About

Professor Marni Boppart holds the Saul J. Morse and Anne B. Morgan Professorship in the College of Applied Health Sciences at the University of Illinois. She serves as Associate Head for Faculty Affairs in the Department of Health and Kinesiology and is a Professor in both Health and Kinesiology and Biomedical and Translational Sciences. Additionally, she is affiliated with the Beckman Institute for Advanced Science and Technology and the Carl R. Woese Institute for Genomic Biology. Professor Boppart's research centers on understanding the molecular and cellular mechanisms that drive skeletal muscle growth following exercise. Her work aims to translate this knowledge into novel cell- and pharmacological-based interventions designed to prevent or treat muscle mass loss due to disuse, with a particular focus on vulnerable populations such as the aging. A significant aspect of her research involves developing therapies based on stem cells, pericytes, and extracellular vesicles (EVs). Through her interdisciplinary approach, Professor Boppart contributes to advancing the fields of skeletal muscle biology, regenerative medicine, and therapeutic development.

Research topics

• Biology
• Endocrinology
• Chemistry
• Biochemistry
• Cancer research
• Internal medicine
• Immunology
• Cell biology
• Medicine
• Genetics
• Neuroscience
• Anatomy

Selected publications

• Human plasma extracellular vesicles as an exercise mimetic to preserve skeletal muscle plasticity during disuse

  npj Microgravity · 2026-03-06

  articleOpen accessSenior author

  The purpose of this study was to determine the extent to which extracellular vesicles (EVs) circulating in blood after exercise training act as an effective mimetic to maintain skeletal muscle mass during unloading and/or accelerate recovery after disuse. Ten healthy males (27.7 ± 7.1 y) were recruited for a 6-week progressive resistance and endurance training program. EVs were isolated from blood before (EVs) or immediately after training (ExerVs). EVs were intraperitoneally injected into male mice (4×; 3 × 108 particles/injection) during 14 days of hindlimb unloading (HU), then the muscles were collected immediately or 7 days after HU. ExerVs did not maintain muscle mass, fiber size (fCSA), or protein synthesis but significantly reduced collagen I during HU. ExerV administration rapidly restored Type I fCSA and capillary quantity concomitant with reduced collagen during the reloading period. Overall, this study demonstrates that ExerVs may represent a novel strategy to preserve skeletal muscle health during disuse.

  PublisherOA PDFDOI

• Exercise-induced plasma-derived extracellular vesicles increase adult hippocampal neurogenesis

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-08-02

  preprintOpen access

  Abstract Aerobic exercise enhances cognition in part by increasing adult hippocampal neurogenesis, angiogenesis, and astrogliogenesis. Since hippocampal atrophy is a hallmark of several neurological and psychiatric conditions—including depression, PTSD, Alzheimer’s disease, and aging—understanding the mechanisms by which exercise increases neurogenesis has broad therapeutic relevance. One potential mechanism involves extracellular vesicles (EVs), lipid bilayer-enclosed particles released by multiple tissues during exercise that transport bioactive molecular cargo to distant organs, including the brain. In this study, we tested whether plasma-derived EVs from exercising mice (ExerVs) are sufficient to promote hippocampal neurogenesis, astrogliogenesis, and vascular density in sedentary mice. EVs were isolated from the plasma of sedentary or exercising C57BL/6J mice and injected intraperitoneally into sedentary recipients twice weekly for four weeks. To evaluate reproducibility, the study was conducted across two independent cohorts using identical procedures. ExerV-treated mice showed a significant increase in BrdU-positive cells in the granule cell layer compared to both PBS- and SedV-treated controls in both cohorts. Approximately 90% of these cells co-expressed NeuN, indicating neuronal differentiation, while 6% co-expressed S100β, indicating astrocyte generation. No changes were observed in vascular density across groups. These findings provide initial evidence that systemically delivered exercise-derived EVs can enhance hippocampal neurogenesis and astrogliogenesis in sedentary mice. This proof-of-concept work supports further investigation into ExerVs as a potential therapeutic strategy for conditions associated with hippocampal atrophy. Highlights ExerVs increase hippocampal neurogenesis and astrogliogenesis in sedentary mice ExerVs do not affect hippocampal vascular area Circulating ExerVs are sufficient to recapitulate key brain benefits of exercise

  PublisherOA PDFDOI

• Plasma-Derived Extracellular Vesicle Proteomics

  Journal of Proteome Research · 2025-08-08 · 8 citations

  reviewOpen access

  Extracellular vesicles (EVs) are nanometer-scale lipid bilayer-enclosed particles released by cells under physiological and pathological conditions. Their molecular cargos, including proteins, can reflect the chemical composition and physiological state of the parent cells, carrying signatures of health and disease. As such, EVs are valuable tools for biomarker discovery and mechanistic studies. Among them, plasma-derived EVs (pEVs) are particularly promising, as sampling plasma allows capture of EVs from virtually all of the tissues and organs. The minimally invasive nature of plasma collection further enhances the diagnostic and therapeutic potential of the pEVs. Proteomic profiling of pEVs enables the identification of disease-specific EV-biomarkers. However, the complexity of plasma, with high levels of abundant proteins and large EV heterogeneity, presents challenges for pEV proteomics. Mass spectrometry (MS) has emerged as the preferred state-of-the-art analytical tool for pEV studies due to its nonbiased ability to characterize thousands of proteins in an experiment and its ability to identify low-abundance EV proteins. Here, a comprehensive overview of the advancements in MS-based pEV proteomics in the recent 5 years is presented with a focus on three key areas: sample preparation methodologies, MS-based approaches for protein identification and quantification, and description of pEV studies for basic and disease research. Technical advancements enable greater proteomic details from pEVs, enhancing biomarker discovery, elucidating disease mechanisms, and advancing an understanding of EVs' biological roles.

  PublisherOA PDFDOI

• Neutrophils exposed to a cholesterol metabolite secrete extracellular vesicles that promote epithelial-mesenchymal transition and stemness in breast cancer cells

  Cancer Letters · 2025-10-29 · 4 citations

  articleOpen access
  PublisherOA PDFDOI

• Real-time label-free dynamic imaging of extracellular vesicles in live tissues

  2025-03-19

  article

  The study of extracellular vesicles (EVs) in live tissues has gained significant attention due to their important role in facilitating intercellular communication and tissue cross-talk. However, the dynamic and real-time imaging of EVs in live tissues remains a challenge due to the limitations of traditional imaging techniques. This study presents the integration of fluorescence lifetime imaging microscopy (FLIM) and coherent anti-Stokes Raman scattering (CARS) into a novel simultaneous label-free autofluorescence multi-harmonic (SLAM) microscopy system. This advanced imaging system enables real-time, label-free dynamic imaging of EVs in live tissues with high spatial and temporal resolution. The SLAM microscopy system leverages the unique autofluorescent properties of EVs, providing a non-invasive and highly sensitive approach to visualize EVs without the need for exogenous labels. The system also captures EVs’ fluorescence lifetime and vibrational information by combining FLIM and CARS, offering a comprehensive understanding of their biochemical composition and dynamics. The system was validated using live tissue samples, demonstrating its capability to monitor EVs’ real-time dynamics, distribution, and interactions with their microenvironment. This innovation opens new avenues for exploring EV-mediated processes in real-time, potentially leading to a deeper understanding of EV dynamics in aging and disease and demonstrating the potential to impact a broad range of biomedical applications, including diagnostics and therapeutic interventions. The results indicate that combining these microscopy modalities is a powerful approach to studying EV biology, offering new insights into their roles in health and disease.

  PublisherDOI

• Cholesterol Metabolite 27-Hydroxycholesterol Enhances the Secretion of Cancer Promoting Extracellular Vesicles by a Mitochondrial ROS-Induced Impairment of Lysosomal Function

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-05-01

  preprintOpen access

  Extracellular vesicles (EVs) serve as crucial mediators of cell-to-cell communication in normal physiology as well as in diseased states, and have been largely studied in regard to their role in cancer progression. However, the mechanisms by which their biogenesis and secretion are regulated by metabolic or endocrine factors remain unknown. Here, we delineate a mechanism by which EV secretion is regulated by a cholesterol metabolite, 27-Hydroxycholesterol (27HC), where treatment of myeloid immune cells (RAW 264.7 and J774A.1) with 27HC impairs lysosomal homeostasis, leading to shunting of multivesicular bodies (MVBs) away from lysosomal degradation, towards secretion as EVs. This impairment of lysosomal function is caused by mitochondrial dysfunction and subsequent increase in reactive oxygen species (ROS). Interestingly, cotreatment with a mitochondria-targeted antioxidant rescued the lysosomal impairment and attenuated the 27HC-mediated increase in EV secretion. Overall, our findings establish how a cholesterol metabolite regulates EV secretion and paves the way for the development of strategies to regulate cancer progression by controlling EV secretion.

  PublisherOA PDFDOI

• Neutrophils exposed to a cholesterol metabolite secrete extracellular vesicles that promote epithelial-mesenchymal transition and stemness in breast cancer cells

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-08-02 · 5 citations

  preprintOpen access

  Small extracellular vesicles (sEVs) are emerging as critical mediators of intercellular communication in the tumor microenvironment (TME). Here, we investigate the mechanisms by which sEVs derived from neutrophils treated with the cholesterol metabolite, 27-hydroxycholesterol (27HC), influence breast cancer progression. sEVs released from 27HC treated neutrophils enhance epithelial-mesenchymal transition (EMT) and stem-like properties in breast cancer cells, resulting in loss of adherence, increased migratory capacity and resistance to cytotoxic chemotherapy. Decreased microRNAs (miRs) within the sEVs resulted in activation of the WNT/β-catenin signaling pathway in recipient cells and suggest that this may be a predominant pathway for stem-like phenotype and EMT. Our findings underscore a novel mechanism by which 27HC-modulated neutrophils contribute to breast cancer pathophysiology through EV-mediated intercellular communication, suggesting potential therapeutic targets in cancer treatment.

  PublisherOA PDFDOI

• 27-Hydroxycholesterol Enhances Secretion of Extracellular Vesicles by ROS-Induced Dysregulation of Lysosomes

  Endocrinology · 2024-09-17 · 9 citations

  articleOpen access

  Extracellular vesicles (EVs) serve as crucial mediators of cell-to-cell communication in normal physiology as well as in diseased states; they have been largely studied in regard to their role in cancer progression. However, the mechanisms by which their biogenesis and secretion are regulated by metabolic or endocrine factors remain unknown. Here, we delineate a mechanism by which EV secretion is regulated by a cholesterol metabolite, 27-hydroxycholesterol (27HC), where treatment of myeloid immune cells (RAW 264.7 and J774A.1) with 27HC impairs lysosomal homeostasis, leading to shunting of multivesicular bodies (MVBs) away from lysosomal degradation, toward secretion as EVs. This altered lysosomal function is likely caused by mitochondrial dysfunction and subsequent increase in reactive oxygen species (ROS). Interestingly, cotreatment with a mitochondria-targeted antioxidant rescued the lysosomal impairment and attenuated the 27HC-mediated increase in EV secretion. Overall, our findings establish how a cholesterol metabolite regulates EV secretion and paves the way for the development of strategies to regulate cancer progression by controlling EV secretion.

  PublisherOA PDFDOI

• Development of an Exercise-based EV Therapy to Improve Skeletal Muscle Recovery After Immobilization

  Physiology · 2024-05-01

  articleSenior author

  Introduction: Immobilization is necessary for recovery from illness or bone fractures; however, prolonged immobilization can result in significant loss of muscle mass and function. It is critical to recover muscle mass quickly following immobilization as severe muscle atrophy is correlated with increased likelihood of metabolic disorders, disability, and mortality. Physical rehabilitation can improve outcomes but is not always feasible. The purpose is to determine the extent to which EVs circulating in blood after endurance exercise training (EnVs) act as a safe and effective therapy to recover skeletal muscle mass following disuse. Methods: Donor C57BL/6 mice (n = 8-10, 4-month-old) were provided access to horizontal running wheels in a locked (sedentary) or unlocked (exercise) condition. After 4 weeks of voluntary running, EVs (SedVs or EnVs) were isolated from plasma using size exclusion chromatography according to manufactures guidelines, and concentration confirmed via nanoparticle tracking analysis (NanoSight NS3000). Recipient C57BL6/J mice (n = 5-8, 4-month-old) were subjected to single limb immobilization for 14 days. Upon remobilization, mice received a single intramuscular injection of PBS, SedVs, EnVs, or endurance plasma proteins, and remobilized for 3 and 14 days. Muscle samples were collected after remobilization and assessed for muscle cross-sectional-area (CSA) and capillarization. Results: Upon 3-day remobilization, EnVs did not significantly recover global fiber CSA and fiber-type specific CSA (Type IIa, Type IIx or Type IIb) or capillarization. Upon 14-day remobilization, EnVs did not significantly improve global fiber CSA and fiber-type specific CSA. However, a significant treatment effect was observed for capillary density (P = 0.0445), with increases observed for both SedV (P = 0.034) and EnV (P = 0.0117). Conclusion: EVs isolated from plasma after exercise can significantly improve skeletal muscle vascularization after immobilization, which may represent an important step toward full recovery of skeletal muscle mass. Partially support by NIH (NIAMS R01AR072735). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

  PublisherDOI

• Development of a cell-free strategy to recover aged skeletal muscle after disuse.

  PubMed · 2023-11-01 · 11 citations

  articleOpen accessSenior author

  -primed pericyte-derived sEVs effectively improve skeletal muscle recovery after immobilization, presenting a novel acellular approach to rebuild muscle mass in older adults after a period of disuse. KEY POINTS: Previous studies suggest that prolonged oxidative stress is a barrier to skeletal muscle recovery after a period of immobilization. In this study we demonstrate that muscle-resident perivascular stromal cells (pericytes) become dysfunctional and lack the capacity to mount an antioxidant defence after disuse in mice. Hydrogen peroxide treatment of healthy pericytes in vitro simulates the release of small extracellular vesicles (sEVs) that effectively recover skeletal muscle fibre size and extracellular matrix remodelling in young adult and aged mice after disuse. Pericyte-derived sEVs present a novel acellular strategy to recover skeletal muscle after disuse.

  PublisherOA PDFDOI

Recent grants

• Alpha7 Integrin-Mediated Hypertrophic Signaling and Growth in Skeletal Muscle

  NIH · $368k · 2014–2017

• Development of a Cell-Based Therapy to Improve Recovery Following Immobilization

  NIH · $1.7M · 2018–2024

• Origins of exercise-brain interactions

  NIH · $403k · 2018–2020

Frequent coauthors

• Laurie J. Goodyear

  Joslin Diabetes Center

  61 shared

• Michael De Lisio

  27 shared

• Heather D. Huntsman

  National Heart Lung and Blood Institute

  26 shared

• Roger A. Fielding

  Tufts University

  26 shared

• Kai Zou

  University of Massachusetts Boston

  25 shared

• Stephen A. Boppart

  University of Illinois System

  25 shared

• Jørgen F. P. Wojtaszewski

  University of Copenhagen

  22 shared

• Ziad S. Mahmassani

  University of Utah

  21 shared

Labs

• Molecular Muscle Physiology LaboratoryPI