Lauren A. Biwer, PhD
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Assistant Professor
Biography
Dr. Biwer (pronounced Bee-were) became passionate about cardiovascular research as a post-bac student in Dr. Taben Hale’s lab at the University of Arizona College of Medicine in Phoenix. She went on to complete her PhD in Molecular Physiology at the University of Virginia School of Medicine with Dr. Brant Isakson and was part of the Robert M. Berne Cardiovascular Research Center. For her post-doctoral training, Dr. Biwer moved to Boston to Dr. Iris Jaffe’s laboratory in the Molecular Cardiology Research Institute at Tufts Medical Center where she received a K99/R00 grant in 2021.
The Biwer lab investigates blood pressure regulation at the intersection of immunology and vascular function to understand female-specific risk factors for cardiovascular disease. Pre-eclampsia, a common pregnancy complication, significantly increases future cardiovascular risk by unknown mechanisms. Research in the Biwer lab focuses on both pregnancy and the post-partum period. Routine techniques in the lab include primary vascular and immune cell culture, molecular biology/microscopy, flow cytometry, ex-vivo physiology of small and large arteries and in-vivo physiology such as vascular ultrasound and long-term blood pressure measurement.
Appointments
Comparative Medicine
Assistant ProfessorPrimaryObstetrics, Gynecology & Reproductive Sciences
Assistant ProfessorSecondary
Other Departments & Organizations
Education & Training
- Post Doctoral Research Fellow
- Tufts Medical Center- Molecular Cardiology Research Institute (2023)
- PhD
- University of Virginia, Molecular Physiology (2017)
- MS
- University of Virginia, Biological Sciences (2014)
- BS
- Baylor University, Health Science Studies (2009)
Research
Overview
Medical Research Interests
Public Health Interests
ORCID
0000-0003-2788-9025
Research at a Glance
Publications Timeline
Research Interests
Myocytes, Smooth Muscle
Endothelial Cells
Hypertension
Vasodilation
Vasoconstriction
Blood Vessels
Publications
Featured Publications
Prior Exposure to Experimental Preeclampsia Increases Atherosclerotic Plaque Inflammation in Atherogenic Mice—Brief Report
Biwer L, Man J, Camarda N, Carvajal B, Karumanchi S, Jaffe I. Prior Exposure to Experimental Preeclampsia Increases Atherosclerotic Plaque Inflammation in Atherogenic Mice—Brief Report. Arteriosclerosis Thrombosis And Vascular Biology 2024, 44: 946-953. PMID: 38450510, PMCID: PMC10978246, DOI: 10.1161/atvbaha.123.320474.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsAtherosclerotic plaque inflammationLDLr-KO micePlaque inflammationAortic root plaque sizeEvidence of premature atherosclerosisFlow cytometryRisk factorsHistory of preeclampsiaIncreased risk of myocardial infarctionPreexisting risk factorsRisk of myocardial infarctionFed high-fat dietExpression of IGFBP6Mouse atherosclerosis modelHigh-density lipoproteinAortic cytokinesNecrotic core areaPreeclampsia exposureSerum sFlt1Normotensive pregnanciesHigh-fat dietPreeclampsia pregnanciesCD3+T cellsHigh-fat feedingLow-density lipoproteinSmooth Muscle Mineralocorticoid Receptor Promotes Hypertension After Preeclampsia
Biwer L, Lu Q, Ibarrola J, Stepanian A, Man J, Carvajal B, Camarda N, Zsengeller Z, Skurnik G, Seely E, Karumanchi S, Jaffe I. Smooth Muscle Mineralocorticoid Receptor Promotes Hypertension After Preeclampsia. Circulation Research 2023, 132: 674-689. PMID: 36815487, PMCID: PMC10119809, DOI: 10.1161/circresaha.122.321228.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsBlood pressureSMC-MRHypertensive stimuliBP responseSmooth Muscle Cell Mineralocorticoid ReceptorsAngII type 1 receptorType 1 receptor expressionMR transcriptional activityIncreased cardiovascular riskElevated blood pressureEnd-organ damageHigh salt intakeHigh blood pressureRisk of hypertensionType 1 receptorSoluble VEGF receptorAngII infusionPrior preeclampsiaMR antagonismCardiovascular riskNormotensive pregnanciesSalt dietAortic stiffnessSalt intakeOrgan damageA Novel Dual-Function Nitric Oxide Donor Therapy for Preeclampsia—A Proof-of-Principle Study in a Murine Model
Pintye D, Sziva R, Biwer L, Karreci E, Jacas S, Mastyugin M, Török M, Young B, Jagtap P, Southan G, Jaffe I, Zsengellér Z. A Novel Dual-Function Nitric Oxide Donor Therapy for Preeclampsia—A Proof-of-Principle Study in a Murine Model. Antioxidants 2023, 12: 2036. PMID: 38136156, PMCID: PMC10741224, DOI: 10.3390/antiox12122036.Peer-Reviewed Original ResearchCitationsConceptsBlood pressureOxidative stressNitric oxide donor therapyPlasma cystatin C.Plasma nitrate levelsHealthy female miceModel of preeclampsiaNitric oxide bioavailabilityEx vivo treatmentPotential therapeutic effectsReduced oxidative stressNovel therapeutic agentsDays of treatmentAnti-angiogenic responseDonor therapyPlacental damageReduced hypertensionHypertensive disordersSubstantial morbidityFetal pathophysiologyResistance vesselsGlomerular endotheliosisPE symptomsVascular disordersFemale miceMineralocorticoid and Estrogen Receptors in Endothelial Cells Coordinately Regulate Microvascular Function in Obese Female Mice
Biwer L, Carvajal B, Lu Q, Man J, Jaffe I. Mineralocorticoid and Estrogen Receptors in Endothelial Cells Coordinately Regulate Microvascular Function in Obese Female Mice. Hypertension 2021, 77: 2117-2126. PMID: 33934622, PMCID: PMC8119365, DOI: 10.1161/hypertensionaha.120.16911.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsEndothelial calreticulin deletion impairs endothelial function in aged mice
Biwer L, Askew-Page H, Hong K, Milstein J, Johnstone S, Macal E, Good M, Bagher P, Sonkusare S, Isakson B. Endothelial calreticulin deletion impairs endothelial function in aged mice. AJP Heart And Circulatory Physiology 2020, 318: h1041-h1048. PMID: 32196361, PMCID: PMC7346539, DOI: 10.1152/ajpheart.00586.2019.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsVascular functionTauroursodeoxycholic acidMesenteric arteryAged miceCalcium signalsImpaired endothelial-dependent vasodilationThird-order mesenteric arteriesEndothelial cellsEndothelial-dependent vasodilationIncubation of arteriesImpairs endothelial functionSmall resistance arteriesMultifunctional calcium binding proteinER stress inhibitor tauroursodeoxycholic acidWk of ageEndoplasmic reticulum stressPE constrictionEndothelial functionVasodilatory functionResistance arteriesCalcium binding proteinAgonist carbacholClinical trialsMuscarinic stimulationVasodilationLoss of Endothelial FTO Antagonizes Obesity-Induced Metabolic and Vascular Dysfunction
Krüger N, Biwer L, Good M, Ruddiman C, Wolpe A, DeLalio L, Murphy S, Macal E, Ragolia L, Serbulea V, Best A, Leitinger N, Harris T, Sonkusare S, Gödecke A, Isakson B. Loss of Endothelial FTO Antagonizes Obesity-Induced Metabolic and Vascular Dysfunction. Circulation Research 2019, 126: 232-242. PMID: 31801409, PMCID: PMC7007767, DOI: 10.1161/circresaha.119.315531.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsMyogenic toneProstaglandin DResistance arteriesDeficient miceHigh-fat diet-induced glucose intoleranceDiet-induced glucose intoleranceObesity-induced hypertensionImpact of obesityPrevalence of obesityNew treatment optionsDevelopment of obesityHigh-fat dietRegulation of obesityDifferent cell typesCell typesGlucose intoleranceVascular alterationsVascular changesVascular dysfunctionControl miceInsulin resistanceTreatment optionsCardiovascular diseaseObesityArteryNon–Endoplasmic Reticulum–Based Calr (Calreticulin) Can Coordinate Heterocellular Calcium Signaling and Vascular Function
Biwer L, Good M, Hong K, Patel R, Agrawal N, Looft-Wilson R, Sonkusare S, Isakson B. Non–Endoplasmic Reticulum–Based Calr (Calreticulin) Can Coordinate Heterocellular Calcium Signaling and Vascular Function. Arteriosclerosis Thrombosis And Vascular Biology 2017, 38: 120-130. PMID: 29122814, PMCID: PMC5746467, DOI: 10.1161/atvbaha.117.309886.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsThird-order mesenteric arteriesBlood pressureMesenteric arteryVascular functionCalcium signalingIEL holesApplication of CChMyoendothelial junctionsCalcium eventsER calciumSmooth muscle cellsInternal elastic laminaVascular reactivityResistance arteriesSmall arteriesSame arteryKnockout miceArteryΔ miceElastic laminaMuscle cellsEndoplasmic reticulum calciumMiceCALRCalcium signals
2024
Mineralocorticoid Receptors in Vascular Smooth Muscle: Blood Pressure and Beyond
Camarda N, Ibarrola J, Biwer L, Jaffe I. Mineralocorticoid Receptors in Vascular Smooth Muscle: Blood Pressure and Beyond. Hypertension 2024, 81: 1008-1020. PMID: 38426347, PMCID: PMC11023801, DOI: 10.1161/hypertensionaha.123.21358.Peer-Reviewed Original ResearchCitationsAltmetricConceptsSmooth muscle cellsSMC-MRMineralocorticoid receptorBlood pressurePulmonary hypertensionHeart failureVascular calcificationAngiotensin II type 1 receptorRegulation of vasomotor functionVascular smooth muscleMR knockout miceType 1 receptorAortic valve diseaseSystemic blood pressureSMC proliferationConnective tissue growth factorMatrix metallopeptidase-2Heart valve dysfunctionDiverse cardiovascular disordersResponse to hypertensionTissue growth factorIn vitro studiesIn vivo findingsMyogenic toneValve dysfunction
2022
Smooth muscle cell FTO regulates contractile function
Luse M, Krüger N, Good M, Biwer L, Serbulea V, Salamon A, Deaton R, Leitinger N, Gödecke A, Isakson B. Smooth muscle cell FTO regulates contractile function. AJP Heart And Circulatory Physiology 2022, 323: h1212-h1220. PMID: 36306211, PMCID: PMC9678421, DOI: 10.1152/ajpheart.00427.2022.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsSmooth muscle cellsThird-order mesenteric arteriesMuscle cellsObesity genesSmooth muscle contractilityRates of obesityHuman coronary arteriesCardiac myocyte contractilityPlasma reninBlood pressureMesenteric arteryMyogenic toneCoronary arteryFat massContractile functionMyocyte contractilityMuscle contractilityHeart rateSerum response factorMuscle depolarizationMouse body massContractilitySignificant decreaseCell deletionMice
2021
A venous-specific purinergic signaling cascade initiated by Pannexin 1 regulates TNFα-induced increases in endothelial permeability
Maier-Begandt D, Comstra H, Molina S, Krüger N, Ruddiman C, Chen Y, Chen X, Biwer L, Johnstone S, Lohman A, Good M, DeLalio L, Hong K, Bacon H, Yan Z, Sonkusare S, Koval M, Isakson B. A venous-specific purinergic signaling cascade initiated by Pannexin 1 regulates TNFα-induced increases in endothelial permeability. Science Signaling 2021, 14 PMID: 33653920, PMCID: PMC8011850, DOI: 10.1126/scisignal.aba2940.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsRNA expression profilingHydrolysis of ATPPannexin-1 channelsExpression profilingArterial endothelial cellsEndothelial cellsArterial endotheliumVenous endothelial cellsBarrier functionProtein analysisLung vascular permeabilityPannexin-1Claudin compositionBarrier function impairmentProinflammatory cytokine TNFαEndothelial cell barrierTargetable pathwaysMurine veinCecal ligationCell barrierFunction impairmentInflammatory insultLife spanDeficient miceVascular leak
Academic Achievements & Community Involvement
honor Bohmfalk Scholar 2024-2025
Yale School of Medicine AwardYale University School of MedicineDetails04/09/2024honor Poster Presentation Award
National AwardGordon Research Conference on Vascular BiologyDetails01/17/2023United Stateshonor Outstanding Post Doctoral Trainee Finalist
National AwardAmerican Physiological Society Cardiovascular SectionDetails04/25/2022United Stateshonor NIH Pathway to Independence Award (K99/R00)
National AwardNHLBIDetails11/30/2021United Stateshonor Appointment to T32 Training Program in Hypertension
National AwardBrigham and Women's HospitalDetails07/02/2018United States
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Postdoc2024 - Present
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