Stuart Campbell

Associate Professor Tenure

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Rational engineering of lung alveolar epitheliumLeiby K, Yuan Y, Ng R, Raredon M, Adams T, Baevova P, Greaney A, Hirschi K, Campbell S, Kaminski N, Herzog E, Niklason L. Rational engineering of lung alveolar epithelium. Npj Regenerative Medicine 2023, 8: 22. PMID: 37117221, PMCID: PMC10147714, DOI: 10.1038/s41536-023-00295-2.
Multi-scale modeling will unravel connections between sarcomeric mutations and cardiomyopathiesCampbell S, Moore J, Rynkiewicz M, Lehman W. Multi-scale modeling will unravel connections between sarcomeric mutations and cardiomyopathies. Journal Of Molecular And Cellular Cardiology Plus 2023, 3: 100025. DOI: 10.1016/j.jmccpl.2022.100025.
Cyclical shortening promotes maturation of atrial engineered heart tissuesGokhan I, Campbell S. Cyclical shortening promotes maturation of atrial engineered heart tissues. Biophysical Journal 2023, 122: 454a. DOI: 10.1016/j.bpj.2022.11.2444.
Predictive genotype-phenotype correlation of four tropomyosin-1 variants of unknown significanceFirlar I, Rynkiewicz M, Creso J, Liu D, Moore J, Lehman W, Campbell S. Predictive genotype-phenotype correlation of four tropomyosin-1 variants of unknown significance. Biophysical Journal 2023, 122: 121a. DOI: 10.1016/j.bpj.2022.11.825.
Mechanisms of pathogenicity in the hypertrophic cardiomyopathy-associated TPM1 variant S215LHalder S, Rynkiewicz M, Creso J, Sewanan L, Howland L, Moore J, Lehman W, Campbell S. Mechanisms of pathogenicity in the hypertrophic cardiomyopathy-associated TPM1 variant S215L. PNAS Nexus 2023, 2: pgad011. PMID: 36896133, PMCID: PMC9991458, DOI: 10.1093/pnasnexus/pgad011.
Increased length-dependent activation of human engineered heart tissue after chronic α1A-adrenergic agonist treatment: testing a novel heart failure therapyRupert C, López J, Cortez-Toledo E, De la Cruz Cabrera O, Chesler N, Simpson P, Campbell S, Baker A. Increased length-dependent activation of human engineered heart tissue after chronic α1A-adrenergic agonist treatment: testing a novel heart failure therapy. AJP Heart And Circulatory Physiology 2023, 324: h293-h304. PMID: 36637971, PMCID: PMC9886349, DOI: 10.1152/ajpheart.00279.2022.
Signaling network model of cardiomyocyte morphological changes in familial cardiomyopathyKhalilimeybodi A, Riaz M, Campbell S, Omens J, McCulloch A, Qyang Y, Saucerman J. Signaling network model of cardiomyocyte morphological changes in familial cardiomyopathy. Journal Of Molecular And Cellular Cardiology 2022, 174: 1-14. PMID: 36370475, PMCID: PMC10230857, DOI: 10.1016/j.yjmcc.2022.10.006.
Abstract 15506: Optical Mapping in Atrial Engineered Heart Tissues Reveals Proarrhythmic Potential of the Anti-AF Agent VernakalantGokhan I, Frimpong A, Cacheux M, Campbell S, Akar F. Abstract 15506: Optical Mapping in Atrial Engineered Heart Tissues Reveals Proarrhythmic Potential of the Anti-AF Agent Vernakalant. Circulation 2022, 146: a15506-a15506. DOI: 10.1161/circ.146.suppl_1.15506.
Humanized Dsp ACM Mouse Model Displays Stress-Induced Cardiac Electrical and Structural PhenotypesStevens TL, Manring HR, Wallace MJ, Argall A, Dew T, Papaioannou P, Antwi-Boasiako S, Xu X, Campbell SG, Akar FG, Borzok MA, Hund TJ, Mohler PJ, Koenig SN, El Refaey M. Humanized Dsp ACM Mouse Model Displays Stress-Induced Cardiac Electrical and Structural Phenotypes. Cells 2022, 11: 3049. PMID: 36231013, PMCID: PMC9562631, DOI: 10.3390/cells11193049.
Physiological calcium combined with electrical pacing accelerates maturation of human engineered heart tissueShen S, Sewanan LR, Shao S, Halder SS, Stankey P, Li X, Campbell SG. Physiological calcium combined with electrical pacing accelerates maturation of human engineered heart tissue. Stem Cell Reports 2022, 17: 2037-2049. PMID: 35931080, PMCID: PMC9481907, DOI: 10.1016/j.stemcr.2022.07.006.
Muscle LIM Protein Force-Sensing Mediates Sarcomeric Biomechanical Signaling in Human Familial Hypertrophic CardiomyopathyRiaz M, Park J, Sewanan LR, Ren Y, Schwan J, Das SK, Pomianowski PT, Huang Y, Ellis MW, Luo J, Liu J, Song L, Chen IP, Qiu C, Yazawa M, Tellides G, Hwa J, Young LH, Yang L, Marboe CC, Jacoby DL, Campbell SG, Qyang Y. Muscle LIM Protein Force-Sensing Mediates Sarcomeric Biomechanical Signaling in Human Familial Hypertrophic Cardiomyopathy. Circulation 2022, 145: 1238-1253. PMID: 35384713, PMCID: PMC9109819, DOI: 10.1161/circulationaha.121.056265.
GSK-3β Localizes to the Cardiac Z-Disc to Maintain Length Dependent ActivationStachowski-Doll MJ, Papadaki M, Martin TG, Ma W, Gong HM, Shao S, Shen S, Muntu NA, Kumar M, Perez E, Martin JL, Moravec CS, Sadayappan S, Campbell SG, Irving T, Kirk JA. GSK-3β Localizes to the Cardiac Z-Disc to Maintain Length Dependent Activation. Circulation Research 2022, 130: 871-886. PMID: 35168370, PMCID: PMC8930626, DOI: 10.1161/circresaha.121.319491.
Increased length-dependent activation of human engineered heart tissue after chronic treatment with alpha-1A-adrenergic agonistRupert C, Cortez-Toledo E, Lopez J, Chesler N, Simpson P, Campbell S, Baker A. Increased length-dependent activation of human engineered heart tissue after chronic treatment with alpha-1A-adrenergic agonist. Biophysical Journal 2022, 121: 397a-398a. DOI: 10.1016/j.bpj.2021.11.785.
Glycogen synthase kinase 3β localizes to the Z-disc to maintain length dependent activationStachowski M, Papadaki M, Martin T, Ma W, Gong H, Shao S, Shen S, Muntu N, Martin J, Moravec C, Campbell S, Irving T, Kirk J. Glycogen synthase kinase 3β localizes to the Z-disc to maintain length dependent activation. Biophysical Journal 2022, 121: 395a. DOI: 10.1016/j.bpj.2021.11.774.
Multiscale characterization of four Tropomyosin-1 variants of unknown significanceRynkiewicz M, Creso J, Li X, Sewanan L, Liu D, Barry M, Moore J, Lehman W, Campbell S. Multiscale characterization of four Tropomyosin-1 variants of unknown significance. Biophysical Journal 2022, 121: 257a. DOI: 10.1016/j.bpj.2021.11.1470.
DCM and HCM mutations to TPM1 differentially alter contractile behavior and gene expression profiles in engineered heart tissuesHalder S, Sewanan L, Li X, Campbell S. DCM and HCM mutations to TPM1 differentially alter contractile behavior and gene expression profiles in engineered heart tissues. Biophysical Journal 2022, 121: 108a. DOI: 10.1016/j.bpj.2021.11.2185.
Engineered Lung Tissues Prepared from Decellularized Lung SlicesLeiby K, Ng R, Campbell S, Niklason L. Engineered Lung Tissues Prepared from Decellularized Lung Slices. Journal Of Visualized Experiments 2022 DOI: 10.3791/63151-v.
Abstract P459: Mavacamten And Danicamtiv Reverse Respective Contractile Abnormalities In Engineered Heart Tissue Models Of Hypertrophic And Dilated CardiomyopathyHalder S, Sewanan L, Rynkiewicz M, Moore J, Lehman W, Campbell S. Abstract P459: Mavacamten And Danicamtiv Reverse Respective Contractile Abnormalities In Engineered Heart Tissue Models Of Hypertrophic And Dilated Cardiomyopathy. Circulation Research 2021, 129: ap459-ap459. DOI: 10.1161/res.129.suppl_1.p459.
Abstract LB210: MicroRNA function is malleable and can be governed by target gene expression levelsSvoronos A, Campbell S, Engelman D. Abstract LB210: MicroRNA function is malleable and can be governed by target gene expression levels. Cancer Research 2021, 81: lb210-lb210. DOI: 10.1158/1538-7445.am2021-lb210.
DANICAMTIV AUGMENTS SYSTOLIC FUNCTION WHILE PRESERVING DIASTOLIC FUNCTION COMPARED TO OMECAMTIV MECARBIL IN HUMAN ENGINEERED MYOCARDIUMSewanan L, Shen S, Campbell S. DANICAMTIV AUGMENTS SYSTOLIC FUNCTION WHILE PRESERVING DIASTOLIC FUNCTION COMPARED TO OMECAMTIV MECARBIL IN HUMAN ENGINEERED MYOCARDIUM. Journal Of The American College Of Cardiology 2021, 77: 577. DOI: 10.1016/s0735-1097(21)01936-7.
MAVACAMTEN PRESERVED LENGTH-DEPENDENT CONTRACTILITY AND IMPROVED DIASTOLIC FUNCTION IN HUMAN ENGINEERED MYOCARDIUMSewanan L, Shen S, Campbell S. MAVACAMTEN PRESERVED LENGTH-DEPENDENT CONTRACTILITY AND IMPROVED DIASTOLIC FUNCTION IN HUMAN ENGINEERED MYOCARDIUM. Journal Of The American College Of Cardiology 2021, 77: 536. DOI: 10.1016/s0735-1097(21)01895-7.
Investigating the Effect of HCM-Associated TPM1 Mutation S215L on Human Engineered Heart TissuesHalder S, Sewanan L, Rynkiewicz M, Howland L, Moore J, Lehman W, Campbell S. Investigating the Effect of HCM-Associated TPM1 Mutation S215L on Human Engineered Heart Tissues. Biophysical Journal 2021, 120: 254a. DOI: 10.1016/j.bpj.2020.11.1645.
Abstract MP103: Methylglyoxal Modifications on Myofilament Proteins Caused by Diabetes Block Heart Failure Drug Targets Through Changing Tropomyosin PositionPapadaki M, Kampaengsri T, Barrick S, Campbell S, Greenberg M, Kirk J. Abstract MP103: Methylglyoxal Modifications on Myofilament Proteins Caused by Diabetes Block Heart Failure Drug Targets Through Changing Tropomyosin Position. Circulation Research 2020, 127 DOI: 10.1161/res.127.suppl_1.mp103.
Mechanical Signatures Driving HCM and DCM Revealed in Human Engineered Heart Tissues Expressing Cardiomyopathy-associated Variants in TPM1Sewanan L, Campbell S. Mechanical Signatures Driving HCM and DCM Revealed in Human Engineered Heart Tissues Expressing Cardiomyopathy-associated Variants in TPM1. Biophysical Journal 2020, 118: 8a. DOI: 10.1016/j.bpj.2019.11.234.
Molecular Mechanisms and Therapeutic Approaches of Myofilament Glycation as a Result of DiabetesPapadaki M, Kampaengsri T, Bonomo R, White C, Aubert V, Aubert G, Campbell S, Kirk J. Molecular Mechanisms and Therapeutic Approaches of Myofilament Glycation as a Result of Diabetes. Biophysical Journal 2020, 118: 327a. DOI: 10.1016/j.bpj.2019.11.1833.
Abstract 525: In vitro Reverse Remodeling After Mechanical Unloading With Engineered Heart TissueShen S, Sewanan L, Campbell S. Abstract 525: In vitro Reverse Remodeling After Mechanical Unloading With Engineered Heart Tissue. Circulation Research 2019, 125 DOI: 10.1161/res.125.suppl_1.525.
Abstract 479: Cardiomyopathy Phenotypes Observed in Human Engineered Heart Tissue Depend on Functional MaturationSewanan L, Shen S, Ng R, Li X, Campbell S. Abstract 479: Cardiomyopathy Phenotypes Observed in Human Engineered Heart Tissue Depend on Functional Maturation. Circulation Research 2019, 125 DOI: 10.1161/res.125.suppl_1.479.
Tissue-Engineered Stem Cell Models of Cardiovascular DiseasesAnderson C, Luo J, Sewanan L, Kural M, Riaz M, Park J, Huang Y, Niklason L, Campbell S, Qyang Y. Tissue-Engineered Stem Cell Models of Cardiovascular Diseases. 2019, 1-18. DOI: 10.1007/978-3-030-20047-3_1.
A New Twist on the Mechanism of Mutation-Induced Tropomyosin DysfunctionRynkiewicz M, Moore J, Campbell S, Lehman W. A New Twist on the Mechanism of Mutation-Induced Tropomyosin Dysfunction. Biophysical Journal 2019, 116: 552a. DOI: 10.1016/j.bpj.2018.11.2966.
Defining a Unifying Mechanism for Select Cardiomyopathy-Linked Variants of DesmoplakinManring H, Ng R, Albertelli T, Dew T, Stevens T, Kilic A, Janssen P, Wright N, Campbell S, Ackermann M. Defining a Unifying Mechanism for Select Cardiomyopathy-Linked Variants of Desmoplakin. Biophysical Journal 2019, 116: 467a. DOI: 10.1016/j.bpj.2018.11.2522.
Power-Load Characteristics of Human-Derived Engineered Heart Tissue in Response to Cardiomyopathy Mutations and Myosin-Targeted DrugsSewanan L, Campbell S. Power-Load Characteristics of Human-Derived Engineered Heart Tissue in Response to Cardiomyopathy Mutations and Myosin-Targeted Drugs. Biophysical Journal 2019, 116: 262a. DOI: 10.1016/j.bpj.2018.11.1425.
Towards the Inhibition of Calpain-Dependent Desmoplakin Cleavage in Arrhythmogenic CardiomyopathiesAlbertelli T, Ott K, Manring H, Campbell S, Borzok M, Wright N. Towards the Inhibition of Calpain-Dependent Desmoplakin Cleavage in Arrhythmogenic Cardiomyopathies. Biophysical Journal 2019, 116: 187a. DOI: 10.1016/j.bpj.2018.11.1039.
Classifying of Arrhythmogenic Cardiomyopathy-Linked Desmoplakin Variants through Molecular Mechanisms of PathogenicityStevens T, Manring H, Albertelli T, Ng R, Wright N, Campbell S, Ackermann M. Classifying of Arrhythmogenic Cardiomyopathy-Linked Desmoplakin Variants through Molecular Mechanisms of Pathogenicity. Biophysical Journal 2019, 116: 183a. DOI: 10.1016/j.bpj.2018.11.1018.
Use of Human Cells and Heart Muscle Tissue Patches as Therapeutics for Heart DiseasesBatty L, Ellis M, Anderson C, Luo J, Riaz M, Park J, Das S, Huang Y, Jacoby D, Campbell S, Qyang Y. Use of Human Cells and Heart Muscle Tissue Patches as Therapeutics for Heart Diseases. 2019 DOI: 10.1016/b978-0-12-801238-3.65542-3.
Abstract 375: Defining a Unifying Mechanism for Select Cardiomyopathy-Linked Variants of DesmoplakinAckermann M, Manring H, Ng R, Albertelli T, Jyothi Bobbili P, Stevens T, Jacoby D, Janssen P, Kilic A, Wright N, Wright N, Qyang Y, Campbell S. Abstract 375: Defining a Unifying Mechanism for Select Cardiomyopathy-Linked Variants of Desmoplakin. Circulation Research 2018, 123 DOI: 10.1161/res.123.suppl_1.375.
Pathogenic Mechanisms of the Cardiomyopathy-Associated Alpha-Tropomyosin Variant E192K as Revealed by Multiscale Modeling and ExperimentsSewanan L, Park J, Rynkiewicz M, Hollenberg S, Papoutsidakis N, Jacoby D, Moore J, Lehman W, Qyang Y, Campbell S. Pathogenic Mechanisms of the Cardiomyopathy-Associated Alpha-Tropomyosin Variant E192K as Revealed by Multiscale Modeling and Experiments. Biophysical Journal 2018, 114: 495a. DOI: 10.1016/j.bpj.2017.11.2714.
Engineered Heart Tissues Expressing Mutant Desmoplakin Exhibit Altered Twitch KineticsNg R, Li X, Manring H, Park J, Luo J, Jacoby D, Ackermann M, Campbell S. Engineered Heart Tissues Expressing Mutant Desmoplakin Exhibit Altered Twitch Kinetics. Biophysical Journal 2018, 114: 550a. DOI: 10.1016/j.bpj.2017.11.3003.
Defining a Unifying Mechanism for Select Cariomyopathy-Linked Variants of DesmoplakinManring H, Ng R, Albertelli T, Bobbili P, Carter O, Stevens T, Jacoby D, Janssen P, Kilic A, Wright N, Campbell S, Ackermann M. Defining a Unifying Mechanism for Select Cariomyopathy-Linked Variants of Desmoplakin. Biophysical Journal 2018, 114: 500a. DOI: 10.1016/j.bpj.2017.11.2734.
Desmoplakin AC Mutations' Affect on Structure and Stability of Its NH2-TerminusAlbertelli T, Manring H, Campbell S, Ackermann M, Wright N. Desmoplakin AC Mutations' Affect on Structure and Stability of Its NH2-Terminus. Biophysical Journal 2018, 114: 48a. DOI: 10.1016/j.bpj.2017.11.315.
Engineering-Based Approaches to Understanding, Diagnosing, and Treating Inherited CardiomyopathiesCampbell S. Engineering-Based Approaches to Understanding, Diagnosing, and Treating Inherited Cardiomyopathies. Biophysical Journal 2018, 114: 1a. DOI: 10.1016/j.bpj.2017.11.030.
Force-Dependent Recruitment of Cross-Bridges from the Myosin Off-State can Contribute to Length-Dependent ActivationCampbell K, Janssen P, Campbell S. Force-Dependent Recruitment of Cross-Bridges from the Myosin Off-State can Contribute to Length-Dependent Activation. Biophysical Journal 2017, 112: 119a-120a. DOI: 10.1016/j.bpj.2016.11.671.
Gap Junction Remodeling in a Novel Engineered Heart Tissue System Cultured under Point StimulationClark J, Ng R, Campbell S. Gap Junction Remodeling in a Novel Engineered Heart Tissue System Cultured under Point Stimulation. Biophysical Journal 2017, 112: 307a. DOI: 10.1016/j.bpj.2016.11.1659.
Investigating the Phenotype of Cardiomyopathy-Associated Alpha-Tropomyosin E192K Mutation in Patient-Derived Engineered Heart TissueSewanan L, Park J, Ren Y, Urdaneta A, Rynkiewicz M, Moore J, Lehman W, Jacoby D, Qyang Y, Campbell S. Investigating the Phenotype of Cardiomyopathy-Associated Alpha-Tropomyosin E192K Mutation in Patient-Derived Engineered Heart Tissue. Biophysical Journal 2017, 112: 260a. DOI: 10.1016/j.bpj.2016.11.1412.
Characterization of a Truncated Cardiac Myosin-Binding Protein C mutation using Patient-Derived Engineered Heart Tissue and Computational ModelingSchwan J, Ren Y, Jacoby D, Qyang Y, Campbell S. Characterization of a Truncated Cardiac Myosin-Binding Protein C mutation using Patient-Derived Engineered Heart Tissue and Computational Modeling. Biophysical Journal 2017, 112: 258a. DOI: 10.1016/j.bpj.2016.11.1404.
Assuming that Myosin-Binding Protein C Interacts with Both Myosin and Actin Can Explain its Role in Skinned Fiber MechanicsSchwan J, Wang C, Campbell S. Assuming that Myosin-Binding Protein C Interacts with Both Myosin and Actin Can Explain its Role in Skinned Fiber Mechanics. Biophysical Journal 2016, 110: 299a-300a. DOI: 10.1016/j.bpj.2015.11.1613.
Modeling Predicts Non-Monotonic Dependence of Myofilament Ca2+ Sensitivity on Tropomyosin StiffnessSewanan L, Campbell S. Modeling Predicts Non-Monotonic Dependence of Myofilament Ca2+ Sensitivity on Tropomyosin Stiffness. Biophysical Journal 2016, 110: 464a. DOI: 10.1016/j.bpj.2015.11.2483.
Polycystin 2 expression alters calcium‐contraction couplingKuo I, Kwaczala A, Nguyen L, Campbell S, Ehrlich B. Polycystin 2 expression alters calcium‐contraction coupling. The FASEB Journal 2015, 29 DOI: 10.1096/fasebj.29.1_supplement.946.1.
Modulation of Cardiac Twitch Dynamics by the Troponin I Inhibitory RegionAboelkassem Y, Bonilla J, Campbell S. Modulation of Cardiac Twitch Dynamics by the Troponin I Inhibitory Region. Biophysical Journal 2015, 108: 201a. DOI: 10.1016/j.bpj.2014.11.1111.
Optogenetic Manipulation of Ca2+ Transients and Contraction in a Mathematical Model of Cardiomyocyte FunctionAboelkassem Y, Campbell S. Optogenetic Manipulation of Ca2+ Transients and Contraction in a Mathematical Model of Cardiomyocyte Function. Biophysical Journal 2015, 108: 268a. DOI: 10.1016/j.bpj.2014.11.1476.
Decreased Polycystin 2 Expression Alters Calcium-Contraction Coupling and Changes Beta-Adrenergic Signaling PathwaysKuo I, Kwaczala A, Nguyen L, Campbell S, Ehrlich B. Decreased Polycystin 2 Expression Alters Calcium-Contraction Coupling and Changes Beta-Adrenergic Signaling Pathways. Biophysical Journal 2015, 108: 177a. DOI: 10.1016/j.bpj.2014.11.980.

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