Yuna Heo

ORCID: 0009-0001-2744-4811
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About
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Research Areas
  • Cell Adhesion Molecules Research
  • Cellular Mechanics and Interactions
  • Caveolin-1 and cellular processes
  • Hippo pathway signaling and YAP/TAZ
  • Tendon Structure and Treatment
  • Knee injuries and reconstruction techniques
  • Sports injuries and prevention
  • Protein Kinase Regulation and GTPase Signaling
  • Nicotinic Acetylcholine Receptors Study
  • Nuclear Structure and Function
  • Bone Tissue Engineering Materials
  • Axon Guidance and Neuronal Signaling
  • Electron Spin Resonance Studies
  • Nitric Oxide and Endothelin Effects
  • Cell Image Analysis Techniques
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Phagocytosis and Immune Regulation
  • Radiopharmaceutical Chemistry and Applications
  • Neuroscience and Neuropharmacology Research

University of Pennsylvania
2024-2025

University at Buffalo, State University of New York
2021-2024

Jacobs (United States)
2024

Meniscus injuries are challenging to treat due the tissue heterogeneity and limited treatment efficacy. Understanding meniscus cell migration, crucial for healing, remains incomplete, especially its zonal dependency. This study explores how epigenetic mechanisms affect migration under inflammation, focusing on healing implications. Distinct histone modifications chromatin dynamics between inner outer cells were observed during emphasizing need consider these differences in repair strategies....

10.1063/5.0239035 article EN cc-by-nc APL Bioengineering 2025-02-20

While advancements in imaging techniques have led to major strides deciphering the human brain, successful interventions are elusive and represent some of most persistent translational gaps medicine. Human restricted CHRFAM7A has been associated with neuropsychiatric disorders.

10.1016/j.ebiom.2023.104725 article EN cc-by-nc-nd EBioMedicine 2023-07-28

ABSTRACT Cell cycle control is a key aspect of numerous physiological and pathological processes. The contribution biophysical cues, such as stiffness or elasticity the underlying extracellular matrix (ECM), critically important in regulating cell progression proliferation. Indeed, increased ECM causes aberrant However, molecular mechanisms that these stiffness-mediated cellular responses remain unclear. Here, we address this gap show good evidence lamellipodin (symbol RAPH1), previously...

10.1242/jcs.257709 article EN Journal of Cell Science 2021-05-25

Vascular dysfunction is a common cause of cardiovascular diseases characterized by the narrowing and stiffening arteries, such as atherosclerosis, restenosis, hypertension. Arterial results from aberrant proliferation vascular smooth muscle cells (VSMCs) their increased synthesis deposition extracellular matrix (ECM) proteins. These, in turn, are modulated arterial stiffness, but mechanism for this not fully understood. We found that survivin an important regulator stiffness-mediated ECM...

10.1063/5.0157549 article EN cc-by APL Bioengineering 2023-10-20

Stiffened arteries are a pathology of atherosclerosis, hypertension, and coronary artery disease key risk factor for cardiovascular events. The increased stiffness triggers phenotypic switch, hypermigration, hyperproliferation vascular smooth muscle cells (VSMCs), leading to neointimal hyperplasia accelerated neointima formation. However, the mechanism underlying this trigger remains unknown. Our analyses whole-transcriptome microarray data from mouse VSMCs cultured on stiff hydrogels...

10.1063/5.0150532 article EN cc-by APL Bioengineering 2023-10-30

Meniscus injuries pose significant challenges in clinical settings, primarily due to the intrinsic heterogeneity of tissue and limited efficacy current treatments. Endogenous cell migration is crucial for healing process, yet regulatory mechanisms meniscus its zonal dependency within are not fully understood. Thus, this study investigates role epigenetic governing under inflammatory conditions, with a focus on their implications injury regeneration. Here, we discovered that proinflammatory...

10.1101/2024.07.22.604178 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-07-23

ABSTRACT Arterial stiffness is a key contributor to cardiovascular diseases, including atherosclerosis, restenosis, and coronary artery disease, it has been characterized be associated with the aberrant migration of vascular smooth muscle cells (VSMCs). However, underlying molecular mechanisms driving VSMC in stiff environments remain incompletely understood. We recently demonstrated that survivin, member inhibitor apoptosis protein family, highly expressed both mouse human VSMCs cultured on...

10.1101/2024.12.11.628062 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-12-12

Abstract Background CHRFAM7A is a human‐restricted gene associated with neuropsychiatric and neurodegenerative disorders. The translated protein incorporates into the α7 nicotinic acetylcholine receptor (α7nAChR) leading to hypomorphic receptor. Mechanistic insight from isogenic iPSC derived neuronal mononuclear cells demonstrated that affects Ca 2+ signaling activates small GTPase Rac1 an actin cytoskeleton gain of function. Fundamental differences in tissue stiffness human rodent brain are...

10.1002/alz.095019 article EN cc-by Alzheimer s & Dementia 2024-12-01

ABSTRACT Vascular dysfunction is a common cause of cardiovascular diseases characterized by the narrowing and stiffening arteries, such as atherosclerosis, restenosis, hypertension. Arterial results from aberrant proliferation vascular smooth muscle cells (VSMCs) their increased synthesis deposition extracellular matrix (ECM) proteins. These, in turn, are modulated arterial stiffness, but mechanism for this not fully understood. We found that survivin (an inhibitor apoptosis) an important...

10.1101/2022.10.24.513582 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2022-10-24

SUMMARY Stiffened arteries are a pathology of atherosclerosis, hypertension, and coronary artery disease key risk factor for cardiovascular events. The increased stiffness triggers the hypermigration hyperproliferation vascular smooth muscle cells (VSMCs), leading to neointimal hyperplasia accelerated neointima formation, but mechanism this trigger is not known. Our analyses whole-transcriptome microarray data sets from mouse VSMCs cultured on stiff hydrogels simulating arterial injured...

10.1101/2022.11.09.515885 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2022-11-10
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