JAK2(V617F)-Mediated Clonal Hematopoiesis Accelerates Pathological Remodeling in Murine Heart Failure

Janus kinase 2 (valine to phenylalanine at residue 617) (JAK2(V617F)) mutations lead to myeloproliferative neoplasms associated with elevated myeloid, erythroid, and megakaryocytic cells. Alternatively these same mutations can lead to the condition of clonal hematopoiesis with no impact on blood cel...

Descripción completa

Detalles Bibliográficos
Autores principales: Sano, Soichi, Wang, Ying, Yura, Yoshimitsu, Sano, Miho, Oshima, Kosei, Yang, Yue, Katanasaka, Yasufumi, Min, Kyung-Duk, Matsuura, Shinobu, Ravid, Katya, Mohi, Golam, Walsh, Kenneth
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2019
Materias:
PRECLINICAL RESEARCH
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6834960/
https://www.ncbi.nlm.nih.gov/pubmed/31709318
http://dx.doi.org/10.1016/j.jacbts.2019.05.013
Descripción
Sumario:Janus kinase 2 (valine to phenylalanine at residue 617) (JAK2(V617F)) mutations lead to myeloproliferative neoplasms associated with elevated myeloid, erythroid, and megakaryocytic cells. Alternatively these same mutations can lead to the condition of clonal hematopoiesis with no impact on blood cell counts. Here, a model of myeloid-restricted JAK2(V617F) expression from lineage-negative bone marrow cells was developed and evaluated. This model displayed greater cardiac inflammation and dysfunction following permanent left anterior descending artery ligation and transverse aortic constriction. These data suggest that JAK2(V617F)mutations arising in myeloid progenitor cells may contribute to cardiovascular disease by promoting the proinflammatory properties of circulating myeloid cells.

Ejemplares similares