Increased mast cell density is associated with decreased fibrosis in human atrial tissue

IMPART Investigator Team Canada

Producción científica: Contribución a una revistaArtículorevisión exhaustiva

8 Citas (Scopus)

Resumen

Fibrotic remodelling of the atria is poorly understood and can be regulated by myocardial immune cell populations after injury. Mast cells are resident immune sentinel cells present in the heart that respond to tissue damage and have been linked to fibrosis in other settings. The role of cardiac mast cells in fibrotic remodelling in response to human myocardial injury is controversial. In this study, we sought to determine the association between mast cells, atrial fibrosis, and outcomes in a heterogeneous population of cardiac surgical patients, including a substantial proportion of coronary artery bypass grafting patients. Atrial appendage from patients was assessed for collagen and mast cell density by histology and by droplet digital polymerase chain reaction (ddPCR) for mast cell associated transcripts. Clinical variables and outcomes were also followed. Mast cells were detected in human atrial tissue at varying densities. Histological and ddPCR assessment of mast cells in atrial tissue were closely correlated. Patients with high mast cell density had less fibrosis and lower severity of heart failure classification or incidence mortality than patients with low mast cell content. Analysis of a homogeneous population of coronary artery bypass graft patients yielded similar observations. Therefore, evidence from this study suggests that increased atrial mast cell populations are associated with decreased clinical cardiac fibrotic remodelling and improved outcomes, in cardiac surgery patients.

Idioma originalEnglish
Páginas (desde-hasta)15-26
Número de páginas12
PublicaciónJournal of Molecular and Cellular Cardiology
Volumen149
DOI
EstadoPublished - dic. 2020

Nota bibliográfica

Funding Information:
We would like to acknowledge Alexander Edgar, Nong Xu, Alec Falkenham, Tanya Myers, Chloe Wong, Kareem Gawdat, Lester Perez-Rodriguez, Christie Aguiar, Ansar Hassan, Thomas Pulinilkunnil, Petra Kienesberger, Jeffrey MacLeod, and Hany Motawea for their contributions to this manuscript as well as all nurses and nurse associates that enabled patient recruitment and clinical sampling/tissues collections obtained from the IMPART investigator team Canada BioBank ( https://impart.team/ ) for their assistance in this work. This work was funded by a CIHR Signature Initiative Team grant in Chronic inflammation Award #THC-135230 and supported by the Dalhousie Medical Research Foundation . SAL is also the recipient of a CIHR doctoral award ( #394140 ), a Dalhousie Medical Research Foundation MacDonald Graduate Studentship , a Killam Predoctoral Award and Nova Scotia Heart and Stroke Foundation Bright Red award.

Funding Information:
We would like to acknowledge Alexander Edgar, Nong Xu, Alec Falkenham, Tanya Myers, Chloe Wong, Kareem Gawdat, Lester Perez-Rodriguez, Christie Aguiar, Ansar Hassan, Thomas Pulinilkunnil, Petra Kienesberger, Jeffrey MacLeod, and Hany Motawea for their contributions to this manuscript as well as all nurses and nurse associates that enabled patient recruitment and clinical sampling/tissues collections obtained from the IMPART investigator team Canada BioBank (https://impart.team/) for their assistance in this work. This work was funded by a CIHR Signature Initiative Team grant in Chronic inflammation Award #THC-135230 and supported by the Dalhousie Medical Research Foundation. SAL is also the recipient of a CIHR doctoral award (#394140), a Dalhousie Medical Research Foundation MacDonald Graduate Studentship, a Killam Predoctoral Award and Nova Scotia Heart and Stroke Foundation Bright Red award.

Publisher Copyright:
© 2020 The Authors

ASJC Scopus Subject Areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine

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