2019
Myeloablation followed by autologous stem cell transplantation normalises systemic sclerosis molecular signatures
Assassi S, Wang X, Chen G, Goldmuntz E, Keyes-Elstein L, Ying J, Wallace PK, Turner J, Zheng WJ, Pascual V, Varga J, Hinchcliff ME, Bellocchi C, McSweeney P, Furst DE, Nash RA, Crofford LJ, Welch B, Pinckney A, Mayes MD, Sullivan KM. Myeloablation followed by autologous stem cell transplantation normalises systemic sclerosis molecular signatures. Annals Of The Rheumatic Diseases 2019, 78: 1371-1378. PMID: 31391177, PMCID: PMC7167108, DOI: 10.1136/annrheumdis-2019-215770.Peer-Reviewed Original ResearchMeSH KeywordsAdultCyclophosphamideDown-RegulationFemaleHematopoietic Stem Cell TransplantationHumansInterferonsMaleMiddle AgedMultilevel AnalysisMyeloablative AgonistsNeutrophilsRandomized Controlled Trials as TopicScleroderma, SystemicTranscriptomeTransplantation ConditioningTransplantation, AutologousTreatment OutcomeUp-RegulationConceptsHaematopoietic stem cell transplantationStem cell transplantationSystemic sclerosisNeutrophil modulesCell transplantationAutologous stem cell transplantationMolecular signaturesImproved clinical outcomesSerum protein levelsDisease-related molecular signaturesCYC armMonths postrandomisationBaseline visitSkin scoreClinical outcomesCyclophosphamide treatmentVital capacityPretreatment baselineSignificant changesControl armBlood transcriptsWhole blood transcriptsConventional treatmentInterferonBaseline samples
2018
The novel adipokine C1q-TNF related protein 9 (CTRP9) is elevated in systemic sclerosis-associated interstitial lung disease.
Korman B, Alejo R, Sudhakar D, Hinchcliff M, Agrawal R, Varga J, Marangoni RG. The novel adipokine C1q-TNF related protein 9 (CTRP9) is elevated in systemic sclerosis-associated interstitial lung disease. Clinical And Experimental Rheumatology 2018, 36 Suppl 113: 184-185. PMID: 30183591, PMCID: PMC7389309.Peer-Reviewed Original Research
2016
Tenascin-C drives persistence of organ fibrosis
Bhattacharyya S, Wang W, Morales-Nebreda L, Feng G, Wu M, Zhou X, Lafyatis R, Lee J, Hinchcliff M, Feghali-Bostwick C, Lakota K, Budinger GR, Raparia K, Tamaki Z, Varga J. Tenascin-C drives persistence of organ fibrosis. Nature Communications 2016, 7: 11703. PMID: 27256716, PMCID: PMC4895803, DOI: 10.1038/ncomms11703.Peer-Reviewed Original ResearchConceptsSystemic sclerosisToll-like receptorsOrgan fibrosisFibrosis resolutionPathogenesis of SScTreatment of SScLevels of tenascinEndogenous danger signalsSSc skin biopsy samplesSkin biopsy samplesMechanism of actionLung fibrosisPathogenic roleTLR activatorsMouse modelBiopsy samplesFibroblast activationDanger signalsMyofibroblast transformationFibrosisSSc fibroblastsCollagen gene expressionSkin fibroblastsAmplification loopTenascin