Shaoning Jiang
Research Scientist in PathologyCards
Appointments
Contact Info
About
Titles
Research Scientist in Pathology
Biography
Dr. Jiang completed her PhD degree in Molecular and cellular Pathology at the University of Alabama at Birmingham (UAB) and received postdoctoral training at UAB and University of Oklahoma health Science Center (OUHSC). Before joining Yale Pathology, Dr. Jiang has started her independent research as an assistant professor at OUHSC in the research areas of diabetes and obesity, focusing on epigenetic mechanisms linking inflammation and energy metabolism in the context of developmental origins of obesity and obesity-related metabolic disorders.
Open position:
A postdoctoral Associate position is currently available for a recent NIH R01 funded project studying cell-type specific functions of microRNAs in regulating beige and brown fat adipogenesis and crosstalk of adipose stem cells and macrophages. Please send a Curriculum Vitae, and names / contact information for three references to Dr. Shaoning Jiang (shaoning.jiang@yale.edu).
Appointments
Pathology
Research ScientistPrimary
Other Departments & Organizations
Education & Training
- Postdoc fellow
- University of Oklahoma Health Science Center
- Postdoc fellow
- University of Alabama at Birmingham
- PhD
- University of Alabama at Birmingham, Pathology
- MM
- Peking University Health Science Center, Gastroenterology
- MD
- Peking University Health Science Center, Medicine
Research
Overview
My main research interest has been studying epigenetic mechanisms linking inflammation and energy metabolism in the pathogenesis of diabetes and obesity and related metabolic disorders. Specifically, my research has focused on two main directions:
1) Macrophages, microRNAs, and adipose stem cells crosstalk in the regulation of brown/beige adipogenesis in obesity. This project studies a bone marrow-derived microRNA cluster of miR-130b and miR-301b, which suppresses adipose tissue stem cells beige differentiation and energy metabolism. By in vivo approaches using a global and a macrophage-specific knockout mouse model for miRNA-130b/301b and in vitro culture of bone marrow and adipose stem cells, the goal is to further delineate cell subtype-specific actions and explore therapeutic potential of extracellular vesicle (EV)-mediated miR-130b/301b inhibition in obesity and related metabolic disorders.
2) Epigenetic mechanisms of developmental programming of metabolic diseases in maternal obesity and diabetes. Adverse intrauterine environment, including diabetes and obesity, impacts fetal development and growth and predispose offspring to type 2 diabetes, obesity, and other metabolic diseases later in life, which has been known as “Developmental Origins of Health and Disease (DoHad)”. The overall aim of my research is to better understand the molecular mechanisms of DoHad and explore new therapeutic options for early prevention of metabolic diseases at the time of their origin, focusing on a) Roles of AMP-activated protein kinase (AMPK) and epigenetic pathways in placenta and fetal development and offspring long-term health in response to maternal overnutrition (obesity and diabetes); b) Effects of maternal overnutrition on peroxisomal and mitochondrial programming during fetal development, and how those alterations impact adipose tissue development and offspring obesity and fatty liver diseases later in life.
Research at a Glance
Yale Co-Authors
Publications Timeline
Wenyi Luo, MD, PhD
Publications
2023
1180-P: Impact of Diabetes Exposure In Utero on Mesenchymal Stem Cell Phenotype and Metabolic Function
HAN LEE W, REDLING D, BROOKS O, TEAGUE A, JIANG S, TRYGGESTAD J. 1180-P: Impact of Diabetes Exposure In Utero on Mesenchymal Stem Cell Phenotype and Metabolic Function. Diabetes 2023, 72 DOI: 10.2337/db23-1180-p.Peer-Reviewed Original ResearchConceptsControl MSCsExposure to diabetesUmbilical cord Wharton's jellyStem cell phenotypeAbsence of CD34Fetal programming eventsIsotype-control antibodyPresence of CD105Maximal respirationMesenchymal stem cell phenotypeCapacity of MSCsDiabetes exposureCharacteristics of MSCsFetal tissuesUteroWharton's jellyDiabetic milieuExposure to DMCell phenotypeMSC abilityPassage 4Adipogenic capacityEnergy expenditureMetabolic characteristicsCD13AMPK Regulates DNA Methylation of PGC-1α and Myogenic Differentiation in Human Mesenchymal Stem Cells
Wu J, Gulati S, Teague A, Kim Y, Tryggestad J, Jiang S. AMPK Regulates DNA Methylation of PGC-1α and Myogenic Differentiation in Human Mesenchymal Stem Cells. Stem Cells And Development 2023, 32: 131-139. PMID: 36594575, PMCID: PMC9986020, DOI: 10.1089/scd.2022.0226.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsActivation of AMP-activated protein kinasePGC-1a expressionMitochondrial programDNA methylationCompound CMitochondrial biogenesisAMPK activationActivation of AMPKAMP-activated protein kinaseAMPK inhibitor compound CInhibition of DNA methylationRegulator of mitochondrial biogenesisRegulate mitochondrial biogenesisPGC-1aInhibitor compound CPromoter methylationIncreased mitochondrial functionRegulation of energy metabolismMitochondrial DNAEpigenetic landscapeDNA demethylationMtDNA abundanceMyogenic differentiationEpigenetic regulationProtein kinase
2022
miR-130b/301b Is a Negative Regulator of Beige Adipogenesis and Energy Metabolism In Vitro and In Vivo.
Luo W, Kim Y, Jensen M, Herlea-Pana O, Wang W, Rudolph M, Friedman J, Chernausek S, Jiang S. miR-130b/301b Is a Negative Regulator of Beige Adipogenesis and Energy Metabolism In Vitro and In Vivo. Diabetes 2022, 71: 2360-2371. PMID: 36001751, PMCID: PMC9630090, DOI: 10.2337/db22-0205.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsBeige adipogenesisMiR-301bMiR-130bPeroxisome proliferator-activated receptor γ coactivator 1αProliferator-activated receptor γ coactivator 1αImproved glucose toleranceReceptor γ coactivator 1αLess weight gainPotential therapeutic targetCold-induced energy expenditureΓ coactivator 1αMitochondrial biogenesisMetabolic complicationsVisceral adiposityGlucose toleranceThermogenic brownCounteract obesityMetabolic disordersTherapeutic targetAdipose tissueBeige phenotypeMetabolic diseasesAdipose progenitor cellsBeige adipocytesCoactivator 1α
2021
AMPK activates Parkin independent autophagy and improves post sepsis immune defense against secondary bacterial lung infections.
Bone NB, Becker EJ Jr, Husain M, Jiang S, Zmijewska AA, Park DW, Chacko B, Darley-Usmar V, Grégoire M, Tadie JM, Thannickal VJ, Zmijewski JW. AMPK activates Parkin independent autophagy and improves post sepsis immune defense against secondary bacterial lung infections. Sci Rep 2021, 11: 12387. PMID: 34117280, DOI: 10.1038/s41598-021-90573-0.Peer-Reviewed Original Research1168-P: Serum MicroRNA-122 and -192 Are Increased in Adolescents with NAFLD: Potential Role as Biomarkers
SHORT K, PALLE S, HELLMAN D, JIANG S, TRYGGESTAD J, GARCIA E. 1168-P: Serum MicroRNA-122 and -192 Are Increased in Adolescents with NAFLD: Potential Role as Biomarkers. Diabetes 2021, 70 DOI: 10.2337/db21-1168-p.Peer-Reviewed Original ResearchCitationsConceptsMiR-122MiR-130bMiR-155MicroRNA-122Abundance of miR-122Serum miR-122Serum microRNA-122Serum miR-155MiR-192Nonalcoholic fatty liver diseaseNonalcoholic fatty liver disease patientsNonalcoholic fatty liver disease groupAlanine aminotransferaseLiver biopsyBiopsy-confirmed nonalcoholic fatty liver disease
2020
Fetal circulating human resistin increases in diabetes during pregnancy and impairs placental mitochondrial biogenesis
Jiang S, Teague A, Tryggestad J, Lyons T, Chernausek S. Fetal circulating human resistin increases in diabetes during pregnancy and impairs placental mitochondrial biogenesis. Molecular Medicine 2020, 26: 76. PMID: 32762639, PMCID: PMC7409642, DOI: 10.1186/s10020-020-00205-y.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAdenosine TriphosphateAdultBiomarkersBlood GlucoseCase-Control StudiesDiabetes, GestationalDNA, MitochondrialFemaleFetal BloodHumansLeukocytes, MononuclearMaternal ExposureMesenchymal Stem CellsMitochondriaOrganelle BiogenesisPlacentaPregnancyPrenatal Exposure Delayed EffectsResistinStress, PhysiologicalTrophoblastsConceptsCord blood mononuclear cellsBlood mononuclear cellsSecretion of resistinHuman resistinMononuclear cellsBeWo cellsCultured cord blood mononuclear cellsMeasures of maternal glycemiaMesenchymal stem cellsLong-term health of offspringExposed BeWo cellsImpact fetal developmentPlacental mitochondrial contentCirculation of infantsPlacental trophoblast cellsHuman placental explantsAdipocyte-derived factorsHealth of offspringMaternal glycemiaResponse to high glucoseDiabetic pregnanciesFetal circulationMaternal diabetesCord bloodCord seraRole of metformin in epigenetic regulation of placental mitochondrial biogenesis in maternal diabetes
Jiang S, Teague A, Tryggestad J, Jensen M, Chernausek S. Role of metformin in epigenetic regulation of placental mitochondrial biogenesis in maternal diabetes. Scientific Reports 2020, 10: 8314. PMID: 32433500, PMCID: PMC7239922, DOI: 10.1038/s41598-020-65415-0.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsMeSH KeywordsAcetylationAdultAMP-Activated Protein KinasesAnimalsCohort StudiesDiabetes, GestationalDiet, High-FatDNA MethylationEpigenesis, GeneticFemaleHistonesHumansMaleMetforminMiceMice, Inbred C57BLMitochondriaOrganelle BiogenesisPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPlacentaPregnancyPregnancy in DiabeticsPromoter Regions, GeneticSex FactorsConceptsActivation of AMP-activated protein kinaseMitochondrial biogenesisPGC-1a expressionH3K27 acetylationAMP-activated protein kinaseRegulator of mitochondrial biogenesisMitochondrial transcription factor ASubgroup of diabetic womenAssociated with epigenetic regulationPGC-1aAberrant epigenetic alterationsLevels of H3K27 acetylationOffspring long-term healthProliferator-activated receptor gamma coactivator 1-alphaPeroxisome proliferator-activated receptor gamma coactivator 1-alphaPromoter methylationTranscription factor AImpaired mitochondrial biogenesisIncreased promoter methylationGamma coactivator 1-alphaDecreased histone acetylationIncreased H3K27 acetylationCoactivator 1-alphaLong-term healthCapability of metforminRole of miR‐130b/301b cluster in macrophage polarization and obesity
Jiang S, McBride A, Luo W, Chernausek S. Role of miR‐130b/301b cluster in macrophage polarization and obesity. The FASEB Journal 2020, 34: 1-1. DOI: 10.1096/fasebj.2020.34.s1.09682.Peer-Reviewed Original ResearchConceptsDevelopment of obesityMacrophage polarizationKnockout miceMacrophage M1/M2 polarizationM1/M2 polarizationPro-inflammatory activationWhole-body energy expenditureHigh-fat dietEnergy expenditureAlternative macrophage activationWild-type miceWhite adipose tissueBody energy expenditureMacrophage activation statusBone marrow macrophagesPresent studyFat dietIL-4M2 polarizationType miceAlternative activationMacrophage activationAdipose tissueMetabolic diseasesActivation status
2019
Macrophage‐Derived microRNA‐155 Increases in Obesity and Influences Adipocyte Metabolism by Targeting Peroxisome Proliferator‐Activated Receptor Gamma
Tryggestad J, Teague A, Sparling D, Jiang S, Chernausek S. Macrophage‐Derived microRNA‐155 Increases in Obesity and Influences Adipocyte Metabolism by Targeting Peroxisome Proliferator‐Activated Receptor Gamma. Obesity 2019, 27: 1856-1864. PMID: 31531958, PMCID: PMC6832842, DOI: 10.1002/oby.22616.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsAdipose tissue macrophagesMiR-155Mesenchymal stem cellsStem cellsPeripheral blood mononuclear cellsPeroxisome proliferator-activated receptor gammaBlood mononuclear cellsImpact of obesityProliferator-activated receptor gammaInfluence adipocyte metabolismMiR-130b expressionCell type-specific fashionIncreased 1.8-foldType-specific fashionPPARG mRNA expressionWestern blot analysisMononuclear cellsPolymerase chain reactionQuantitative polymerase chain reactionMiRNA expressionHuman mesenchymal stem cellsTissue macrophagesDifferentiated 3T3-L1 adipocytesMRNA expressionObesity
2018
Metformin reverses established lung fibrosis in a bleomycin model.
Rangarajan S, Bone NB, Zmijewska AA, Jiang S, Park DW, Bernard K, Locy ML, Ravi S, Deshane J, Mannon RB, Abraham E, Darley-Usmar V, Thannickal VJ, Zmijewski JW. Metformin reverses established lung fibrosis in a bleomycin model. Nat Med 2018, 24: 1121-1127. PMID: 29967351, DOI: 10.1038/s41591-018-0087-6.Peer-Reviewed Original Research
Get In Touch
Contacts
Locations
Lauder Hall
Academic Office
310 Cedar Street, Rm 108G
New Haven, CT 06510