JAK2V617F-mutant vascular niche contributes to JAK2V617F clonal expansion in myeloproliferative neoplasms

The myeloproliferative neoplasms (MPNs) are characterized by hematopoietic stem/progenitor cell (HSPC) expansion and overproduction of blood cells. The acquired mutation JAK2V617F plays a central role in these disorders. Mechanisms responsible for MPN HSPC expansion is not fully understood, limiting...

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Published inBlood cells, molecules, & diseases Vol. 62; pp. 42 - 48
Main Authors Lin, Chi Hua Sarah, Kaushansky, Kenneth, Zhan, Huichun
Format Journal Article
LanguageEnglish
Published Elsevier Inc 01.11.2016
Subjects
Endothelial cells
Hematopoietic stem/progenitor cells
JAK2V617F
Microenvironment
MPL
Myeloproliferative neoplasms
Hematopoietic stem/progenitor cells
MPL
Microenvironment
JAK2V617F
Endothelial cells
Myeloproliferative neoplasms
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Abstract The myeloproliferative neoplasms (MPNs) are characterized by hematopoietic stem/progenitor cell (HSPC) expansion and overproduction of blood cells. The acquired mutation JAK2V617F plays a central role in these disorders. Mechanisms responsible for MPN HSPC expansion is not fully understood, limiting the effectiveness of current treatments. Endothelial cells (ECs) carrying the JAK2V617F mutation can be detected in patients with MPNs, suggesting that ECs are involved in the pathogenesis of MPNs. Here we report that JAK2V617F-bearing primary murine ECs have increased cell proliferation and angiogenesis in vitro compared to JAK2WT ECs. While there was no difference between JAK2V617F and JAK2WT HSPC proliferation when co-cultured with JAK2WT EC, the JAK2V617F HSPC displayed a relative growth advantage over the JAK2WT HSPC when co-cultured on JAK2V617F EC. In addition, the thrombopoietin (TPO) receptor MPL is up regulated in JAK2V617F ECs and contributes to the maintenance/expansion of the JAK2V617F clone over JAK2WT clone in vitro. Considering that ECs are an essential component of the hematopoietic niche and most HSPCs reside in the perivascular niche, our studies suggest that the JAK2V617F-bearing ECs form an important component of the MPN vascular niche and contribute to mutant stem/progenitor cell expansion, likely through a critical role of the TPO/MPL signaling axis.
AbstractList The myeloproliferative neoplasms (MPNs) are characterized by hematopoietic stem/progenitor cell (HSPC) expansion and overproduction of blood cells. The acquired mutation JAK2 V617F plays a central role in these disorders. Mechanisms responsible for MPN HSPC expansion is not fully understood, limiting the effectiveness of current treatments. Endothelial cells (ECs) carrying the JAK2 V617F mutation can be detected in patients with MPNs, suggesting that ECs are involved in the pathogenesis of MPNs. Here we report that JAK2 V617F -bearing primary murine ECs have increased cell proliferation and angiogenesis in vitro compared to JAK2 WT ECs. While there was no difference between JAK2 V617F and JAK2 WT HSPC proliferation when co-cultured with JAK2 WT EC, the JAK2 V617F HSPC displayed a relative growth advantage over the JAK2 WT HSPC when co-cultured on JAK2 V617F EC. In addition, the thrombopoietin (TPO) receptor MPL is up regulated in JAK2 V617F ECs and contributes to the maintenance/expansion of the JAK2 V617F clone over JAK2 WT clone in vitro . Considering that ECs are an essential component of the hematopoietic niche and most HSPCs reside in the perivascular niche, our studies suggest that the JAK2 V617F -bearing ECs form an important component of the MPN vascular niche and contribute to mutant stem/progenitor cell expansion, likely through a critical role of the TPO/MPL signaling axis.
The myeloproliferative neoplasms (MPNs) are characterized by hematopoietic stem/progenitor cell (HSPC) expansion and overproduction of blood cells. The acquired mutation JAK2V617F plays a central role in these disorders. Mechanisms responsible for MPN HSPC expansion is not fully understood, limiting the effectiveness of current treatments. Endothelial cells (ECs) carrying the JAK2V617F mutation can be detected in patients with MPNs, suggesting that ECs are involved in the pathogenesis of MPNs. Here we report that JAK2V617F-bearing primary murine ECs have increased cell proliferation and angiogenesis in vitro compared to JAK2WT ECs. While there was no difference between JAK2V617F and JAK2WT HSPC proliferation when co-cultured with JAK2WT EC, the JAK2V617F HSPC displayed a relative growth advantage over the JAK2WT HSPC when co-cultured on JAK2V617F EC. In addition, the thrombopoietin (TPO) receptor MPL is up regulated in JAK2V617F ECs and contributes to the maintenance/expansion of the JAK2V617F clone over JAK2WT clone in vitro. Considering that ECs are an essential component of the hematopoietic niche and most HSPCs reside in the perivascular niche, our studies suggest that the JAK2V617F-bearing ECs form an important component of the MPN vascular niche and contribute to mutant stem/progenitor cell expansion, likely through a critical role of the TPO/MPL signaling axis.
Author Kaushansky, Kenneth
Zhan, Huichun
Lin, Chi Hua Sarah
AuthorAffiliation 1 Department of Medicine, Division of Hematology-Oncology, Stony Brook University, Stony Brook, NY
2 Office of the Sr. Vice President, Health Sciences, Stony Brook Medicine, NY
3 Northport VA Medical Center, Northport, NY
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  givenname: Huichun
  surname: Zhan
  fullname: Zhan, Huichun
  email: Huichun.Zhan@stonybrookmedicine.edu, Huichun.Zhan@va.gov
  organization: Department of Medicine, Division of Hematology-Oncology, Stony Brook University, Stony Brook, NY, USA
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Keywords Hematopoietic stem/progenitor cells
MPL
Microenvironment
JAK2V617F
Endothelial cells
Myeloproliferative neoplasms
Language English
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Snippet The myeloproliferative neoplasms (MPNs) are characterized by hematopoietic stem/progenitor cell (HSPC) expansion and overproduction of blood cells. The...
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SubjectTerms Endothelial cells
Hematopoietic stem/progenitor cells
JAK2V617F
Microenvironment
MPL
Myeloproliferative neoplasms
Title JAK2V617F-mutant vascular niche contributes to JAK2V617F clonal expansion in myeloproliferative neoplasms
URI https://dx.doi.org/10.1016/j.bcmd.2016.09.004
https://search.proquest.com/docview/1842553334
https://pubmed.ncbi.nlm.nih.gov/PMC5135612
Volume 62
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