About

Dr. Beth L. Pruitt is a Professor of Bioengineering at UC Santa Barbara, where she moved in 2018 to help launch the biological engineering degree program. She served as the founding program director and department chair of the Bioengineering Department. Her research broadly focuses on mechanobiology, specifically the role of mechanical perturbations in the evolution of mechanosignaling, structure, and function, including cell adhesion, cell and matrix remodeling, and downstream genetic and phenotypic changes. Her lab develops technologies to enhance the maturity of human pluripotent stem cell-derived cardiomyocytes, manipulate various cell types in micro physiological systems, and make quantitative measurements of cell responses to drugs, mechanical stimuli, or disease mutations. Dr. Pruitt's work spans from designing microtechnologies for small-scale mechanical measurements to investigating how mechanics mediate biological signaling, with an emphasis on reliable, quantitative biophysical measurements to address questions in physiology, cardiology, stem cell biology, and neuroscience.

Research topics

• Political Science
• Computer Science
• Medicine
• Sociology
• Engineering ethics
• Engineering
• Social Science
• Genetics
• Medical education
• Biology
• Public relations
• Internal medicine
• Materials science
• Nanotechnology
• Cardiology
• Cell biology
• Chemistry
• Biochemistry
• Microbiology
• Pedagogy

Selected publications

• Viscoelasticity of the Heart: An Overview of Viscoelastic Measurements at Different Scales

  Annual Review of Biomedical Engineering · 2026-05-01

  articleOpen accessSenior author

  The heart is viscoelastic and exhibits both viscous and elastic behavior with deformation. Cardiac viscoelasticity influences heart function by regulating the volume of blood that can fill, and subsequently be pumped from, the cardiac chambers. Tissue viscoelasticity can also influence cellular functions, motivating the need to measure and model viscoelasticity from the cellular to the organ scale under healthy and disease conditions. Here, we review current protocols, instrumentation, and results from cardiac viscoelastic measurements from the organ to the subcellular level. Since viscoelasticity is regulated by tissue structure and composition, we describe what is known about the viscoelasticity of intracellular and extracellular proteins, cardiac cells, and cardiac tissue, as well as how changes in these proteins with disease progression may influence cardiac viscoelasticity. Finally, we discuss the outlook for the field, including recommendations for standardizing reports of cardiac viscoelastic measurements to increase their utility for biomaterials design for tissue engineering, cardiovascular modeling, and diagnosis.

  PublisherOA PDFDOI

• Spontaneous and Induced Oscillations in Confined Epithelia

  PRX Life · 2025-01-09 · 2 citations

  articleOpen access

  The feedback between mechanical and chemical signals plays a key role in controlling many biological processes and collective cell behavior. Here we focus on the emergence of spatiotemporal density waves in a one-dimensional “cell train.” Combining a minimal theoretical model with experiments on MDCK epithelial cells confined to a linear pattern, we examine the spontaneous oscillations driven by feedback between myosin activation and mechanical deformations, as well as their effect on the response of the tissue to externally applied deformations. We show that the nature and frequency of spontaneous oscillations is controlled by the size of the cell train, with a transition from size-dependent standing waves to intrinsic spontaneous waves at the natural frequency of the tissue. The response to external boundary perturbations exhibits a resonance at this natural frequency, providing a possible venue for inferring the mechanochemical couplings that control the tissue behavior from rheological experiments.

  PublisherDOI

• E-cadherin mechanotransduction activates EGFR-ERK signaling in epithelial cells by inducing ADAM-mediated ligand shedding

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-03-06

  preprint

  Abstract The behavior of cells is governed by signals originating from their local environment, including mechanical forces that cells experience. Forces are transduced by mechanosensitive proteins, which can impinge on signaling cascades that are also activated by growth factor receptors upon ligand binding. We investigated the crosstalk between these mechanical and biochemical signals in the regulation of intracellular signaling networks in epithelial monolayers. Phosphoproteomic and transcriptomic analyses on epithelial monolayers subjected to mechanical strain revealed ERK signaling as a predominant strain-activated hub, initiated at the level of the upstream epidermal growth factor receptor (EGFR). Strain-induced EGFR-ERK signaling depends on mechanosensitive E-cadherin adhesions. Proximity labeling identified the metalloproteinase ADAM17, an enzyme that mediates shedding of soluble EGFR ligands, to be closely associated with E-cadherin. We developed a novel probe for monitoring ADAM-mediated shedding, which demonstrated that mechanical strain induced ADAM activation. Mechanically-induced ADAM activation was essential for mechanosensitive signaling from E-cadherin adhesions towards EGFR-ERK. Collectively, our data demonstrate that mechanical strain transduced by E-cadherin adhesion triggers the shedding of EGFR ligands that stimulate downstream downstream ERK activity. Our findings illustrate how mechanical signals and biochemical ligands can operate within a single, linear signaling cascade. Significance statement Cells integrate different types of information that they receive from their local environment to regulate their behavior. This includes biochemical signals, such as growth factors binding to their dedicated receptor. Similarly, cells respond to mechanical forces that they are subjected to. Although biochemical and mechanical signals can elicit similar signaling responses in cells, the interplay between these types of signals is not well understood. Here we unveil that mechanical strain of epithelia modulates the activity of the EGFR-ERK signaling pathway by controlling the availability of growth factors that bind and activate EGFR. This finding demonstrates that biochemical and mechanical signals do not act in a segregated fashion, but rather can function in a linear cascade, shedding light on fundamental principles governing cellular regulation.

  PublisherDOI

• E-cadherin mechanotransduction activates EGFR-ERK signaling in epithelial monolayers by inducing ADAM-mediated ligand shedding

  Science Signaling · 2025-05-13 · 7 citations

  articleOpen access

  The behavior of cells is governed by signals originating from their local environment, including mechanical forces exerted on the cells. Forces are transduced by mechanosensitive proteins, which can impinge on signaling cascades that are also activated by growth factors. We investigated the cross-talk between mechanical and biochemical signals in the regulation of intracellular signaling networks in epithelial monolayers. Phosphoproteomic and transcriptomic analyses on epithelial monolayers subjected to mechanical strain revealed the activation of extracellular signal-regulated kinase (ERK) downstream of the epidermal growth factor receptor (EGFR) as a predominant strain-induced signaling event. Strain-induced EGFR-ERK signaling depended on mechanosensitive E-cadherin adhesions. Proximity labeling showed that the metalloproteinase ADAM17, an enzyme that mediates shedding of soluble EGFR ligands, was closely associated with E-cadherin. A probe that we developed to monitor ADAM-mediated shedding demonstrated that mechanical strain induced ADAM activation. Mechanically induced ADAM activation was essential for mechanosensitive, E-cadherin-dependent EGFR-ERK signaling. Together, our data demonstrate that mechanical strain transduced by E-cadherin adhesion triggers the shedding of EGFR ligands that stimulate downstream ERK activity. Our findings illustrate how mechanical signals and biochemical ligands can operate within a linear signaling cascade.

  PublisherOA PDFDOI

• Cyclic stretch regulates epithelial cell migration in a frequency dependent manner via intercellular vinculin recruitment

  npj Biological Physics and Mechanics. · 2024-11-06 · 5 citations

  articleOpen accessSenior author

  Abstract The epithelial microenvironment is incredibly dynamic, subjected to mechanical cues including cyclic stretch. While cyclic cell stretching platforms have revealed epithelial cell reorientation and gap formation, few studies have investigated the long-term effects of cyclic stretch on cell migration. We measured the migratory response of the epithelium to a range of physiologically relevant frequencies and stretch. Our results indicate that lower stretch frequencies (i.e., 0.1 Hz) suppress epithelial migration, accompanied by cell reorientation and high cell shape solidity. We found that this response is also accompanied by increased recruitment of vinculin to cell-cell contacts, and this recruitment is necessary to suppress cell movements. These results confirm the mechanosensitive nature of vinculin within the adherens junction, but independently reveal a novel mechanism of low frequency stress response in supporting epithelial integrity by suppressing cell migration.

  PublisherOA PDFDOI

• YAP dysregulation triggers hypertrophy by CCN2 secretion and TGFβ uptake in human pluripotent stem cell-derived cardiomyocytes

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-06-03 · 1 citations

  preprintOpen accessSenior authorCorresponding

  Hypertrophy Cardiomyopathy (HCM) is the most prevalent hereditary cardiovascular disease - affecting >1:500 individuals. Advanced forms of HCM clinically present with hypercontractility, hypertrophy and fibrosis. Several single-point mutations in b-myosin heavy chain (MYH7) have been associated with HCM and increased contractility at the organ level. Different MYH7 mutations have resulted in increased, decreased, or unchanged force production at the molecular level. Yet, how these molecular kinetics link to cell and tissue pathogenesis remains unclear. The Hippo Pathway, specifically its effector molecule YAP, has been demonstrated to be reactivated in pathological hypertrophic growth. We hypothesized that changes in force production (intrinsically or extrinsically) directly alter the homeostatic mechano-signaling of the Hippo pathway through changes in stresses on the nucleus. Using human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs), we asked whether homeostatic mechanical signaling through the canonical growth regulator, YAP, is altered 1) by changes in the biomechanics of HCM mutant cardiomyocytes and 2) by alterations in the mechanical environment. We use genetically edited hiPSC-CM with point mutations in MYH7 associated with HCM, and their matched controls, combined with micropatterned traction force microscopy substrates to confirm the hypercontractile phenotype in MYH7 mutants. We next modulate contractility in healthy and disease hiPSC-CMs by treatment with positive and negative inotropic drugs and demonstrate a correlative relationship between contractility and YAP activity. We further demonstrate the activation of YAP in both HCM mutants and healthy hiPSC-CMs treated with contractility modulators is through enhanced nuclear deformation. We conclude that the overactivation of YAP, possibly initiated and driven by hypercontractility, correlates with excessive CCN2 secretion (connective tissue growth factor), enhancing cardiac fibroblast/myofibroblast transition and production of known hypertrophic signaling molecule TGFβ. Our study suggests YAP being an indirect player in the initiation of hypertrophic growth and fibrosis in HCM. Our results provide new insights into HCM progression and bring forth a testbed for therapeutic options in treating HCM.

  PublisherOA PDFDOI

• C. elegans touch receptor neurons direct mechanosensory complex organization via repurposing conserved basal lamina proteins

  Current Biology · 2024-07-01 · 9 citations

  articleOpen access
  PublisherOA PDFDOI

• Spontaneous and Induced Oscillations in Confined Epithelia

  arXiv (Cornell University) · 2024-08-05

  preprintOpen access

  The feedback between mechanical and chemical signals plays a key role in controlling many biological processes and collective cell behavior. Here we focus on the emergence of spatiotemporal density waves in a one-dimensional "cell train." Combining a minimal theoretical model with observations in an in vitro experimental system of MDCK epithelial cells confined to a linear pattern, we examine the spontaneous oscillations driven by the feedback between myosin activation and mechanical deformations and their effect on the response of the tissue to externally applied deformations. We show that the nature and frequency of spontaneous oscillations is controlled by the size of the cell train, with a transition from size-dependent standing waves to intrinsic spontaneous waves at the natural frequency of the tissue. The response to external boundary perturbations exhibit a resonance at this natural frequency, providing a possible venue for inferring the mechanochemical couplings that control the tissue behavior from rheological experiments.

  PublisherOA PDFDOI

• Cell Architecture and Dynamics of Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes (hiPSC-CMs) on Hydrogels with Spatially Patterned Laminin and N-Cadherin

  ACS Applied Materials & Interfaces · 2024-12-16 · 4 citations

  articleOpen accessSenior authorCorresponding

  Controlling cellular shape with micropatterning extracellular matrix (ECM) proteins on hydrogels has been shown to improve the reproducibility of the cell structure, enhancing our ability to collect statistics on single-cell behaviors. Patterning methods have advanced efforts in developing human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) as a promising human model for studies of the heart structure, function, and disease. Patterned single hiPSC-CMs have exhibited phenotypes closer to mature, primary CMs across several metrics, including sarcomere alignment and contractility, area and aspect ratio, and force production. Micropatterning of hiPSC-CM pairs has shown further improvement of hiPSC-CM contractility compared to patterning single cells, suggesting that CM-CM interactions improve hiPSC-CM function. However, whether patterning single hiPSC-CMs on a protein associated with CM-CM adhesion, like N-cadherin, can drive similar enhancement of the hiPSC-CM structure and function has not been tested. To address this, we developed a novel dual-protein patterning process featuring covalent binding of proteins at the hydrogel surface to ensure robust force transfer and force sensing. The patterns comprised rectangular laminin islands for attachment across the majority of the cell area, with N-cadherin "end caps" to imitate CM-CM adherens junctions. We used this method to geometrically control single-cell CMs on deformable hydrogels suitable for traction force microscopy (TFM) to observe cellular dynamics. We seeded α-actinin::GFP-tagged hiPSC-CMs on dual-protein patterned hydrogels and verified the interaction between hiPSC-CMs and N-cadherin end caps via immunofluorescent staining. We found that hiPSC-CMs on dual-protein patterns exhibited higher cell area and contractility in the direction of sarcomere organization than those on laminin-only patterns but no difference in sarcomere organization or total force production. This work demonstrates a method for covalent patterning of multiple proteins on polyacrylamide hydrogels for mechanobiological studies. However, we conclude that N-cadherin only modestly improves single-cell patterned hiPSC-CM models and is not sufficient to elicit increases in contractility observed in hiPSC-CM pairs.

  PublisherDOI

• Stress relaxation rates of myocardium from failing and non-failing hearts

  Biomechanics and Modeling in Mechanobiology · 2024-12-31 · 5 citations

  articleOpen access

  The heart is a dynamic pump whose function is influenced by its mechanical properties. The viscoelastic properties of the heart, i.e., its ability to exhibit both elastic and viscous characteristics upon deformation, influence cardiac function. Viscoelastic properties change during heart failure (HF), but direct measurements of failing and non-failing myocardial tissue stress relaxation under constant displacement are lacking. Further, how consequences of tissue remodeling, such as fibrosis and fat accumulation, alter the stress relaxation remains unknown. To address this gap, we conducted stress relaxation tests on porcine myocardial tissue to establish baseline properties of cardiac tissue. We found porcine myocardial tissue to be fast relaxing, characterized by stress relaxation tests on both a rheometer and microindenter. We then measured human left ventricle (LV) epicardium and endocardium tissue from non-failing, ischemic HF and non-ischemic HF patients by microindentation. Analyzing by patient groups, we found that ischemic HF samples had slower stress relaxation than non-failing endocardium. Categorizing the data by stress relaxation times, we found that slower stress relaxing tissues were correlated with increased collagen deposition and increased α-smooth muscle actin (α-SMA) stress fibers, a marker of fibrosis and cardiac fibroblast activation, respectively. In the epicardium, analyzing by patient groups, we found that ischemic HF had faster stress relaxation than non-ischemic HF and non-failing. When categorizing by stress relaxation times, we found that faster stress relaxation correlated with Oil Red O staining, a marker for adipose tissue. These data show that changes in stress relaxation vary across the different layers of the heart during ischemic versus non-ischemic HF. These findings reveal how the viscoelasticity of the heart changes, which will lead to better modeling of cardiac mechanics for in vitro and in silico HF models.

  PublisherOA PDFDOI

Recent grants

• NIH Grant R01EB006745

  NIH · $3.1M · 2016

• Shear Stress Measurement in Liquid Environments Using MEMS Sensor Arrays

  NSF · $391k · 2004–2008

• Effect of Microgravity on Drug Responses Using Engineered Heart Tissues

  NIH · $1.5M · 2018–2020

• NER: Processing and Characterization of Functionalized Polymers for Micro/Nano Systems

  NSF · $116k · 2004–2006

• From proteins to cells to tissues: A multi-scale assessment of biomechanical regulation by the myosin molecular motor

  NIH · $8.2M · 2019–2025

Frequent coauthors

• Alexandre J. S. Ribeiro

  Gladstone Institutes

  66 shared

• Gaspard Pardon

  Stanford University

  50 shared

• Miriam B. Goodman

  Stanford University

  37 shared

• Joseph C. Wu

  37 shared

• M. Taher A. Saif

  University of Illinois Urbana-Champaign

  36 shared

• Martin A. Schmidt

  36 shared

• Kimberly L. Turner

  Washington University in St. Louis

  36 shared

• Reza Ghodssi

  University of Maryland, College Park

  36 shared

Education

• B.S., Mechanical Engineering

  Massachusetts Institute of Technology (MIT)

• M.S., Manufacturing Systems Engineering

  Stanford University

• Ph.D., Mechanical Engineering

  Stanford University

Awards & honors

• Elected Fellow of AAAS
• Elected Fellow of BMES
• Elected Fellow of AIMBE
• Elected Fellow of ASME
• Senior Member of IEEE