Aug 20, 2020
This month on Episode 15 of the Discover CircRes podcast, host Cindy St. Hilaire highlights three featured articles from the July 31 and August 14 issues of Circulation Research. This episode features an in-depth conversation with Drs Venu Venna and Juneyoung Lee from the Department of Neurology at the McGovern Medical School at the University of Texas Health Science Center at Houston regarding their study Gut Microbiota-Derived Short-Chain Fatty Acids Promote Post-Stroke Recovery in Aged Mice. This episode also includes a brief discussion with BCVS Outstanding Early Career Investigator Award competition finalists, Drs Shyam Bansal from Ohio State University, Emmanouil Tampakakis from Johns Hopkins University, and Yang Zhou from the University of Alabama, Birmingham.
Article highlights:
Veys, et al. GLUT1 in Angiogenesis and BBB Integrity
Zhang, et al. Self-Renewal of Local Macrophages Attenuates DiCM
Lerchenmüller, et al. CITED4 in Cardiac Remodeling
Dr Cindy St. Hilaire: Hi. Welcome to Discover CircRes, the podcast of the American Heart Association's journal, Circulation Research. I'm your host, Dr Cindy St. Hilaire from the Vascular Medicine Institute at the University of Pittsburgh.
Today I'm going to share with you three articles selected from the late July and early August issues of Circulation Research. I'm also excited to share with you my discussions with Drs Venugopal Venna and Juneyoung Lee, who are from the group of Louise McCullough at the University of Texas Health Science Center, regarding their study Gut Microbiota-Derived Short-Chain Fatty Acids Promote Post-Stroke Recovery in Aged Mice.
I also speak with the finalists of the BCVS Outstanding Early Career Investigator Award, Shyam Bansal from Ohio State University, Emmanouil Tampakakis from Johns Hopkins University, and Yang Zhou from the University of Alabama, Birmingham.
So first the highlights. The first article I'm sharing with you is titled Role of the GLUT1 Glucose Transporter in Postnatal CNS Angiogenesis and Blood-Brain Barrier Integrity. The first author is Koen Veys and the corresponding author is Katrin De Bock from ETH Zurich.
The primary energy source for the brain is glucose and the blood vessel endothelial cells which from the blood-brain barrier supplied glucose to the brain via the glucose transporter protein GLUT1. Patients with genetic mutations in GLUT1 have neurological problems, including seizures, movement disorders, and delayed neurological development. Low GLUT1 levels in the blood-brain barrier have also been linked to Alzheimer's disease in humans and have been known to exacerbate the disease in a mouse model.
In this study, the group examined the role of GLUT1 in blood-brain barrier endothelial cells in more detail. They found that while structural integrity of the blood-brain barrier remained intact, inhibiting the activity of GLUT1 in newborn mice impaired aspects of normal blood vessel growth in the brain, and inhibiting GLUT1 in adult mice led to progressive neuron loss, behavioral abnormalities, reduced movement, seizures, and signs of inflammation.
The results highlight GLUT1's importance in the brain endothelial cells, and the role of GLUT1 in glucose utilization in overall brain function.
The second article I want to share with you is titled Self-Maintenance of Cardiac Resident Reparative Macrophages Attenuates Doxorubicin-induced Cardiomyopathy Through the SR-A1-c-Myc Axis. The first authors are Hanwen Zhang, Andi Xu, Xuan Sun, and the corresponding author is Qi Chen and the work was completed at Nanjing Medical University in China.
Doxorubicin and it's analogues are commonly used chemotherapeutic agents. However, the use of these drugs is limited by dose-dependent cardiotoxicity. Doxorubicin-induced cardiomyopathy presents with dilated and poorly functioning left ventricle in the absence of abnormal loading conditions. This may induce cardiac systolic dysfunction.
Accumulating clinical evidence suggests that inflammation contributes to doxorubicin-induced cardiomyopathy pathogenesis. Several studies suggest that the inhibition of cardiac inflammation can improve cardiac function; however, the underlying mechanisms remain unclear.
This group wanted to explore the role of cardiac resident macrophages during doxorubicin-induced cardiomyopathy progression. They found that cardiac resident macrophages were vulnerable to doxorubicin insult but that monocyte-derived macrophages survived. Further, these surviving monocyte-derived macrophages exhibited a proinflammatory phenotype which contributed to impaired cardiac function.
Scavenger receptors are expressed on macrophages and help to modulate their inflammatory response. Global, or myeloid-specific deletion of class A1 scavenger receptor, also called SR-A1, inhibited proliferation of resident reparative macrophages and this inhibition exacerbated cardiomyopathy.
At the mechanistic level, this group identified that the transcription factor c-Myc mediated the effect of SR-A1 in reparative macrophage proliferation in doxorubicin-induced cardiomyopathy.
The last article I want to share with you before we switch to our interviews is titled CITED4 Protects Against Adverse Remodeling in Response to Physiological and Pathological Stress. The first author is Carolin Lerchenmüller and the corresponding author is Anthony Rosenzweig, and they're from Massachusetts General Hospital.
Exercise is good for the heart. It increases cardiac mass which is called physiological hypertrophy, which appears to induce cardiac benefits. However, pathological stimuli, such as hypertension and aortic stenosis, can lead to pathological hypertrophy which is associated with adverse outcomes and can lead to heart failure. Cardiac CITED4 is a protein that is induced by exercise and is sufficient to cause physiological hypertrophy and mitigate adverse ventricular remodeling after ischemic injury. However, the role of endogenous CITED4 in response to physiological or pathological stress is unknown. To understand the role of endogenous cardiomyocyte CITED4, this groups generated cardiomyocyte specific knockouts of CITED4.
These mice were analyzed at baseline. They were subjected to a swimming protocol which provided physiological stimuli or they underwent transverse aortic constriction, also called TAC, which causes pressure overload and served as the pathological stimulus for heart remodeling.
CITED4 knockout mice developed modest cardiac dysfunction and dilation in response to exercise. After TAC, these knockouts developed severe heart failure with left ventricular dilation and impaired cardiomyocyte growth.
The study goes on to show that CITED4 protects against pathological cardiac remodeling by regulating mTOR activity and also a network of microRNAs which control cardiomyocyte to fibroblast crosstalk.
So for our interview of this episode, I have with me Drs Venugopal Venna and Juneyoung Lee from the Department of Neurology at the McGovern Medical School at the University of Texas Health Science Center at Houston.
Today we're going to be discussing their manuscript titled Gut Microbiota-Derived Short-Chain Fatty Acids Promote Post-Stroke Recovery in Aged Mice. Thank you both very much for joining me today.
Dr Venu Venna: Thank you Cindy for having us. It's a pleasure.
Dr Juneyoung Lee: Yeah, thank you for the opportunity.
Dr Cindy St. Hilaire: It's a wonderful paper. Actually I really enjoyed the nice graphical abstract, that really made a good visual of what this papers about, so I encourage everyone to go take a peek at that. Could you introduce yourselves and tell us a little bit about your lab group?
Dr Venu Venna: Yeah, sure, I'm Venu Venna, it's my third year at McGovern Medical School UT Health, and we are a part of a large research group in the Department of Neurology here. This is headed by Dr Louise McCullough. She's also a co-corresponding author on this paper.
Unfortunately she's not here today, but it's basically her idea and her initiative that led us to drive this huge project. We are very excited to share with you more details today.
Dr Juneyoung Lee: Hi, my name is Juneyoung Lee. I'm postdoctoral fellow here and I'm working with Dr McCullough and Dr Venna.
Dr Cindy St. Hilaire: So this manuscript is testing the general hypothesis that the gut microbiome can influence stroke recovery but before we dig into the details of your study, can you give us a little bit of background about what the microbiota gut brain axis is?
Dr Venu Venna: That's a great question. Thank you for asking that. So recent advances in 16S sequencing, metagenomics, and metabolic analysis lead us to specifically identify the role of gut microbiota. We have... Everybody consists of large number of microbiota in the gut, so particularly the microbiota's role is largely remains unknown, as of now.
The recent advances helped us to understand whether it's for communication of the microbiome, how it actually influences our health, and how the metabolites that are released by the microbiota can actually influence the brain-gut.
So this is where the concept of microbiota gut-brain axis continues to evolve and we rely on 16S metagenomics, as well as metabolomics to understand if the microbiome itself has a specific role in the stroke recovery and stroke in this paper.
Dr Cindy St. Hilaire: Great, so I know that previous research by you specifically, and also you mentioned your fellow corresponding author, Dr Louise McCullough, your prior work has shown that stroke can cause aberrant changes in the gut regarding things like motility, permeability, activation of gut-immune cells. So this to me suggested that aberrant signaling can come from the brain and affect the gut, but your study is kind of now flipping that.
You want to ask the question is changing the gut microbiome after the stroke also beneficial? So there's kind of a chicken and egg type conundrum going on. Is there a preceding event, is it the stroke that alters the gut microbiome primarily, or is the gut microbiome maybe deficient in different people and therefore their stroke outcomes are different?
Dr Venu Venna: Yeah, I mean this is a very new emerging field and what's very interesting about this is the brain gut microbiota axis, it's a bi-directional axis. In this case, what we think is if we have a stroke, it may actually directly influence the gut.
There is a brain-gut axis. At the same time, the changes in the microbiome can actually trigger an inflammatory state where it can actually contribute to the worst stroke outcomes. It's a chicken and egg relationship as you rightly mentioned, but at the same time what is not known is whether if we can simply manipulate the microbiota, can you actually improve the stroke outcomes or can you improve the age associated outcomes?
Because what we found in previous studies is age itself causes changes in the microbiome.
Dr Cindy St. Hilaire: Interesting, so just being young or old, if you were to compare those microbiomes of old individuals and young individuals, you see differences that are I guess negatively impactful on things like stroke and disease?
Dr Venu Venna: That's exactly right, so the more imaging data coming out from the literature, not just our group, but all other groups, on humans and animal studies, do suggest that age itself is associated with changes in the gut microbiome.
Dr Cindy St. Hilaire: So the overall goal of this specific study was to determine if replacing the gut microbiota of an older mouse with the microbiota from a younger mouse would help in the recovery after an ischemic stroke. Can you talk about the design of that study and the different aspects that you had to consider when designing these experiments?
Dr Venu Venna: Yeah, absolutely. This was a great question. The initial experiments, like what we were trying to do before, was whether we can actually even manipulate the microbiome in an aged animal. In our previous study, what we did is we took a young animal and we transplanted the biome from an aged animal. We used a combination of antibiotics to actually deplete the existing biome and that's what gave us susceptibility to transplant.
Once you transplant the biome into a donor from a host, so the biome can actually sustain for quite a bit of time. This gave us an opportunity to study the direct role of microbiome. Later, what we did was we subjected these animals to the stroke and then what we found is when we induced this stroke in an animal that received aged biome, despite being young, the animal that received aged biome, can itself contribute to the worst stroke outcomes and increased mortality.
In this follow-up study, what we decided to do was can we even manipulate the microbiome after stroke? So this is particularly important because most of the clinical patients don't come into medical attention until after stroke. Transplanting the microbiome or even manipulating the microbiome after stroke can have a broader clinical relevance.
In this particular study we decided to see if we can actually manipulate the microbiome after several days or several hours after the stroke happens. We decided to test if we can wait for three days. This is a particular time where we can actually see the infarcts get mature and all the injury in all groups of animals are same, and then we transplanted the aged animals with the young microbiome.
So this gives us an opportunity to actually study the role of microbiome, independent of infarct. Meaning, all animals have a similar degree of injury, so now whatever the beneficial affects you are seeing because of the microbiome transplant, are potentially due to, not because of the size of the injury, because they have a smaller injury they have better recovery, but it's basically because their infarcts are the same and whatever you're seeing is because of the manipulation of the microbiome.
Dr Cindy St. Hilaire: Interesting. Juneyoung, would you like to tell me a little bit about what you found then? Using these interesting fecal transplant models, what are the key results that you found in this study?
Dr Juneyoung Lee: Great question. As Dr Venna explained, we treated young biome to aged stroke mice, after stroke. We found that young biome contributes to better behavior outcomes and they regulate the immune system in the brain and the gut and increase the short term brain-gut axis in the aged stroke recipient mice.
One interesting finding is that we found dominant T-cells, which are very small number of T-cells in the host, but they secrete proinflammatory cytokines which is IL-17. Cytokines exacerbate new inflammation in the brain so if we treat the young biome, we found that the level of proinflammatory cytokine IL-17 decrease cytokines compared to aged biome.
Dr Cindy St. Hilaire: You also focused on short-chain fatty acids, SCFA producing bacteria. What is it about these short-chain fatty acids that are beneficial and what are the signaling pathways that you found to be activated or things that were present that helped to promote better stroke recovery?
Dr Juneyoung Lee: Short-chain fatty acids are key metabolites produced by bacterial fermentation of dietary fiber in the gut. These are suspected to play an important role in microbiota gut-brain crosstalk. Also, in our previous study we found that young fecal biome has higher levels of short-chain fatty acid compared to aged biome so we think that the short-chain fatty acid has a beneficial role in our mild level stroke.
Dr Cindy St. Hilaire: So are you focusing more on identifying the metabolites or trying to move into humans? What do you think the next step of this vein of research is?
Dr Venu Venna: So what we think is right now, this is a very interesting and fascinating finding, even for us. We're trying to understanding what other metabolites could be involved and what other ways as you previously asked, what other pathways these bacteria itself are triggering or contributing to actually enhance this recovery, that's what we are seeing from the young microbiome.
As a future direction, we are also seeing if this transplant of biome can have a broader therapeutic relevance, meaning is it only specific to the stroke related outcomes or can it be beneficial in large settings of other age relate diseases like what we are seeing, again as I mentioned before like age related diseases such as... Many age related diseases like cognitive dementia, or Parkinson's disease, any neurodegenerative disease.
Dr Cindy St. Hilaire: Well thank you, Drs Venu Venna and Juneyoung Lee for joining me today. I really appreciate it and congratulations again on this wonderful story.
Dr Venu Venna: Thank you very much for having us, Cindy, and for this work I would like to acknowledge the funding agency. This work is funded by NIH and also the American Heart Association, both for my Scientist Development Grant and also as well as for Juneyoung Lee's postdoctoral fellowship. This funding helped us to perform these highly innovative studies in gut microbiome axis.
Dr Cindy St. Hilaire: Wonderful. Yes, well, we love seeing AHA funded research published in AHA journals, so thank you.
Right so now we're going to have our interview with the BCVS Outstanding Early Career Investigator Award competition finalists. I have with me today, Shyam Bansal from Ohio State University, Emmanouil Tampakakis from Johns Hopkins University, and Yang Zhou from the University of Alabama, Birmingham.
So congratulations to all of you for being recognized for your outstanding science. These topics are great. The timing of T-cells activity in chronic heart failure, sympathetic neuron signaling, circadian genes and cardiomyocyte proliferation, and the identification of a transcription factor that helps promote maturation of reprogrammed cardiomyocytes.
So, Dr Bansal, your abstract that's recognized, is titled Novel Inhibitors For Temporal Modulation Of T-lymphocytes During Chronic Heart Failure. Where was this study conducted and where are you now?
Dr Shyam Bansal: Right now I'm at Ohio State University. I joined here in July 2019 and I've been setting up my lab. While doing that, we conducted all this work. This work, most of it is done here, and we have been looking to identify certain inhibitors that can be used for T-cell modulation.
Dr Cindy St. Hilaire: Excellent so why should I care about T-cells in the heart? And what did you all find in this paper?
Dr Shyam Bansal: The right question is why shouldn't you? T-cells are coming out to be involved in almost every chronic disease. We have heard about CAR T-cell therapy. Recently it revolutionized the whole cancer research field. The heart failure and cardiovascular diseases has also been realizing the importance of T-cells. They're important in a way because they are kind of a two-edged blade. They are protective because we need them to initiate those wound healing cascades so the tissue can regain its original function. But then, too much activation of T-cells can be injurious and lead to autoimmune reactions.
In 2017 I published a paper during my postdoc with Dr Sumanth Prabhu at UAB where we showed that these T-cells get activated during chronic heart failure.
It's a double-sided activation to get activated immediately after injury but then they go down and they come back again, during chronic heart failure. That's where the two-edged blade comes into picture. If you alter these T-cells during this acute phase, during the cardiac infarction, the animals always do worse, right? They are protective because they are needed for wound healing pathways.
Dr Cindy St. Hilaire: We can't just stop them at the start, we need to fine tune.
Dr Shyam Bansal: Yes.
Dr Cindy St. Hilaire: So what's this temporal aspect you looked at?
Dr Shyam Bansal: So that's what we found in my postdoc in 2017 paper. If you inhibit these during the chronic phase, in mouse, in rodents, it was whole weeks after infarction, then you can actually stop maladaptive remodeling. You can complete shut it down, it doesn't get better but you at least shut it down completely.
We did those studies by using some antibodies, again CD4+ T-cells, and using genetic mouse models.
Dr Cindy St. Hilaire: So do you think anything that you found can quickly or soon translate to humans?
Dr Shyam Bansal: That's exactly what we did after we came here, right? So we compared what happens during this chronic heart failure, what happens to these T-cells. We identified one molecular pathway that's associated with receptor signaling, being activated in these T-cells. The interesting thing is, these T-cells came from male mice, not from females. Still, they had strong activation of the surge in receptor signaling.
We found a drug molecule that can activate another pathway that inhibits this pathway, so indirectly we're able to inhibit this pathway. We did those studies and found that we can actually stop T-cells from getting activated during chronic heart failure and when we do that, this drug can actually, again, inhibit left ventricular remodeling significantly.
Dr Cindy St. Hilaire: Wow.
Dr Shyam Bansal: And if you give this drug early in myocardial infarction, again, animals died.
Dr Cindy St. Hilaire: It's going to be very important to fine tune when that drug could potentially be administered to humans.
Dr Shyam Bansal: Yes, and that's the first drug in our knowledge that can actually target specific antigen activated T-cells.
Dr Cindy St. Hilaire: Super exciting, well congratulations again. Well done and well earned. Dr Tampakakis, your study is titled Sympathetic Innervation Negatively Regulates Postnatal Cardiomyocyte Proliferation Through Circadian Genes. So where was this conducted and what position are you in now?
Dr Emmanouil Tampakakis: This research was conducted at Johns Hopkins University and I'm currently part of the... I'm Assistant Professor within the Division of Cardiology in the School of Medicine. Pretty much for my curiosity and the fact that we know a lot about the role of neurons for adult heart disease but we really don't know what much about neurons are doing at the neonatal stages in heart development.
We know at least in preterm babies where the innervation is really affected, some of them do develop changes in their heart geometry, and there might be a role there, plus there is some data to suggest that the autonomic nervous system does manipulate or does affect the neonatal heart regeneration.
The role of neurons to me was really intriguing.
Dr Cindy St. Hilaire: So this is linking together sympathetic nervous signaling, circadian genes, and postnatal cardiomyocyte proliferation. Why do I care about all these things fitting together?
Dr Emmanouil Tampakakis: Yes, so apart from the fact that it's fascinating knowing that each individual organ has in their body its own circadian genes that regulate actually, several functions. Without being affected by the central nervous system and what's happening in the hypothalamus, which to me is really fascinating, is we really don't know much about what actually regulates and synchronizes the circadian cycle of the heart.
We, in this study, showing that actually the innervation that happens in neonatal stages, already aaffects how certain genes are circulating within the heart. That appears to be through one of the adrenergic pseudoephedrine way that the sympathetic nerves are secreted.
Again, by affecting this, we are showing that there is more proliferation of neonatal cardiomyocytes which can be important for disease at later time points, and we're also showing that if you mess up two specific circadian genes, Period 1 and Period 2, that are transcription regulators, and are some of the masterminds of this phenomenon, you can actually still affect neonatal cardiomyocyte proliferation which can be important for diseases like heart degeneration and whether we're thinking about manipulating other pathways to induce more regeneration and induce healing in the heart.
The novelty of our work is we see that there's a link between that cell cycle and the circadian genes, at least at neonatal time points when myocytes proliferate a little more.
Dr Cindy St. Hilaire: So neat. Congratulations again, it's a wonderful story and I'm really happy it's being recognized. And Dr Zhou, you're being recognized for your work that's titled TBX20 Activates Cardiac Maturation Gene Programs Promoting Direct Human Cardiac Reprogramming. So where was this study started and where are you now?
Dr Yang Zhou: So I started as an Assistant Professor of Biomedical Engineering at UAB in January 2019. Before I moved to Birmingham, I did my postdoc training at the University of North Carolina at Chapel Hill in Dr Li Qian's lab. I basically studied direct cardiac programming which directly convert non-myocyte cell type to the functional cardiomyocytes.
I did a lot of work and found the epigenetic barriers and I find that the features of these direct programming cells and almost in the mouse cells, but we know that we have to move that to the human cells, so then when I moved to Birmingham and then I studied the cardio programming from the cells.
Dr Cindy St. Hilaire: Excellent, so your study is looking for ways to really kind of push the direct conversion of cardiomyocytes into a more fully differentiated state. Why is that an important question and what did you find in this study?
Dr Yang Zhou: Yeah, it is still challenging to gather a functional beating cardiomyocytes from human fibroblast by the direct reprogramming method. We want to get the functional cardiomyocytes to do the cell therapy. Also this method has promise to do the in situ heart regeneration because we use the transcription factors we can inject these factors to the injured heart then directly convert those cardiac fibroblasts into the cardiomyocytes.
So we have to study, we have to know how to get the functional work that cardiomyocytes.
Dr Cindy St. Hilaire: That is so neat. So really you're hoping to harness those fibroblasts in the heart that everyone kind of ignores because they're not contractile and you're hoping to really take them and transition them to these fully functioning beating cardiomyocytes.
Dr Yang Zhou: Right, so we know that the stuff we are coding are very important for the contractility, the myocyte contractility, so we find that a lot of missing protein expression in the current direct programming cells, so my hypothesis is they might be missing key regulators and can promote expression of those coding in the genes.
My computational analysis of the transcription data, I find that this T-box, transcription factor Tbx20, that can highly promote those unexpressed genes in the reprogrammed human cardiomyocyte.
Dr Cindy St. Hilaire: That's wonderful. Well congratulations again on some excellent work. So I want to ask you all, early career question, you're all within I think the first couple years of starting up your lab, and we're in the midst of a pandemic which means none of us are in the labs. Maybe staff is at reduced numbers, but first, how's it going?
And second is, you're kind of still fresh in terms of transitioning. So I'm wondering if there's any one piece of advice that you'd like to share with maybe someone who's in the middle of transitioning or just about to.
Or if there's something you wish you knew ahead of time that you'd love to tell your pre-faculty self?
Dr Emmanouil Tampakakis: Yeah, I don't know if I can give advice, already I think I'm too junior to do this. I would say that-
Dr Cindy St. Hilaire: What, too traumatized?
Dr Emmanouil Tampakakis: Maybe. Probably, or will be traumatized, but I would say for me at least, the things that kept me sane during this is my son, who's three and a half years old and lives in a complete different world, so that helps me balance what's happening out there.
Dr Cindy St. Hilaire: That's so important.
Dr Emmanouil Tampakakis: Probably some good alcohol at the end of the day but both those two things combined actually helped me maintain my sanity. In terms of advice, I would say to try to enjoy science. Try to stay focused and productive and at the end of the day, enjoy what you do. I think that if you are creative and if you like what you do, find the right people to collaborate and work with and you can hope that you will do well.
Dr Cindy St. Hilaire: I agree. Excellent advice.
Dr Shyam Bansal: I also have two kids, three years and eight years old, so we were at home for two and a half months or so. I think those kids were really helpful in keeping my sanity because the weather was getting better so we had to put in a swing set for them, get some play items and stuff, so they kept me busy. That was good that way.
The advice that I will have for junior investigators is be collaborative. Try to see how you can help others because when you help others, others are ready to help you as well. Remember science is a collaborative field, the more you collaborate with people, the more you get to know many more stuff.
Dr Cindy St. Hilaire: I think that's so important.
Dr Shyam Bansal: I was able to get done a lot of whatever work we presented. I was able to set up my lab, get some work done, and be at a position that I was able to summit my first abstract to BCVS for my independent own work, just because I had good collaborations here. I had good people who helped me stand on my feet and obviously I was working and helping them also.
Dr Cindy St. Hilaire: Yeah, and it also sounds like you have good colleagues so that's another key to it.
Dr Shyam Bansal: Yeah, I'm really lucky that way. Our whole department is really great. We have several senior faculty who are always ready to help us out in whatever issues we have, personal, professional, scientific, they're always here for us.
Dr Cindy St. Hilaire: That's great. Yang, how about you?
Dr Yang Zhou: I think the pandemic is very challenging for our junior faculty and for research and career developments but we have to balance between the work and the family, like kids. You might have an issue because we have two PIs in our lab.
Dr Cindy St. Hilaire: Oh gosh.
Dr Yang Zhou: Yeah, but I learned a lot these two years before this position. I think the most important thing I feel like is you have to talk to people. You always can find people that can help you to find answers. You need a mentor because they are more senior, they have more experience, even in this pandemic, if you find someone to share even just your feelings, that's very helpful.
Dr Cindy St. Hilaire: We're almost lucky that this happened now where we can have platforms like Zoom, and Adobe Connect, where we can have these virtual conferences because at least on all the different committees I'm on, ATVB and BCVS, we can have these discussions and break-out sessions, so I think it's really... We're lucky it's happening now and not 1997 when there's no video.
Dr Yang Zhou: Concerns... We all feel that the University and the Department, they all responded very quickly and they have much more support here than before.
Dr Emmanouil Tampakakis: As a more senior, what advice can you give us as a more senior person?
Dr Cindy St. Hilaire: Oh gosh, more senior? Well thank you. My advice? I definitely agree on the collaboration, I think that's key. Finding sponsors is equally important, someone who's going to go to bat for you. Finding a safety net where you can send someone a half-baked game page and have them tell you just how bad it is and be honest and be willing to give you that kind of critical feedback is really important.
Building your network is key, and getting involved in societies and getting people to know you independently from your former mentor, I think is really critical. Yes, you want to collaborate but you also got to make sure that you have your own path in the sand, to make sure you can move forward independently, and have fun while you're doing it, like you said.
Great, well I wish you all the best of luck. Congratulations again on being recognized and I'll see you on the BCVS webinar.
That's it for our highlights from the late July and early August issues from Circulation Research. Thank you for listening. Please check out the Circulation Research Facebook page and follow us on Twitter and on Instagram with the handle @CircRes and #discoverCircRes.
Thank you to our guests, Drs Venu Venna and Juneyoung Lee, and to the BCVS Outstanding Early Career Investigator Finalists, Shyam Bansal, Emmanouil Tampakakis, and Yang Zhou. This podcast is produced by Rebecca McTavish and Ishara Ratnayake, edited by Melissa Stoner, and supported by the editorial team at Circulation Research. Some of the copy text for the highlighted articles is provided by Ruth Williams. I'm your host, Dr Cindy St. Hilaire and this is Discover CircRes, your on-the-go source for the most exciting discoveries in basic cardiovascular research.