Kanika Jain, PhD
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Associate Research Scientist
Biography
Dr. Jain obtained her PhD in Life Sciences (Cardiovascular Biology) from India. Her PhD work focused on identifying the effect of high altitude hypoxia on rodent heart and further investigating the role of the Proteostasis network in the cardiovascular system. Her work has contributed to understanding the mechanism behind the differential hypoxic tolerance and has published several research articles during her PhD.
Currently her projects at the Hwa lab at Yale, involve the study of platelets, the anucleate cells in the blood stream. Dr. Jain is doing extensive work on exploring the role of stress induced signaling cascades in the platelets, more specifically in context of protein misfolding and ER Stress. Using a combination of basic and advanced techniques, involving both human and rodent samples, her studies involve a wide range of pathophysiological conditions including Diabetes Mellitus, Aging and Neurodegenerative diseases.
Appointments
Cardiovascular Medicine
Associate Research ScientistPrimary
Other Departments & Organizations
Education & Training
- PhD
- DIPAS, DRDO, Life Sciences (2015)
- MSc
- Jamia Hamdard University, Biochemistry (2009)
Research
Overview
Medical Subject Headings (MeSH)
ORCID
0000-0003-1826-4402- View Lab Website
Hwa Lab
Research at a Glance
Yale Co-Authors
Publications Timeline
Research Interests
Tarun Tyagi, PhD
John Hwa, MD, PhD, FRACP
Jing Du, MD, PhD
Sean Gu, MD/PhD
John Kadado
Kathleen Martin, PhD
Oxidative Stress
Blood Platelets
Cardiovascular Diseases
Protein Folding
Aging
Diabetes Mellitus
Publications
Featured Publications
Unfolded Protein Response Differentially Modulates the Platelet Phenotype
Jain K, Tyagi T, Du J, Hu X, Patell K, Martin KA, Hwa J. Unfolded Protein Response Differentially Modulates the Platelet Phenotype. Circulation Research 2022, 131: 290-307. PMID: 35862006, PMCID: PMC9357223, DOI: 10.1161/circresaha.121.320530.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsUPR pathwayProtein responseMouse plateletsUnfolded protein responseActivation of UPRPlatelet phenotypeTranscriptional regulationGenomic regulationProtein misfoldingAnucleate plateletsProtein aggregationUPR activationPhosphorylation of PLCγ2Chemical chaperonesXBP1 pathwayP38 MAPKPERK pathwayUPRPKCδ activationPlatelet physiologyActivation pathwayPathwayPhenotypeIRE1α inhibitionSelective inductionA guide to molecular and functional investigations of platelets to bridge basic and clinical sciences
Tyagi T, Jain K, Gu S, Qiu M, Gu V, Melchinger H, Rinder H, Martin K, Gardiner E, Lee A, Tang W, Hwa J. A guide to molecular and functional investigations of platelets to bridge basic and clinical sciences. Nature Cardiovascular Research 2022, 1: 223-237. PMID: 37502132, PMCID: PMC10373053, DOI: 10.1038/s44161-022-00021-z.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsCitationsAltmetricConceptsVascular smooth muscle cellsPlatelet functional assaysCoronavirus disease 2019Smooth muscle cellsImmune cellsImmune regulationVascular remodelingDisease 2019Pathophysiological processesTranslational relevancePatient diagnosisFlow cytometryMuscle cellsPlatelet biologyFunctional assaysPlatelet investigationsHomeostatic processesPlateletsPhenotypic heterogeneityFunctional stateClinical scienceCellsAdditional roleThrombosisSuch diverse functionsThrombocytopathy and endotheliopathy: crucial contributors to COVID-19 thromboinflammation
Gu SX, Tyagi T, Jain K, Gu VW, Lee SH, Hwa JM, Kwan JM, Krause DS, Lee AI, Halene S, Martin KA, Chun HJ, Hwa J. Thrombocytopathy and endotheliopathy: crucial contributors to COVID-19 thromboinflammation. Nature Reviews Cardiology 2020, 18: 194-209. PMID: 33214651, PMCID: PMC7675396, DOI: 10.1038/s41569-020-00469-1.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAdministration, InhalationAnticoagulantsBlood Coagulation DisordersBlood Platelet DisordersCOVID-19COVID-19 Drug TreatmentEndothelium, VascularEndothelium-Dependent Relaxing FactorsEpoprostenolHeart Disease Risk FactorsHumansIloprostInflammationNitric OxidePlatelet Aggregation InhibitorsSARS-CoV-2Systemic Inflammatory Response SyndromeThrombosisThrombotic MicroangiopathiesVascular DiseasesVasodilator AgentsVenous ThromboembolismConceptsCardiovascular risk factorsRisk factorsCOVID-19Severe acute respiratory syndrome coronavirus 2Pre-existing cardiovascular diseaseAcute respiratory syndrome coronavirus 2Traditional cardiovascular risk factorsAcute respiratory distress syndromeRespiratory syndrome coronavirus 2Respiratory distress syndromeManagement of patientsSyndrome coronavirus 2COVID-19 pathologyCoronavirus disease 2019Potential therapeutic strategyCytokine stormEndothelial dysfunctionThrombotic complicationsDistress syndromeExcessive inflammationCoronavirus 2Severe outcomesAdvanced ageCardiovascular diseaseDisease 2019Age associated non-linear regulation of redox homeostasis in the anucleate platelet: Implications for CVD risk patients
Jain K, Tyagi T, Patell K, Xie Y, Kadado AJ, Lee SH, Yarovinsky T, Du J, Hwang J, Martin KA, Testani J, Ionescu CN, Hwa J. Age associated non-linear regulation of redox homeostasis in the anucleate platelet: Implications for CVD risk patients. EBioMedicine 2019, 44: 28-40. PMID: 31130473, PMCID: PMC6604369, DOI: 10.1016/j.ebiom.2019.05.022.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAdaptation, PhysiologicalAge FactorsAgedAged, 80 and overAgingAnimalsAntioxidantsApoptosisBiomarkersBlood PlateletsCardiovascular DiseasesComorbidityDisease Models, AnimalFemaleHomeostasisHumansMaleMiceMiddle AgedOxidation-ReductionOxidative StressPlatelet ActivationPlatelet AdhesivenessReactive Oxygen SpeciesRisk AssessmentRisk FactorsConceptsRisk patientsMouse studiesPlatelet phenotypeMajor adverse cardiovascular eventsHigh cardiovascular risk patientsAdaptive increaseAdverse cardiovascular eventsCentral pathophysiological roleCVD risk patientsCardiovascular risk patientsAggressive antiplatelet therapyEffect of comorbidityAge group 40Young healthy subjectsAntiplatelet therapyCardiovascular eventsYear age cohortAdvanced ageCVD patientsGroup 40Healthy subjectsPathophysiological roleElderly populationCardiovascular pathologyPatientsPlatelet-derived TLT-1 promotes tumor progression by suppressing CD8+ T cells
Tyagi T, Jain K, Yarovinsky TO, Chiorazzi M, Du J, Castro C, Griffin J, Korde A, Martin KA, Takyar SS, Flavell RA, Patel AA, Hwa J. Platelet-derived TLT-1 promotes tumor progression by suppressing CD8+ T cells. Journal Of Experimental Medicine 2022, 220: e20212218. PMID: 36305874, PMCID: PMC9814191, DOI: 10.1084/jem.20212218.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsCD8 T cellsT cellsTLT-1Non-small cell lung cancer patientsCell lung cancer patientsTREM-like transcript-1Tumor immunosuppressive mechanismsT cell suppressionLung cancer patientsPatient T cellsNF-κB pathwayPatient-derived tumorsDistinct activation phenotypesNSCLC patientsImmunosuppressive mechanismsSyngeneic tumorsHumanized miceImmunoregulatory rolePrognostic significanceImmunocompetent miceCancer patientsCell suppressionActivation phenotypeReduced tumorTumor growth
2023
Lipid remodeling in megakaryocyte differentiation and platelet biogenesis
Jain K, Tyagi T, Hwa J. Lipid remodeling in megakaryocyte differentiation and platelet biogenesis. Nature Cardiovascular Research 2023, 2: 803-804. PMID: 37736249, PMCID: PMC10512809, DOI: 10.1038/s44161-023-00324-9.Peer-Reviewed Original ResearchCitationsAltmetricSOD2 in platelets: with age comes responsibility
Jain K, Gu S, Hwa J. SOD2 in platelets: with age comes responsibility. Journal Of Thrombosis And Haemostasis 2023, 21: 1077-1081. PMID: 36716965, DOI: 10.1016/j.jtha.2023.01.016.Peer-Reviewed Original Research
2022
High Altitude Induced Thrombosis: Challenges and Recent Advancements in Pathogenesis and Management
Tyagi T, Jain K. High Altitude Induced Thrombosis: Challenges and Recent Advancements in Pathogenesis and Management. 2022, 85-101. DOI: 10.1007/978-981-19-1008-1_6.ChaptersConceptsMolecular pathogenesisAvailable treatment optionsBlood clot formationPulmonary embolismVenous thrombosisTreatment optionsClinical managementRisk factorsAnimal studiesHigh-altitude hypoxic environmentClot formationSerious disorderPathogenesisThrombosisHypoxic environmentVTEDisordersNumber of humanEmbolismA guide to molecular and functional investigations of platelets to bridge basic and clinical sciences
Tyagi, T., Jain, K., Gu, S.X. et al. A guide to molecular and functional investigations of platelets to bridge basic and clinical sciences. Nat Cardiovasc Res 1, 223–237 (2022). https://doi.org/10.1038/s44161-022-00021-zPeer-Reviewed Original Research
2021
Low-dose Aspirin prevents hypertension and cardiac fibrosis when thromboxane A2 is unrestrained
D'Agostino I, Tacconelli S, Bruno A, Contursi A, Mucci L, Hu X, Xie Y, Chakraborty R, Jain K, Sacco A, Zucchelli M, Landolfi R, Dovizio M, Falcone L, Ballerini P, Hwa J, Patrignani P. Low-dose Aspirin prevents hypertension and cardiac fibrosis when thromboxane A2 is unrestrained. Pharmacological Research 2021, 170: 105744. PMID: 34182131, DOI: 10.1016/j.phrs.2021.105744.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsMeSH KeywordsAdultAnimalsAntifibrotic AgentsAntihypertensive AgentsAspirinBiomarkersBlood PlateletsBlood PressureCardiomyopathiesCase-Control StudiesCells, CulturedDisease Models, AnimalEssential HypertensionFemaleFibrosisHumansMaleMice, Inbred C57BLMice, KnockoutMiddle AgedMyocytes, CardiacMyofibroblastsPlatelet Aggregation InhibitorsReceptors, EpoprostenolReceptors, ThromboxaneThromboxane A2ConceptsProfibrotic gene expressionEnhanced blood pressureBlood pressureCardiac fibrosisPlatelet TXAHypertensive patientsOverload-induced cardiac fibrosisLow-dose aspirin administrationEarly cardiac fibrosisPlatelet-derived thromboxaneLow-dose aspirinEssential hypertensive patientsEssential hypertension patientsHigh-salt dietSalt-sensitive hypertensionCardiac collagen depositionNumber of myofibroblastsSelective inhibitionGene expressionPrevents hypertensionTP overexpressionUrinary TXMAspirin administrationHypertensive miceAspirin treatment
Academic Achievements and Community Involvement
activity Blood
Journal ServiceReviewerDetails2022 - Presentactivity EMBO Molecular Medicine
Journal ServiceReviewerDetails2022 - Presentactivity Pharmacological Research
Journal ServiceReviewerDetails2020 - Presentactivity Oxidative Medicine and Cellular Longevity
Journal ServiceReviewerDetails2020 - Presentactivity Expert Reviews in Molecular Medicine
Journal ServiceReviewerDetails2020 - Present
Links & Media
Media
- Confocal microscopy image of platelets (green) from patients with Type II Diabetes Mellitus stained for UPR markers , GRP78 (red) and IRE (blue). Image from Jain et al. 2022, Circ Res (10.1161/CIRCRESAHA.121.320530 )
- Figure from Jain et al. Circ Res 2022 (10.1161/CIRCRESAHA.121.320530 )
- Platelet phenotype differs distinctly with age and is likely due to the age associated adaptive changes in platelet antioxidant levels.
News
- January 09, 2024
Recap & Reflections: Vascular Biology & Therapeutics Program & Cardiovascular Research Center 2023 Retreat
- December 07, 2023
Decoding Female-Specific Mechanisms in Cardiovascular Disease: A Captivating Conversation with Dr. Lauren Biwer
- October 26, 2023
Unraveling the Mysteries of type 1 Diabetes and Cardiovascular Disease: A Conversation with Dr. David Alagpulinsa.
- October 16, 2023
Recap & Reflections: the Chalk Talk event