these different things or diet.

We've been looking at how, um, the microbiome impacts. Repair on a muscle, right? So, so all these different things, talking to each other and that variation in people makes it much harder to develop a single therapy.

Yeah. Uh, one more question for you, and I think it's sort of just more a big picture. I mean, it's always kind of interesting to hear people in various positions of, you know, you, you're a leader in your field, um, you know, what does the future look like?

You're looking 10, 20 years down the line. What's some of the. Breakthrough in tissue engineering that you're potentially most excited about, that you see that there's, wow, that could potentially be something really big.

Ooh, distilling that to a single one is a little tough, I would say. Um, I've been so excited with the big data opportunities in tissue engineering that weren't there before.

Right. So, you know, now we can break apart tissues and. Learn what every single cell is doing in there and how they're talking to each other, right? And understanding that network of communication and how it changes with aging or with fibrosis or things like that. And that's giving us the foundation to then, you know, start playing and tweaking with it.

And, and you know, I mentioned the heterogeneity, then we need to personalize that. Because we all have different, um, weaknesses or aging, right? So are you gonna age more in your liver or your hearts or you know, your pancreas, right? So figuring out that personalized aging, um, and, and using that base of information, uh, really starting to understand what every cell in the body is doing, um, and understanding that it's not always just one thing you have to hit.

You have to do a combination therapy to, to be able to regulate all the pieces of the tissue, the matrix, the vascularity, the immune component, and of course, whatever function that tissue has.

So artificial intelligence, um, how much of that is being used right now? Are we still, are, are we actually

definitely a lot.

So, so all the methods that, um, I mentioned you really understand what each cell is doing and how it's regulating, um, how the cell's regulating itself and how it's talking to other people, uh, other cells in the tissue. Um, and that network, we're definitely using, um, artificial intelligence to help us do that.

Fantastic. Thanks so much for being on the show today. Um, uh, it's been, uh, it's been a pleasure and we learned a lot. And, uh, where can we learn a little bit more if, you know, people are just interested in tissue engineering and regenerative medicine, this kind of stuff. Like what, what, what would you suggest the resources for them?

Oh, well, I would say, um, you know, it's now really very accessible, the researchers in the field, so you can. See open source publications. All our publications are open source now. Um, and, and a lot of the information is out on the web and always feel free to contact us. We're usually pretty happy to talk to people about, uh, what we're doing and, and the science that's moving forward.

So. Thank you for having me.

Yeah, thank

you.

Thanks for listening. A quick reminder that while I am in fact a surgeon, nothing I say should be construed as medical advice. Now, make sure to include your physician in any medical decisions you make, and also, if you're enjoying the show, please make sure to show your support with the like, share, or scribe.