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Updated: Jun 19, 2026

A Mouse Model of Vascularized Heterotopic Spleen Transplantation for Studying Spleen Cell Biology and Transplant Immunity

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Published on: June 11, 2019

Splenectomy normalizes hematocrit in murine polycythemia vera.

Jan-Rung Mo¹, Anjili Mathur, Minilik Angagaw

¹Department of Oncology-Pharmacology, Merck Research Laboratories, Boston, Massachusetts, United States of America.

|October 1, 2009

Summary

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The spleen is essential for developing elevated hematocrit in polycythemia vera (PV) driven by JAK2(V617F). Removing the spleen prevents or reverses this PV hallmark, indicating a critical spleen-PV cell interaction.

Area of Science:

Hematology
Oncology
Pathophysiology

Background:

Splenic enlargement (splenomegaly) is common in disease, but its specific role is often unclear.
Polycythemia vera (PV) involves JAK2(V617F) mutation, causing splenomegaly and high hematocrit.
Splenectomy is rarely done in PV due to surgical risks, leaving the spleen's role in PV pathogenesis unknown.

Purpose of the Study:

To investigate the spleen's specific role in the pathogenesis of JAK2(V617F)-driven polycythemia vera (PV).

Main Methods:

A murine model of JAK2(V617F)-driven PV was used.
Mice underwent either sham (SH) surgery or splenectomy (SPL).
JAK2(V617F) was transplanted, and hematocrit, disease burden, and bone marrow changes were assessed.

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A Mouse Model of Vascularized Heterotopic Spleen Transplantation for Studying Spleen Cell Biology and Transplant Immunity

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Published on: June 11, 2019

Bone Marrow Transplantation Procedures in Mice to Study Clonal Hematopoiesis

Bone Marrow Transplantation Procedures in Mice to Study Clonal Hematopoiesis

Published on: May 26, 2021

Main Results:

Splenectomized mice failed to develop elevated hematocrit compared to sham-operated mice after JAK2(V617F) transplantation.
Bone marrow disease burden, fibrosis, and osteosclerosis were similar in both groups.
Splenectomy after PV establishment normalized hematocrit but did not prevent bone marrow fibrosis or osteosclerosis.

Conclusions:

The spleen is required for the development of elevated hematocrit in JAK2(V617F)-driven murine PV.
This PV phenotype may necessitate a specific interaction between mutant cells and the spleen.
Splenectomy effectively reduces hematocrit in PV, independent of bone marrow pathology.