About

David Wood is a Professor and the Director of Graduate Studies in the Department of Biomedical Engineering at the University of Minnesota. His research focuses on building benchtop systems that mimic human disease outside the human body, utilizing microfluidics and microfabrication to create engineered tissues. These systems allow for control over biological components and transport processes at relevant physiological scales, aiming to elucidate fundamental disease mechanisms, improve diagnosis, and develop new therapies. His work includes efforts to better understand treatments for sickle cell anemia, prevent tumor metastasis, and develop platforms for new disease therapies. Dr. Wood's educational background includes a BS in Physics from North Carolina State University and a PhD in Physics from the University of California, Santa Barbara. He completed postdoctoral training at the Massachusetts Institute of Technology in the Laboratory for Multiscale Regenerative Technologies. His contributions to the field are reflected in numerous publications, and his research is characterized by a focus on biomedical device development and disease modeling.

Research topics

• Biology
• Cell biology
• Medicine
• Pathology
• Genetics
• Biochemistry
• Cancer research
• Chemistry
• Internal medicine

Selected publications

• Quantitative Engineering Approaches to Understand the Multiscale Biophysical, Biomechanical, and Rheological Pathophysiology of Sickle Cell Disease

  2026-01-01

  book-chapterSenior author
  PublisherDOI

• Suspension physics govern the multiscale dynamics of blood flow in sickle cell disease

  Science Advances · 2026-01-01

  articleOpen accessSenior authorCorresponding

  From diabetes to malaria, altered blood flow contributes to poor clinical outcomes. Heterogeneity in red blood cell (RBC) properties within and across individuals has hindered our ability to establish the multiscale mechanisms driving pathological flow dynamics in such diseases. To address this, we develop microfluidic platforms to measure RBC properties and flow dynamics in the same blood samples from patients with sickle cell disease (SCD). We find that effective blood viscosity across individuals is explained by the proportion of stiff RBCs, exhibiting qualitative similarities to rigid-particle suspensions, despite considerable mechanical heterogeneity. By combining simulations with spatially resolved measurements of cell dynamics, we show how features of emergent rheology are governed by spatiotemporal cell organization, via margination at intermediate oxygen tensions, and localized jamming caused by spatial hematocrit variations under hypoxia. Our work defines the suspension physics underlying pathological blood flow in SCD and, more broadly, emergent rheology in heterogeneous particle suspensions.

  PublisherDOI

• Collagen-Based Tumor Spheroid Model for Investigating Tumor-Macrophage Interactions through Extracellular Matrix Remodeling

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-10-03

  preprintOpen accessSenior authorCorresponding

  Macrophages in the tumor microenvironment (TME) can constitute up to 50% of tumor mass and play a critical role in cancer cell proliferation, invasion, and metastasis. While their contribution to extracellular matrix (ECM) degradation through matrix metalloproteinases (MMPs) has been explored, the role of other macrophage-derived factors in ECM remodeling and their impacts beyond degradation remain poorly understood. Here, we describe the development of a 3D collagen-based tumor spheroid model to investigate the impact of peripheral blood mononuclear cell (PBMC)-derived macrophages on cancer cell-ECM and cancer cell-macrophage interactions within the TME. We observed that cancer cells stimulated PBMC-derived macrophages into an M2-like phenotype and that tumor spheroid conditioned macrophages (TSCMs) shifted cancer cell populations toward phenotypes with greater invasion distances and reduced circularity, indicative of increased malignancy. Such observations can be explained by macrophage-mediated ECM remodeling. Specifically, we demonstrate that TSCMs secreted a variety of soluble factors that are known to contribute to ECM remodeling, including ECM degradation and fiber realignment. These processes collectively create a tumor-favoring environment by loosening the collagen matrix and aligning fibers that serve as invasion tracks for migrating tumor cells that facilitate cancer cell migration and invasion. This model provides a robust platform to study the interactions between cellular and non-cellular components in the TME and to identify the molecular mechanisms underlying cancer progression. These insights may aid in the development of novel therapeutic strategies targeting macrophage-mediated processes in cancer.

  PublisherOA PDFDOI

• A human microbiome-derived therapeutic for ulcerative colitis promotes mucosal healing and immune homeostasis

  medRxiv · 2025-04-20 · 2 citations

  preprintOpen access

  Abstract The gut microbiome is central to the pathogenesis of ulcerative colitis (UC), and microbiome-derived therapeutics are a promising new treatment option. Using a metagenome-guided, large cohort-based approach, we identified Hominenteromicrobium mulieris as prevalent in healthy individuals but depleted in UC. Here, we present a Live Biotherapeutic Product (LBP) candidate, MAP 315, derived from a newly isolated strain of this species (MH27-2). In mouse colitis models, MH27-2 improved disease pathology, and accelerated gut healing, marked by epithelial restitution and reduced immune cell infiltration. In vitro studies showed that MH27-2 promotes mucosal healing through accelerated epithelial cell migration and proliferation, accelerated wound closure, and improved gut barrier integrity. Importantly, MH27-2 supports immune homeostasis through the promotion of regulatory T-cells, suppression of TL1A signaling, and induction of anti-inflammatory IL-10. Manufacturing processes were developed, and MH27-2 drug product (MAP 315) demonstrated to be safe and well-tolerated in a first-in-human Phase 1 clinical trial.

  PublisherOA PDFDOI

• Author response for "Oxygen-tunable endothelialized microvascular chip to assess hypoxia–reperfusion in sickle cell disease"

  2025-07-02

  peer-reviewSenior author
  PublisherDOI

• Quantifying the unique mechanical properties of irreversibly sickled cells in sickle cell disease

  Blood Vessels Thrombosis & Hemostasis · 2025-05-26 · 2 citations

  articleOpen accessSenior author

  • Irreversibly sickled cells are twenty times stiffer than non-sickled cells and six times less stiff than reversibly sickled cells. • Irreversibly sickled cell fractions have a negative correlation patient fetal hemoglobin fraction. We developed a platform to measure the oxygen dependent mechanical properties and oxygen saturation of individual irreversibly sickled cells (ISC). We identified and measured ISCs from a cohort of 10 individuals with SCD. ISCs were found to have an average shear surface modulus twenty times that of non-sickled cells and a sixth that of red blood cells with detectable hemoglobin polymer. We found that the number of ISCs was significantly reduced at 53 mmHg oxygen compared to 91 mmHg oxygen and above, suggesting these RBCs can still form polymer under hypoxia. We also found that the fraction of ISCs present in a blood sample had a negative correlation with donor fetal hemoglobin fraction, suggesting HbF could play a role in mitigating occurrence of irreversibly sickled cells.

  PublisherDOI

• Deciphering Colorectal Cancer–Hepatocyte Interactions: A Multiomics Platform for Interrogation of Metabolic Crosstalk in the Liver–Tumor Microenvironment

  International Journal of Molecular Sciences · 2025-02-25 · 5 citations

  articleOpen access

  Metabolic reprogramming is a hallmark of cancer, enabling tumor cells to adapt to and exploit their microenvironment for sustained growth. The liver is a common site of metastasis, but the interactions between tumor cells and hepatocytes remain poorly understood. In the context of liver metastasis, these interactions play a crucial role in promoting tumor survival and progression. This study leverages multiomics coverage of the microenvironment via liquid chromatography and high-resolution, high-mass-accuracy mass spectrometry-based untargeted metabolomics, 13C-stable isotope tracing, and RNA sequencing to uncover the metabolic impact of co-localized primary hepatocytes and a colon adenocarcinoma cell line, SW480, using a 2D co-culture model. Metabolic profiling revealed disrupted Warburg metabolism with an 80% decrease in glucose consumption and 94% decrease in lactate production by hepatocyte–SW480 co-cultures relative to SW480 control cultures. Decreased glucose consumption was coupled with alterations in glutamine and ketone body metabolism, suggesting a possible fuel switch upon co-culturing. Further, integrated multiomics analysis indicates that disruptions in metabolic pathways, including nucleoside biosynthesis, amino acids, and TCA cycle, correlate with altered SW480 transcriptional profiles and highlight the importance of redox homeostasis in tumor adaptation. Finally, these findings were replicated in three-dimensional microtissue organoids. Taken together, these studies support a bioinformatic approach to study metabolic crosstalk and discovery of potential therapeutic targets in preclinical models of the tumor microenvironment.

  PublisherOA PDFDOI

• Nonclinical evaluation of renizgamglogene autogedtemcel for SCD and TDT

  Molecular Therapy · 2025-09-24 · 3 citations

  articleOpen access
  PublisherOA PDFDOI

• Single-cell transcriptomics reveals heterocellular γ-globin gene expression in Aγδβ-thalassemia

  Blood Advances · 2025-12-06 · 2 citations

  articleOpen access
  PublisherOA PDFDOI

• Sticking together: Polymerization of sickle hemoglobin drives the multiscale pathophysiology of sickle cell disease

  Biophysics Reviews · 2025-03-01 · 2 citations

  reviewOpen accessSenior author

  Sickle cell disease is a hereditary disorder in which the pathophysiology is driven by the aggregation of a mutant (sickle) hemoglobin (HbS). The self-assembly of deoxygenated sickle hemoglobin molecules into ordered fiber structures has consequences extending to the cellular and rheological levels, stiffening red blood cells and inducing pathological flow behavior. This review explores the current understanding of the molecular processes involved in the polymerization of hemoglobin in sickle cell disease and how the molecular phase transition creates quantifiable changes at the cellular and rheological scale, as well as, identifying knowledge gaps in the field that would improve our understanding of the disease and further improve treatment and management of the disease.

  PublisherOA PDFDOI

Recent grants

• Developing a multiscale understanding of biophysical processes in sickle cell disease

  NIH · $4.6M · 2017–2025

• NIH Grant R56HL132906

  NIH · $402k · 2017

• Carcinoma Cell Hyaluronan as a Therapeutic Target in Metastasis

  NIH · $363k · 2016–2019

• Collaborative Research: High-throughput microliver platform for drug toxicity screening

  NSF · $300k · 2017–2021

• Dissecting the origins of fetal hemoglobin modulation of sickle cell vaso-occlusion

  NIH · $435k · 2016–2019

Frequent coauthors

• John M. Higgins

  Center for Systems Biology

  49 shared

• Sangeeta N. Bhatia

  43 shared

• Roger V. Lloyd

  University of Memphis

  35 shared

• Alexandra L. Crampton

  University of Minnesota

  30 shared

• James B. McCarthy

  University of Minnesota

  24 shared

• Katherine A. Cummins

  University of Minnesota

  23 shared

• A. N. Cleland

  22 shared

• Wilbur A. Lam

  Emory University

  21 shared

Labs

• Tissue Mechanics LaboratoryPI

Education

• Ph.D., Physics

  University of California, Santa Barbara

  2007

• B.S., Physics

  North Carolina State University

  2001