Scientists, engineers and clinicians are working together at Duke University’s Renegeration Next Initiative to learn how human tissue might be repaired and replaced, using the body’s own innate biological mechanisms.
By Ken Kingery
This article first appeared on Duke’s Pratt School of engineering, and is reposted here in its entirety.
Biomedical engineers at Duke University have created a fully functioning artificial human heart muscle large enough to patch over damage typically seen in patients who have suffered a heart attack. The advance takes a major step toward the end goal of repairing dead heart muscle in human patients.
The study appears online in Nature Communications on November 28, 2017.
“Right now, virtually all existing therapies are aimed at reducing the symptoms from the damage that’s already been done to the heart, but no approaches have been able to replace the muscle that’s lost, because once it’s dead, it does not grow back on its own,” said Ilia Shadrin, a biomedical engineering doctoral student at Duke University and first author on the study. “This is a way that we could replace lost muscle with tissue made outside the body.”
Unlike some human organs, the heart cannot regenerate itself after a heart attack. The dead muscle is often replaced by scar tissue that can no longer transmit electrical signals or contract, both of which are necessary for smooth and forceful heartbeats.
The end result is a disease commonly referred to as heart failure that affects over 12 million patients worldwide. New therapies, such as the one being developed by Shadrin and his advisor Nenad Bursac, professor of biomedical engineering at Duke, are needed to prevent heart failure and its lethal complications.
Current clinical trials are testing the tactic of injecting stem cells derived from bone marrow, blood or the heart itself directly into the affected site in an attempt to replenish some of the damaged muscle. While there do seem to be some positive effects from these treatments, their mechanisms are not fully understood. Fewer than one percent of the injected cells survive and remain in the heart, and even fewer become cardiac muscle cells.
Heart patches, on the other hand, could conceivably be implanted over the dead muscle and remain active for a long time, providing more strength for contractions and a smooth path for the heart’s electrical signals to travel through. These patches also secrete enzymes and growth factors that could help recovery of damaged tissue that hasn’t yet died.
For this approach to work, however, a heart patch must be large enough to cover the affected tissue. It must also be just as strong and electrically active as the native heart tissue, or else the discrepancy could cause deadly arrhythmias.
This is the first human heart patch to meet both criteria. “Creating individual cardiac muscle cells is pretty commonplace, but people have been focused on growing miniature tissues for drug development,” said Bursac. “Scaling it up to this size is something that has never been done and it required a lot of engineering ingenuity.”
The cells for the heart patch are grown from human pluripotent stem cells — the cells that can become any type of cell in the body. Bursac and Shadrin have successfully made patches using many different lines of human stem cells, including those derived from embryos and those artificially forced or “induced” into their pluripotent state.
Various types of heart cells can be grown from these stem cells: cardiomyocytes, the cells responsible for muscle contraction; fibroblasts, the cells that provide structural framework for heart tissue; and endothelial and smooth muscle cells, the cells that form blood vessels. The researchers place these cells at specific ratios into a jelly-like substance where they self-organize and grow into functioning tissue.
Finding the right combination of cells, support structures, growth factors, nutrients and culture conditions to grow large, fully functional patches of human heart tissue has taken the team years of work. Every container and procedure had to be sized up and engineered from scratch. And the key that brought it all together was a little bit of rocking and swaying.
“It turns out that rocking the samples to bathe and splash them to improve nutrient delivery is extremely important,” said Shadrin. “We obtained three-to-five times better results with the rocking cultures compared to our static samples.”
The results improved on the researchers’ previous patches, which were one square centimeter and four square centimeters. They successfully scaled up to 16 square centimeters and five to eight cells thick. Tests show that the heart muscle in the patch is fully functional, with electrical, mechanical and structural properties that resemble those of a normal, healthy adult heart.
“This is extremely difficult to do, as the larger the tissue that is grown, the harder it is to maintain the same properties throughout it,” said Bursac. “Equally challenging has been making the tissues mature to adult strength on a fast timescale of five weeks while achieving properties that typically take years of normal human development.”
Bursac and Shadrin have already shown that these cardiac patches survive, become vascularized and maintain their function when implanted onto mouse and rat hearts. For a heart patch to ever actually replace the work of dead cardiac muscle in human patients, however, it would need to be much thicker than the tissue grown in this study. And for patches to be grown that thick, they need to be vascularized so that cells on the interior can receive enough oxygen and nutrients. Even then, researchers would have to figure out how to fully integrate the heart patch with the existing muscle.
“Full integration like that is really important, not just to improve the heart’s mechanical pumping, but to ensure the smooth spread of electrical waves and minimize the risk of arrhythmias,” said Shadrin.
“We are actively working on that, as are others, but for now, we are thrilled to have the ‘size matters’ part figured out,” added Bursac.
The research is part of a seven-year, $8.6 million grant from the National Institutes of Health. With the large heart patches in hand, the Bursac team is collaborating with researchers at the University of Alabama at Birmingham to develop procedures to successfully integrate the patch onto the hearts of pigs. Another affiliated team of researchers at the University of Wisconsin-Madison is working to develop improved stem cells for creating the main cell types that compose these heart patches, in the hopes of minimizing an immune response to the delivery of the engineered tissues.
This research was supported by Foundation Leducq and the National Institutes of Health (R01HL104326, R01HL12652, UG3TR002142, U01HL134764, 5T32GM007171, F30HL122079).
CITATION: “Cardiopatch platform enables maturation and scale-up of human pluripotent stem cell-derived engineered heart tissues,” Ilya Y. Shadrin, Brian W. Allen, Ying Qian, Christopher P. Jackman, Aaron L. Carlson, Mark E. Juhas, and Nenad Bursac. Nature Communications, 2017. DOI: 10.1038/s41467-017-01946-x
Dysfunction of intricate astrocyte cells may underlie devastating diseases like autism, schizophrenia and epilepsy
By Kara Manke
Brains are made of more than a tangled net of neurons. Star-like cells called astrocytes diligently fill in the gaps between neural nets, each wrapping itself around thousands of neuronal connections called synapses. This arrangement gives each individual astrocyte an intricate, sponge-like structure.
New research from Duke University finds that astrocytes are much more than neurons’ entourage. Their unique architecture is also extremely important for regulating the development and function of synapses in the brain.
When they don’t work right, astrocyte dysfunction may underlie neuronal problems observed in devastating diseases like autism, schizophrenia and epilepsy.
The Duke team identified a family of three proteins that control the web-like structure of each astrocyte as it grows and encases neuronal structures such as synapses. Switching off one of these proteins not only limited the complexity of the astrocytes, but also altered the nature of the synapses between neurons they touched, shifting the delicate balance between excitatory and inhibitory neural connections.
“We found that astrocytes’ shape and their interactions with synapses are fundamentally important for brain function and can be linked to diseases in a way that people have neglected until now,” said Cagla Eroglu, an associate professor of cell biology and neurobiology at Duke. The research was published in the Nov. 9 issue of Nature.
Astrocytes have been around almost as long as brains have. Even simple invertebrates like the crumb-sized roundworm C. elegans has primitive forms of astrocytes cloaking their neural synapses. As our brains have evolved into complex computational machines, astrocyte structure has also grown more elaborate.
But the complexity of astrocytes is dependent on their neuronal companions. Grow astrocytes and neurons together in a dish, and the astrocytes will form intricate star-shaped structures. Grow them alone, or with other types of cells, and they come out stunted.
“It didn’t matter if the neurons were dead or alive — either way, contact between astrocytes and neurons allowed the astrocyte to become complex,” Stogsdill said. “That told us that there are interactions between the cell surfaces that are regulating the process.”
Stogsdill searched existing genetic databases for cell surface proteins known to be expressed by astrocytes, and identified three candidates that might help direct their shape. These proteins, called neuroligins, play a role in building neural synapses and have been linked to diseases like autism and schizophrenia. Previously, their functions had been primarily studied in neurons.
To find out what role neuroligins play in astrocytes, Stogsdill tinkered with astrocytes’ ability to produce these proteins. He found that when he switched off the production of neuroligins, the astrocytes grew small and blunt. But when he boosted the production of neuroligins, astrocytes grew to nearly twice the size.
“The shape of the astrocytes was directly proportional to their expression of the neuroligins,” Stogsdill said.
Tweaking the expression of neuroligins didn’t just change the size and shape of the astrocytes. They also had a drastic effect on the synapses that astrocyte touched.
When Stogsdill switched off a single neuroligin — neuroligin 2 — the number of excitatory or “go” synapses dropped by 50 percent. The number of inhibitory or “stop” synapses stayed the same, but their activity increased.
“We are learning now that one of the hallmarks of neurological disorders like schizophrenia, autism and epilepsy is an imbalance between excitation and inhibition,” Stogsdill said. “Which just drives home that these disease-associated molecules are potentially functioning in astrocytes to shift this balance.”
Ben Barres, a professor of neurobiology at Stanford University who was not involved with the study, praised the findings as “a profoundly important, revolutionary advance” for understanding how interactions between neurons and astrocytes can affect synapse formation.
“These findings vividly illustrate once again how any important process in the brain can only be understood as a dialogue between astrocytes and neurons,” Barres said. “To ignore the astrocytes, which are vastly more numerous than neurons, is always a mistake.”
Other authors on the study are Juan Ramirez, Katherine T. Baldwin, Eray Enustun, Tiffany Ejikeme from Duke University Cell Biology Department and Ru-Rong Ji, Di Liu, Yong-Ho Kim from Duke University Department of Anesthesiology.
This research was supported by grants from the National Institutes of Health (RO1 DA031833, RO1 DE022743 and F31 NS092419) and a Holland Trice Brain Research Award. Additional support was provided by the Foerster-Bernstein Family and the Hartwell Foundation.
CITATION: “Astrocyte Neuroligins Control Astrocyte Morphogenesis and Synaptogenesis,” Jeff A. Stogsdill, Juan Ramirez, Di Liu, Yong-Ho Kim, Katherine T. Baldwin, Eray Enustun, Tiffany Ejikeme, Ru-Rong Ji and Cagla Eroglu. Nature, Nov. 9, 2017. DOI: 10.1038/nature24638
“Cell Biology of Astrocyte-Synapse Interactions,” Nicola J. Allen and Cagla Eroglu. Neuron, Nov. 1, 2017. DOI: 10.1016/j.neuron.2017.09.056
We are pleased to announced the winners of Cycle 2 of the Regeneration Next student travel grants. Congratulations to:
Shaunak Adkar (Gersbach lab) to travel to the Orthopaedic Research Society annual symposium in March 2018 to present his work: Purification of hiPSC-derived chondrocyte-like cells using a CRISPR-Cas9-generated collagen II reporter enhances chondrogenesis and cartilaginous matrix production.
Victoria Deneke (DiTalia lab) to travel to the ASCB/EMBO joint annual meeting in December 2017 to present her work: Mechanisms regulating the emergence of tissue-wide synchrony in Drosophila early embryos.
The next round of travel grant applications will open in January 2018. All students presenting work relevant to tissue regeneration are encouraged to apply!
By Marla Vacek Broadfoot
This article first appeared on Duke Today and is reposted here in its entirety. This work represents a collaborative effort across multiple departments at Duke University: School of Medicine, Pratt School of Engineering, and Trinity School of Arts and Sciences.
By taking videos of a tiny beating zebrafish heart as it reconstructs its covering in a petri dish, scientists have captured unexpected dynamics of cells involved in tissue regeneration. They found that the depleted heart tissue regenerates itself in a wave, led by a front of fast-moving, supersized cells and trailed by smaller cells that multiply to produce others.
The nature of this wavefront — and the success of the tissue regeneration that follows — is determined by mechanical tension that acts upon the cells. The results, published September 25 in the journal Developmental Cell, indicate a new paradigm for how forces acting in tissues can direct the decisions that cells make to regenerate lost tissues.
“Our findings open avenues for the study of cell cycle dynamics in regenerating tissue,” said Jingli Cao, PhD, lead study author and a postdoctoral fellow in Ken Poss’s lab at Duke University School of Medicine. “By manipulating the mechanical tension of cells, we also might be able to develop new bioengineering or translational approaches.”
While the human heart can’t fully heal itself after a heart attack, the zebrafish heart can easily replace cells lost to damage or disease. Scientists have spent many years probing the regenerative powers of this small striped fish in the hopes of uncovering clues that could improve therapy for human heart disease.
In 2015, Cao showed that he could remove the hearts from zebrafish and grow them in dishes in the laboratory, where the tiny two-chambered organs continued to beat and behave as if they were still tucked inside the animal. In this study, Cao and his colleagues exploited this system to monitor the regeneration of the epicardium, a thin layer of cells that cover the heart’s surface.
The researchers destroyed most of the heart’s epicardial layer, and then put the “explanted” organs under the microscope to capture the regeneration in action. They expected to see a population of cells that had rapidly replicated their DNA content and divided into new cells replenish the surface of the organ. While these cells definitely played a part, they were not leading the charge. Instead, regeneration was led by cells that replicated their DNA without dividing, effectively creating supersized cells with two times the cell machinery or more.
“Imagine you have a wound on your skin and you want to cover it as soon as possible, but you don’t have enough cells,” said Cao. “By making cells become larger, you could efficiently cover the wound. We think this tactic could increase the regenerative capacity of this population by covering the surface in an efficient manner.”
The researchers measured a number of properties of the cells in the regenerative wavefront. They found that the bigger leader cells migrated across the surface of the heart at higher speeds than the smaller follower cells. When they measured the levels of tension experienced by the cells, they found that leader cells recoiled faster than follower cells when tiny incisions were applied, much like the surface of an inflated balloon retracts after bursting. Poss said that mechanical tension seems to keep the cells from dividing after DNA replication.
“This study is trying to understand the basic decisions cells make when they regenerate,” said Poss, professor of cell biology at Duke University School of Medicine and director of the Regeneration Next Initiative at Duke. “If there are methods we could use to guide their decisions, to determine whether they generate larger cells or more cells through division, it could be one way to influence the ability of a tissue to repair.”
The researchers plan to use their zebrafish heart explant culture system to screen for small molecules that could potentially increase the regenerative capacity of heart tissues. Such chemicals could one day form the basis for new drugs to repair the damage caused by a heart attack or other cardiovascular diseases.
This study was a collaboration between several research groups at Duke led by Poss, Stefano Di Talia, Daniel Kiehart, and Nenad Bursac, as well as Eric Small’s group at University of Rochester. It was supported by the American Heart Association (14POST20230023, 16POST30230005, 16PRE30490009, and 15SDG25710444), the National Science Foundation (2013126035, 2014175655), the National Institutes of Health (T32-GM007184, T32-HL066988-15, R00 HD074670, R01 HL120919, R01 GM033830, R01 HL132389, R01 HL131319, and R01 HL081674), and the Leducq Foundation.Office
CITATION: “Tension Creates an Endoreplication Wavefront That Leads Regeneration of Epicardial Tissue,” Jingli Cao, Jinhu Wang, Christopher P. Jackman, Amanda H. Cox, Michael A. Trembley, Joseph J. Balowski, Ben D. Cox, Alessandro De Simone, Amy L. Dickson, Stefano Di Talia, Eric M. Small, Daniel P. Kiehart, Nenad Bursac, and Kenneth D. Poss. Developmental Cell, September 25, 2017. DOI:10.1016/j.devcel.2017.08.024
Regeneration Next (RNI) is a venture to advance discovery research and education in the broad field of tissue regeneration, and to enable applications for regenerative medicine. RNI is partnering with the Department of Cell Biology and the Department of Biomedical Engineering to hire tenure-track faculty members at the rank of Assistant Professor. An appointment at the Associate or Full Professor level may be possible for exceptional senior applicants.
We invite applications from accomplished candidates with expertise in developmental and cell biology, quantitative biology, imaging, stem cell biology, mechanisms of tissue regeneration, mechanobiology, tissue engineering or related areas. One appointment will be in the Department of Cell Biology in the School of Medicine, while the other will be in the Department of Biomedical Engineering in the School of Engineering. Joint appointments across departments will be considered for qualified candidates. Candidates must have a Ph.D., M.D., or equivalent degree. Women and underrepresented minority candidates are especially encouraged to apply.
Applicants should submit a curriculum vitae, a 3-page total summary of accomplishments and research plans, a teaching statement, and at least 3 letters of recommendation by November 15, 2017 to AcademicJobsOnline. Questions may be directed to: Ken Poss, Director, RNI.
Duke University is an Affirmative Action/ Equal Opportunity Employer committed to providing employment opportunity without regard to an individual’s age, color, disability, genetic information, gender, gender identity, gender expression, national origin, race, religion, sexual orientation, or veteran status.
By Marla Vacek Broadfoot
This article was originally posted on the Duke Today blog and is re-posted here in its entirety.
Duke researchers have discovered a unique repair mechanism in the developing backbone of zebrafish that could give insight into why spinal discs of longer-lived organisms like humans degenerate with age.
The repair mechanism apparently protects the fluid-filled cells of the notochord, the precursor of the spine, from mechanical stress as a young fish begins swimming. Notochord cells go on to form the gelatinous center of intervertebral discs, the flat, round cushions wedged between each vertebrae that act as shock absorbers for the spine.
The disappearance of these cells over time is associated with degenerative disc disease, a major cause of human pain and disability worldwide.
“It is not difficult to speculate that these same mechanisms of repair and regeneration are present in humans at very early stages, but are lost over time,” said Michel Bagnat, Ph.D., senior author of the study and assistant professor of cell biology at Duke University School of Medicine. “If we are going to think about techniques that foster intervertebral disc regeneration, this is the basic biology we need to understand.”
The study appears June 22, 2017, in Current Biology.
Bagnat likens the notochord to a garden hose filled with water. The hardy structure consists of a sheath of epithelial cells surrounding a collection of giant fluid-filled or “vacuolated” cells. During development, these vacuolated cells rarely pop, despite being under constant mechanical stress. Recent research has suggested that tiny pouches known as caveolae (Latin for “little caves”) that form in the plasma membrane of these cells can provide a buffer against stretching or swelling.
To see whether the caveolae protected vacuoles from bursting, his team and collaborators from Germany generated mutants of three caveolar genes in their model organism, the zebrafish. Because these small aquarium fish are transparent as embryos, the scientists could easily visualize any spinal defects triggered by the loss of caveolae.
The researchers found that when the mutant embryos hatched and started swimming, exerting pressure on their underdeveloped backbones, their vacuolated cells started to break up. While the finding confirmed their suspicions, it turned up a puzzling discovery. “In the caveolar mutants, you see these serial lesions up and down the notochord, and yet the mature spine formed normally,” said Bagnat. “That was very puzzling to us.”
To figure out how that was possible, lead authors Jamie Garcia and Jennifer Bagwell took a closer look at the notochord of mutant fish. They marked the vacuolated cells green and the surrounding epithelial sheath cells red and then filmed the fish shortly after they hatched and started swimming. First, they could see an occasional vacuolated cell break and spill its contents like a water balloon. Then, over the course of fifteen hours, a nearby epithelial sheath cell would move in, crawl over the detritus of the collapsed cell, and morph into a new vacuolated cell.
They performed a few more experiments and found that the repair response was triggered by the release of the cell contents, specifically the basic molecular building blocks known as nucleotides. The researchers then isolated live epithelial sheath cells and treated them with nucleotide analogs to show that they turned into vacuolated cells.
“These cells, which reside in the discs of both zebrafish and man, seem capable of controlling their own repair and regeneration,” said Bagnat. “Perhaps it is a continuous release of nucleotides that is important for keeping the disc in good shape.”
The study may offer insight not only into the development of back and neck pain, but also into the origins of cancer. Their data suggests that chordomas, rare and aggressive notochord cell tumors, may begin when epithelial sheath cells leave the notochord and invade the skull and other tissues.
The research was supported by National Institutes of Health (AR065439, AR065439-04S1, T32DK007568-26, and CA193256), a Capes-Humboldt Fellowship, the Max Planck Society, and a Faculty Scholar grant from the Howard Hughes Medical Institute.
CITATION: “Sheath cell invasion and trans-differentiation repair mechanical damage caused by loss of caveolae in the zebrafish notochord,” Jamie Garcia, Jennifer Bagwell, Brian Njaine, James Norman, Daniel S. Levic, Susan Wopat, Sara E. Miller, Xiaojing Liu, Jason W. Locasale, Didier Y.R. Stainier and Michel Bagnat. Current Biology, June 22, 2017. DOI# 10.1016/j.cub.2017.05.035
Earlier this spring, a group of Wake Early College of Health and Sciences (WECHS) high school students left their classrooms to spend the day learning about cardiovascular research. The students visited the labs of Dr. Ravi Karra and Dr. Doug Marchuk, and toured the Duke zebrafish core facility. The students, many with plans to attend graduate or medical school, listened to presentations explaining basic concepts and methodologies of cardiovascular research work.
This program came to fruition under the leadership of Dr. Maria Rapoza, executive director of the Duke Cardiovascular Research Center (CVRC), Dr. Sharlini Sankaran, the executive director of Duke’s Regeneration Next Initiative, and Sruthi Valluru, a WECHS senior high schooler.
Sruthi, like many of her Wake Early College classmates, has already taken college-level courses and has been granted experiential learning opportunities in the field of medicine through WakeMed Hospital. However, when her interests turned toward medical research, she ran into roadblocks.
“[Finding ways to interact with research] was such a tricky thing for me. I had to go out and email people or have connections…It’s so difficult for any high schooler (even though there are so many smart and capable students)…to penetrate the field of research when they don’t have the proper connections.”
Valluru hopes that launching a tour program at WECHS will help her peers gain first-hand exposure to medical research. After working in both a Duke-based start-up and research lab, Valluru’s career interests turned towards medical research as a platform to transform the lives of so many. She will be studying biomedical engineering at North Carolina State University beginning this fall semester.
Valluru emphasizes the collaborative nature of research. “As we bring more people to the field, we are creating a wider community that can help us move forward in discovering new things.” Exposing students to the work of research laboratories early on in their careers helps broaden the pipeline of scientsts and cultivate interest and talent in young people.
Students enjoyed walking through Duke’s winding halls of countless lab facilities and touring Duke’s beautiful medical campus. “One of the things I enjoyed the most was the bus ride home listening to the excited chatter of my fellow classmates about how much they enjoyed [the tour],” Valluru noted.
Popular culture often portrays researchers as socially awkward science nerds who work in a dimly-lit basement. The societal conceptions of research work are not aligned with the reality that researchers enjoy rich social lives and span a wide range of types of research.
Many WECHS students expressed that participating in the tour changed their perspectives on the research work. One student said, “This isn’t what I expected research to be like. I expected research to be this one person working by themselves.” At the end of each lab visit, WECHS students asked the lab members for contact information, eager to continue learning about research work at Duke.
The Duke CVRC, Regeneration Next Initiative, and WECHS team would like to thank everyone who made this program possible. The team looks forward to scaling future collaborations to a wider scale with high schools and research universities across the Triangle area.
Guest blog post by Jacqueline Xu, Duke Department of Medicine undergraduate intern.
As a scientist, it is easy to get caught up in the day-to-day workflow of research and lose sight of the bigger picture. We are often so focused on generating and reporting solid, exciting data that we neglect another major aspect of our job; sharing our work and its impacts with the broader community. On Tuesday May 23rd, a group of graduate students from Duke went to the North Carolina legislative building to do just that.
Dr. Sharlini Sankaran, Executive Director of Duke’s Regeneration Next Initiative, organized a group of graduate students to attend the North Carolina Hospital Associations (NCHA) “Partnering for a Healthier Tomorrow!” advocacy day at the state legislature in Raleigh. The event gave representatives from various hospital systems an opportunity to interact with state legislators about the work they do and issues affecting healthcare in the state. Andrew George, a graduate student in the McClay Lab, Will Barclay, a graduate student in the Shinohara Lab, and I joined Dr. Sankaran to share some of the great tissue regeneration-related research going on at Duke.
Our morning was busy as elected officials, legislative staff, executive branch agency officials, and staff from other hospital systems stopped by our booth to hear what Regeneration Next is all about. We talked about the focus on harnessing Duke’s strengths in fundamental research on molecular mechanisms underlying regeneration and development, then pairing that with the expertise of our engineers and clinicians. We discussed topics including spine and heart regeneration mechanisms from the Poss Lab, advances in engineering skeletal muscle from the Bursac Lab, and clinical trials of bioengineered blood vessels for patients undergoing dialysis from Duke faculty Dr. Jeffrey Lawson.
It was remarkable to hear how engaged everyone was, we got great questions like ‘what is a zebrafish and why do you use them?’ and ‘why would a bioengineered ligament be better than one from an animal model or cadaver?’. Every person who stopped by was supportive and many had a personal story to share about a health issue experienced by friends, family, or even themselves. As a graduate student who does basic research, it really underscored how important these personal connections are to our work, even though it may be far removed from the clinic.
Communicating our research to legislators and others at NCHA advocacy day was a great and encouraging experience. Health issues affect all of us. Our visit to the legislature on Tuesday was a reminder that there is support for the work that we do in hopes it will help lead to a healthier tomorrow.
Guest blog post by Dan Keeley, graduate student in Biology
Regeneration Next is pleased to announce travel grants to support six students. The travel award supports graduate students who present tissue regeneration-related research at relevant scientific meetings. Our first round of awardees are:
- Erez Cohen, Fox lab, department of Pharmacology and Cancer Biology. Erez will attend the Gordon Research Conference on Tissue Repair and Regeneration to present his work on “Switching Injury Response: Polyploidy Associated Hypertrophy as An Alternative to Compensatory Proliferation.”
Colleen Drapek, Benfey Lab, Department of Biology. Colleen will attend the American Society of Plant Biology meeting and will present her work on “The Minimal Gene Regulatory network for Arabidopsis Root Endodermis differentiation.”
Lauren Heckelman, DeFrate lab, Department of Biomedical Engineering. Lauren attended the Orthopaedic Research Society conference and presented two projects: “In Vivo Behavior of Patellar Cartilage in Response to and Twenty-Four Hours following Running” and “In Vivo Exercise-Induced Glenohumeral Cartilage Strains.”
Jennifer Kwon, Gersbach lab, Department of Biomedical Engineering. Jennifer will attend the International Society for Stem Cell Research meeting to present her work on “Directing skeletal myogenic progenitor cell lineage specification with CRISPR/Cas-9 based transcriptional activators.”
Jason Wang, Bursac lab, Department of Biomedical Engineering. Jason will attend the EMBO conference on Muscle Wasting and will present his work on “Developing an in-vitro model for human skeletal muscle regeneration.”
Lifeng Yuan, Wang Lab, Department of Pharmacology and Cancer Biology. Lifeng will attend the International Society for Stem Cell Research meeting and will present work on “Negative regulation of mitochondrial intermembrane peptidase drives metabolic alteration and cell death blockage for initiating cellular senescence.”
Congratulations to these deserving students! The next deadline for the Regeneration Next travel grants will be September 28, 2017. Details and application instructions are here.