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Injury to heart tissue results in non-functional scar tissue that compromises cardiac function. A new approach combines targeted lipid nanoparicles and mRNAs to reprogram immune cells to seek and destroy the pathogenic fibroblasts that limit heart function. Results from mice are promising, and indicate that these approaches may have significant value in treating a suite of human disorders.
Talking Biotech is a weekly podcast that uncovers the stories, ideas and research of people at the frontier of biology and engineering.
Each episode explores how science and technology will transform agriculture, protect the environment, and feed 10 billion people by 2050.
Interviews are led by Dr. Kevin Folta, a professor of molecular biology and genomics.
353 CAR-T Therapies to Reverse Cardiac Fibrosis
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Kevin Folta: [00:00:00] Hi everybody. And welcome to this. Week's talking biotech podcast by collabora. Now, if you are a cellular and molecular biology geek like me, you're going to love today's podcast. So animal organ cells, they, they all have special needs for rigidity and structure. And there's a cell type called a fiberblast that has an important role in many of these processes.
So think about something like wound healing or scar formation. The fiberblast contains this intracellular cocktail of molecules like collagens and, and proteoglycans fiber and other matrix proteins that are the basis for for its function as a fiberblast and for repairing tissue. But this is a Razor's edge because you can imagine a fibroblast can become pathogenic and ultimately problematic in many different contexts.
There's injury to organs that leads to changes in cells that transform them from normal functioning cells to cells that can't perform their normal function, or maybe [00:01:00] do so at a much diminished capacity. And, and we frequently think of this as scar. So you know, in, in the liver and the heart and other cases, this tissue doesn't work the same way.
If you take away a heart cell's ability to contract, normally you affect the heart and, and scar tissue occurs after injury, like things like heart attack or chronic blood pressure, and that scar tissue can exacerbate patient decline from other conditions such as congestive heart failure. So what if there was a clever merging of new technologies, including the ones used in COVID 19 vaccines that could correct damaged heart tissue.
So today we're going to talk to Joe Rorick. He's a PhD candidate at Penn medicine at the university of Pennsylvania, and we're going to cover the technology that is covered in his most recent science paper. So welcome to the podcast, Joe.
Joel Rurik: Great. Thank you so much for having me. I'm excited to be here.
Kevin Folta: [00:02:00] Yeah, it's really cool. I'm glad to have you on. I always like having PhD candidates. So when you say D candidate, it means you've been through your you know, the, the grilling parts of the program and your classes are done. You're wrapping up research. And how far along are you in the program?
Exactly.
Joel Rurik: So I have finished the didactic portions of my training and I'm onto full-time research. I have been here for four years now and I'm looking forward to trying to defend my thesis in about a year.
Kevin Folta: That's pretty cool. So what's next after you're done with this?
Joel Rurik: So my plan right now is to pursue postdoc in academics.
This is on on the way towards applying for faculty positions to be a full-time scientist.
Kevin Folta: Yeah, that's cool. And, and the best part is, is that I bet that this project in which we'll get to in a second, I bet that this concept that you were working on didn't exist when you started the program.
Joel Rurik: Exactly.
I think, you know, and we'll start talking about it shortly. It's [00:03:00] really exciting cuz sitting here at Penn, it's a little unique and we get to pull experts in from multiple different domains and kind of compile them into really exciting new technologies.
Kevin Folta: Oh, yeah. So you're a Pence. Are you down the hall from Weisman?
I am. Yeah.
Joel Rurik: So we actually have several years of collaboration with drew and he's a fantastic scientist and, and collaborator. Well, that
Kevin Folta: explains a lot because, and I didn't put two and two together with that until you mentioned that. So that's pretty cool. Right. So let's start at the beginning. What is fibrosis and what are some of the major causes and the problems that it contributes to.
Joel Rurik: So fibrosis on the, as a high level overview is, is fairly simple. This is the extracellular matrix or what I think of as the structural scaffolding of the heart. So the heart is comprised of many different things. The cardiomyocytes or the muscle cells of the heart that do the actual contracting.
They need to pull against something and they [00:04:00] need to sit in some form of structure. And so the extracellular matrix. Is a very normal, healthy part of the heart that these heart muscle cells sit in and pull against. But in the settings of disease, there's a real shift from a healthy dynamic pliable, extracellular matrix towards way too much.
What we call fibrosis is a real. Over abundance or accumulation and a stiffening of the matrix. And it can have a lot of downstream effects. You mentioned stiffening in the heart, making it harder to contract, but it also can interrupt the metabolics, the inflammation baseline inflammation of the heart and, and other you know, non structural type interactions with the other cells in the heart that usually are negative in the long term, in the chronic.
Kevin Folta: And fibrosis is in other organs as well. So maybe in the liver. Yeah. So in the liver it's normally fi fibrosis is cirrhosis, right? Where your [00:05:00] actually cells are becoming less functional metabolically.
Joel Rurik: Yep. And in the lung, the same thing, you know, the gas exchange doesn't happen as, as easily and as frequently kidney, the Cerus and other structures can't filter blood appropriately.
It's a very common. Pathology across many organs and many diseases.
Kevin Folta: Yeah. I was really surprised by that from your paper and from the analysis of your paper, I think it affects something like 40% of well you tell me, but what exa how prevalent is this problem and does it just kind of exacerbate other conditions or does it really, is it really primarily primary causal to many different health conditions?
Well,
Joel Rurik: it's an interesting question because it's actually a bit hard to disentangle the fibrosis from its effects versus is it accumulating as downstream of other disease you know, portions of diseases. So it's a bit [00:06:00] complicated in that regard, but we think of it as both positive in terms of pathology and also.
Resulting from other disease processes. It certainly doesn't help.
Kevin Folta: Yeah. Yeah. My grandfather had a viral infection of the heart mm-hmm and led the significant scarring that gave him really diminished function and ultimately had to have a heart transplant.
Joel Rurik: Yeah. Yeah. That's exactly what we're looking to to ameliorate and to fix.
Kevin Folta: So when we talk about this, this whole area of fibrosis, as it occurs in different organs, what are the current therapies for treating.
Joel Rurik: Sure. So there's, there's a number of different inhibitors. These are small molecules. Sometimes there's been a few antibodies blocking antibodies proposed that help to stop the process from.
Getting out of control. These tend to work quite well. In preclinical trials, in clinical trials, they're better than nothing. But we think [00:07:00] that, you know, it, it's trying to put the breaks on a process. That's pretty powerful. And once fibrosis is established, there's nothing on the market or even in early clinical trials to help reverse the fibrosis.
Once it's established.
Kevin Folta: Yeah. So that was really my next question. So this is a one way street, right?
Joel Rurik: Exactly. That's how we think of it right now.
Kevin Folta: Yeah. So the therapies that you've proposed are really cool. They, they or you've proposed, you've actually performed That integrate a number of different approaches that we'll talk about in a moment, but let's start, let's talk about car T-cell and this is something we've covered on the podcast many times in different context, but what is a car T-cell and where we seen them successfully implemented?
Joel Rurik: Right. So car TCE, this, this name, car stands for chimeric antigen receptor T cells. So the chimeric part refers to a very engineered protein. So in the laboratory, we can [00:08:00] design these targeting receptors that essentially tell this T-cell, which is a normal part of our adaptive immunity that seeks out and kills very specifically its target cell.
And so we engineer these cars to, to seek out and find only one cell very specifically across the whole body. In in the clinic, the car Ts are mainly approved for use in lymphomas and leukemias. So these are blood cancers. They work extremely well for people that have failed first line therapeutics like chemotherapy and radiation, and they are very good at durable remission in these patients, especially the pediatric popul.
Kevin Folta: Yeah, they're really important in the pediatric populations, because they don't induce certain other secondary problems that pediatric treatment sometimes can cause. Right. And one of the interesting things about [00:09:00] car T-cell, so just to kind of summarize for the audience, it's kind of a way of genetically engineering, a cell to produce a surface.
Molecule that it makes it like a guided missile. It knows exactly where it's going. And, and well, I shouldn't say that it knows the cell type it needs to interact with, because it has a specific handshake with that cell type. It now guides this, this T-cell this normal part of the immune system to that specific cell type.
And it, it, it has been, as you mentioned, has been used in. In blood cancers pocito therapeutics. We did, I don't know the number off the top of my head, but they've been using the same type of approach to deliver specific compounds to prostate cancer cells, for instance, that's one of the episodes in our series.
Yeah. Mm-hmm
Joel Rurik: so, yeah, exactly. And, and I think what's really exciting is there's. Hundreds of new cars in the pipeline of development, and it's going to really expand in terms of scope and what we're able to treat. [00:10:00]
Kevin Folta: Yeah. It's pretty exciting stuff. So your team did this in a little bit different way, and we'll talk about that on the other side of the break where you're really merging.
Some of the newest technologies to make a potent way to address the problem of fibrosis. So we're speaking with Joe Rorick, he's a PhD candidate at Penn medicine at the university of Pennsylvania. This is collaborative talking biotech podcast, and we'll be back with you in just a moment. And now we're back on collaborative talking biotech podcast, and you should check out collaborative suite of tools that can make your laboratory more efficient and help curate the data that's present in your laboratory.
So let's talk about a question that I left out. So. We talk about normal functioning, somatic cells or fibroblast that are there because they're important structural parts of cells or of tissues. What makes a fibroblast that's normal [00:11:00] different from one that's problematic,
Joel Rurik: right? So this is really central to what we're doing.
There are many different types of cells in the heart, aside from the cardiomyocytes. And we're using the heart as a typical organ in a way that we think this biology extends to other major organs in the disease settings, that's relevant to them, but essentially a fibroblast is responsible for this extracellular matrix.
And in normal, healthy states, it's very dynamic and it's constantly making and maintaining this extracellular matrix of which the other functional cells of the organ are, are embedded in and, and rely on. And so in the setting of disease and for us, we use a high blood pressure model. So this mimics a type of chronic heart disease, like heart failure.
These cells, which start as, as kind of a loosely similar cell type [00:12:00] in terms of fibroblast, they then. Become probably four or five different cell states or different flavors of fibroblasts. And only a very few of them in terms of number are very pathogenic. And they're the ones that are ultimately responsible for the fibrosis or this excess accumulation of extracellular matrix.
Kevin Folta: And what's happening at the, you know, biochemical, molecular level to make them a fibroblast. What are they accumulating or how are they coordinating structure to make themselves this kind of fibroblast that's or, or fibroblast that's associated with the scar tissue?
Joel Rurik: Right. So we call these activated fibroblasts and they have been studied in quite great depth over the last several decades.
And there's a, there's an intermingling of different cell stimuli coming from multiple different places. So one is. Biomechanical strain or stress. So excess stress on the heart. One, [00:13:00] another source of signal is ischemia and reactive species from dying cardiomyocytes after myocardial infarction TGF beta and interleukin 11 are known potent players in the activation of fibroblasts and other immune components.
You mentioned earlier that there was a viral infection caus. The, you know, heart damage, that's a known pathway to activate these fibroblasts form fibrosis.
Kevin Folta: No, very good. Yeah. It's important to have a idea of the, the, the organic basis of this. Exactly. So now let's go to car T cells in a normal.
Car T-cell environment, which sounds funny to say that because it's such new stuff, but you, you take a cell type out of a, a patient and you engineer that cell to have this surface antigen that targets like locking key to a specific cell type and then put those back in. That's normally how it's done, or they've had other ones that have been stripped of surface [00:14:00] antigens to be a kind of a generic cell type that has more AP.
Anyway, the bottom line is, is. The problem. And the, one of the drawbacks to car T-cell therapies is that you need to start the first step by this removal of cells from the body. And then, and then identifying the cell types you want and then modifying them and then putting 'em back in. So adds tremendous expense and hassle to the, to the process.
And please correct me if I'm wrong on this. I don't do this every day. No, that's,
Joel Rurik: that's absolutely correct. Yeah, it's, it's a very expensive and. Tailored process. So every patient that receives car T therapy, their own T cells get modified. This is as it currently stands there is a vast amount of work being done to broaden this process and streamline it, make it more efficient and cost effective.
But what we have done is, is kind of side. All of that manufacturing process.
Kevin Folta: and the, well, how did you do it?
Joel Rurik: So we teamed up with drew Weisman. Who's a RNA expert [00:15:00] in in developing therapeutic RNA for both vaccines and for other indications. So we have essentially taken what is a, the COVID 19.
Which is mRNA encoding for us, our custom car, and then that's encapsulated in a lipid nano particle. That is exactly what we, what I have received is the COVID 19 vaccine we know is, is very manufacturable and doable. The step that we have added is a targeting antibody on the exterior shell of the lip nanoparticle.
And this is what tells T cells to take up and express the RNA for the
Kevin Folta: car. Yeah. So, so just to kind of recap, this, you're using the same technology that was used in the COVID. Vaccine and, and drew Weisman just for what it's worth. He was with cattle in Carrico many years ago, like 2000 [00:16:00] in, throughout the nineties and then two thousands early, two thousands worked on developing.
The coding of mRNA so that it would not cause collateral effects and that would be serve as an effective template to create antigens in vivo. So in your muscle cells, you create the COVID vaccine antigen the spike protein antigen. Now you can use that same technology. And in this case, they're taking that they're creating.
They're giving the information in that lipid nanoparticle to change the, T-cell but then putting a coating on the outside an antibody that directs it to the T-cell. So this way that, that mRNA message that's going to be translated into a protein. That's going to give the cell new function. Is going to the T-cell specifically.
so, so exactly. Did I, so I recap that correctly. Yeah. Yeah. That's
Joel Rurik: exactly right. I frankly, am quite amazed that this actually works
Kevin Folta: well, this is like the [00:17:00] weirdest ven diagram of really cool technologies, right. Where, you know, right at that little intersection. And that's why, and I wanna be so clear about this because the listener needs to be conversant with what this is, because this is so cool.
And well, we'll talk about this maybe more at the end. So. You're using a lipid nanoparticle to target an mRNA to a T-cell and correct. Now, all of a sudden this T-cell can specifically go to cardiac fibroblasts. And how, how does, how does it know, what does that mRNA Inco?
Joel Rurik: Right. So the mRNA and codes, our custom car, this is the receptor on the surface of the T-cell that now targets the T-cell into the heart and into these.
Spaces of injury, where the fibroblasts have activated they're now expressing a different suite of proteins than the homeostatic or normal fibroblasts. So we are now selectively [00:18:00] killing with these car. T-cell. Only the pathogenic fibroblasts in the heart after injury. It has no effect if the heart is not injured and there's no real that we know of yet a downstream effect outside of the injured heart.
Kevin Folta: Yeah, so that, but so it only removes these these pathogenic fiberglass are the things that we would colloquially refer to as scar tissue.
Joel Rurik: Exactly. Yeah. And, and we're, at this point, we're a little unclear exactly how the mechanism works, because what we're doing is we're killing these problematic cells.
And then this is allowing through some mechanisms the remodeling of the extracellular space likely. The rest of the homeostatic fibroblasts as well as other infiltrating immune cells, such as macrophages, which are really good at cleaning up environments and returning them back to their healthier state.
Kevin Folta: And I should emphasize that this, all this [00:19:00] work was done in mouse in these first trials, but what were the results?
Joel Rurik: Correct? So, you know, the first thing we had to show is that we could actually engineer these T cells. Because T cells don't really like to express any form of foreign genetic material or RNA.
And so first we demonstrated that what we can do is we could take these LMP or lipid nanoparticles that contain the RNA. We can directly inject them into mice. And that will form for a brief, you know, a couple of days, maybe three days a targeted T-cell against activated fibroblast. And so what we then moved on to, after showing that they have the capability of expressing the car in T cells in the mouth, then we moved on to a injury model.
So this model is essentially a high blood pressure chronic model that induces [00:20:00] scar formation in the heart, just like we see in humans. Over time, then we administer just a single dose of these LMP. They'll make a transient wave of T cells that are targeting and eliminating the activated fibroblasts.
Again, about three days, then those T cells will return to normal. The extracellular matrix will get remodeled within the hearts, and then we demonst. Via histology. So looking at the actual tissue itself, that the fibrosis has been resolved. And more importantly, we look via echocardiography, which is an ultrasound picture of the heart.
This is over time. So we get a movie of the heart and it can watch how it contracts, how freely it can move and relax. And we show that one dose of these lipid nano particles is sufficient to restore. The mouse heart back to its baseline or, [00:21:00] or normal wild type uninjured controls. And so we see both in systolic, which is the pumping, you know, the forceful contraction of the heart, as well as diastolic or the relaxation of the heart.
Both parameters have returned essentially to normal, which is incredibly exciting.
Kevin Folta: Yeah, this is really cool because in the introduction I talked about scar tissue in the heart as still serving some sort of structural C component, although right. Not pumping. And what you're telling me is that you can remove these if you and if you remove them molecularly, then you can have other types of events that cause remodeling of the cardiac tissue to restore full function.
That
Joel Rurik: is exactly what we have seen so far. Which is really crazy. I mean, it's, it's somehow specific for only the, a acute excess accumulation of fibrosis. And what we've done is by [00:22:00] eliminating these. These most pathogenic of cells of fibroblasts. It really allows the homeostatic mechanisms, this kind of balance of production and remodeling of extracellular matrix to regain the PRI you know, priority in the heart.
And so we're not eliminating all fi you know, all extracellular matrix. We're really just almost surgically taking out the extra and leaving the normal.
Kevin Folta: Yeah. Like it knows what has to be there. Right?
Joel Rurik: Yeah. , it's, it's
Kevin Folta: quite amazing. Yeah. It's pretty cool. You know, in, in the series, I hate keep going back to the series, but we've done this for seven years now.
And so there's a lot of different examples of this, like Michael Levin, who I talked with from Tufts, a lot of examples of this, about how, how cells know where they are. Right. And, and how organs and tissues. Kind of know their neighbor and, and have the ability to regenerate and correct problems that they sense.
So this fits right in there. So what about cases where there's a lot of sta scarring? Where, [00:23:00] how, how does that impair a car TCEs ability to even get to the places it needs to work?
Joel Rurik: Right. So we know that. Larger, you know, bulky scars are still ized, so they still have fibroblasts in them. And we, we are not quite certain how the therapy will respond.
There may be a scenario where a, a certain scar is, is quote too far gone or too established to be. You know, functionally resolved. But we're not entirely sure yet that's something we are actively working on with different models, as well as large animal models. This is in preparation towards heading towards early clinical trials.
You know, where our predominant goal is addressing exactly this question, you know you know, the first and foremost is, is the, is the. And then the second question is, is it effective for more chronic type, you know, really dense scars?[00:24:00] What's really exciting about the technology that we propose is that we can dose it as many times as we need.
You know, I have received three vaccinations so far with mRNA and we'll get more in the future likely. And, and so, you know, I don't have any ill effects from that. So there's not much in terms of formulation that we. Inhibits repeat dosing as needed. And maybe we can start to remodel these big dense scars from the outside in.
Yeah.
Kevin Folta: And then T cells are terminally differentiated. So they have a finite life. They, they, they, once they're once they've been transformed with this and become the car T sells themselves, they have a finite halflife.
Joel Rurik: Because we use mRNA. We only get a very transient wave of expression of the car.
And after about three days or even two days, these T cells will return to normal. And then, like you just mentioned, these T cells have a finite lifespan. [00:25:00] And so we're not continually targeting fibrosis forever.
Kevin Folta: Yeah, but the nice part is, is you get, as you mentioned, you go get another dose. If there's still impairment of function that can be ascribed to fibroblast or pathogenic fibroblast.
That's really cool. So are there groups that are taking parallel tracks? A friend of mine wants to know if they're working on livers.
Joel Rurik: Absolutely. So that is something that we are working on with collaborators right now. And we're very excited, but it's a little bit early to tell.
Kevin Folta: Yeah. Well, what are the next steps for the cardiac project?
Joel Rurik: So in terms of cardiac, we really want to show safety profile. We have done this in the mouse, but as you well know, and the audience knows very well, the mouse is not a human. And so we need to demonstrate that this therapy is safe for humans. So the next steps for us are are, are translating this to large animal models and then eventually to early proof of concept in clinical trials.
And, and we'll hope that. You know, we think that the FQ efficacy will [00:26:00] also follow.
Kevin Folta: So, if you had to take a crystal ball guess here, how far are, are we from the first human clinical trials?
Joel Rurik: Well, we're hoping for about three to five years to start the first trials. There's some, some engineering that needs to happen.
And then there's some, some large animal studies that need to happen. Both of which are currently underway both in our lab and also with our collaborators. And what's been really exciting for me is a. You know, more on the academic side of life than on the, the therapy development side. Although it's really fascinating is, you know, we're really trying to understand some biology and one of the cool you.
Side effects, if you will, is that we can use this as a tool to start understanding what fibrosis really means in the disease context. And if you take out the fibrosis, is there other pathology that's still there that's latent that will need to be addressed with other types of, of therapies that are either co-administered or taken at [00:27:00] the same time.
Kevin Folta: Yeah. Yeah. That's a really good point, but you know, something's gonna get you right. yeah. , there's always, so, you know, you take away one problem and another one emerges, but the, but exactly the beauty of this, though, for me in, in thinking about this is that in the past, when I've talked about car T-cell therapy, which I've just been so excited about as it's been as proposed for use on aggressive cancers, like glioblastoma and other types of things, right.
That is that I imagined a day and I actually had a discussion with the GE the guests that we may come a day where you go to a car T-cell therapy clinic. That's almost like a Jiffy lube where you pull in, they pull your cells out, engineer 'em and put 'em back in and it's 75 bucks and go home and be well where, because it's, it's such.
I don't wanna say simple in a bad way, but it's such a straightforward therapy and such a straightforward approach that if we could get some parts of it to be a little more generic, and that's what you've accomplished with lipid nanoparticle, [00:28:00] mRNA, just like we, you know, pulled into a tent in Jacksonville to get my COVID shot.
I could, I could probably get this at a CVS. If I had a prescription from my physician that said, you've got some evidence of scar tissue you know, you're showing some evidence of, of diminished heart capacity or cirrhosis or whatever, you know, go in and get this shot. And so it modularizes treatment for really severe disease that currently doesn't have a treatment.
I, I just love
Joel Rurik: that. Absolutely. I'm, I'm really excited about that aspect. And, you know, I think it really democratizes car T therapy as you probably well know, you know, the. Recipients are very fortunate and they have to have a lot of resources behind them to actually get this therapy. And it's not really accessible, especially outside of you know westernized, you know, developed countries.
And so what's really exciting is, is we can mass mass manufacture this therapy and we can preserve it and [00:29:00] dose it anywhere in the world. Hopeful.
Kevin Folta: yeah, just like the COVID vaccine. You can take us to places where people normally don't have the access. To medical care and it, it also, but it, it, it, it really lowers the price point.
And, but this is, what's so exciting to me is that when we talk about cancer therapies or in this case, heart, or, you know, other types of treatments for fibrosis, there's so many people that are affected by this for something. So something like 40% in one of the reviews. Exactly. And, and, and, and if we could get this.
Through. And, and, and I think what my, my way I always like to conclude is for those of you who have family members who are suffering from these issues, there's hope on the horizon. So you, so, and the reason that's so exciting is because it means, you know, tell them about this, share this story, tell them about this technology, because this is something that can affect them if they can make it that far.
So so, yeah. Yeah, absolutely. [00:30:00] I know a lot of sick people who just gave. And I think knowing that there is a treatment on the horizon, if you can get there maybe is something that just the hope alone can help them surf through a couple of years and maybe be able to receive it. So that, that's why this is so cool.
So congratulations, Joel. Really nice stuff.
Joel Rurik: Thank you so much. I appreciate it. And, and just like you said, I'm very hopeful.
Kevin Folta: I am too. And the best part is, is, you know, like we started with is, I've said, I bet that at the beginning of your project, you didn't know you would be doing this. You, you have absolutely no idea what you will ultimately do in a faculty position.
Exactly.
Joel Rurik: Yeah. I think it's, it's equal parts, terrifying and exciting.
Kevin Folta: Yeah, but that's good. I tell all my students, I'm like, you guys are alive at the best time to do this. And I wish I was at the beginning of my career because this is where like the innovators are gonna grab it and the people who can do what, what was done in, in your laboratory.
You know you're combining the best of the new technologies to create [00:31:00] new solutions. And, and maybe you should give a little shout out to the lab and your PI and some of the folks who participated in the project.
Joel Rurik: Yeah, absolutely. You know, this type of thing does not happen alone. There's big teams that are involved and, and, you know, as, as the saying goes, we stand on the shoulder of giants.
You know, I'm happy to talk about this work, but there were many people involved. My mentor, Jonathan Epstein. Who's a professor here at. Drew Weisman, who, as you, we talked about earlier is a RNA expert. You know, both of our laboratories were critical ha agen who was key to starting this whole concept.
And Hamid par is who's works as a group leader in Drew's lab and is their own faculty position now who's, who's really working on exciting things in terms of, you know, we demonstrate RNA deliver. To T cells for the, you know, the therapy of fibrosis, but that's not the only TCE that, or that's not the only cell in the body [00:32:00] that can take up LMPs and that's not the only RNA that can be expressed.
And so I think you can let your imagination run wild in terms of, of which cells we want to address and what we want to do in those cells. And I think there's, we're, we're really standing at the top of a watershed looking down at just what seems like an almost infinite number of possibilities that.
Really exciting.
Kevin Folta: Extremely well put, I won't try to, I won't try to put any additional shine on that. So if people wanna learn more about this where they, where can they follow you on social media and maybe the Epstein lab?
Joel Rurik: Absolutely. So my Twitter handle is probably the best way to keep track of me.
It's at dev bio academic, and then also our laboratory is John Epstein lab.
Kevin Folta: Yeah, very good. So follow those on Twitter, and I'll also include those in the show notes. So Joel Rorick thank you so much for contacting me and after your Dr. Joel Rorick, if you want to get back in touch with me about your next big [00:33:00] breakthroughs gimme a holler and we'll talk about 'em again.
Thank you very much for a great episode.
Joel Rurik: Fantastic. Thank you so much for having me and for
Kevin Folta: the listeners. Again, thank you for listening to the talking biotech podcast. This is the kind of technology that combines the best of the best. What are we doing with this lipid nanoparticle delivery of mRNA to specific cell types to give them new programming, to solve problems?
I mean, this is amazing stuff, and I hope you share this podcast episode and the information within. With the people you care about, because this is the kind of thing that gives us hope and helps us correct the misinformation. That's out there about what these technologies really are, because the thing that will stand between their innovation and their deployment is the false information that will be given by the folks out there who, for some reason, find these kinds of technologies in genetic engineering.
Unaccept. So share this kind of information. Thank you for listening. This is the talking biotech podcast by collab. And we'll talk [00:34:00] to you again next week.