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Updated: May 12, 2026

Retroviral Infection of Murine Embryonic Stem Cell Derived Embryoid Body Cells for Analysis of Hematopoietic Differentiation

Retroviral Infection of Murine Embryonic Stem Cell Derived Embryoid Body Cells for Analysis of Hematopoietic Differentiation

Published on: October 20, 2014

Rb regulates interactions between hematopoietic stem cells and their bone marrow microenvironment.

Carl R Walkley¹, Jeremy M Shea, Natalie A Sims

¹Department of Pediatric Oncology, Dana-Farber Cancer Institute, Division of Hematology/Oncology and Stem Cell Program, Children's Hospital Boston, Harvard Stem Cell Institute, Harvard Medical School, Boston, MA 02115, USA.

|June 19, 2007

Summary

The retinoblastoma protein (RB) regulates cell cycle and hematopoiesis. Inactivating RB causes myeloproliferation, not by affecting stem cells directly, but by disrupting their bone marrow niche interactions.

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Bioengineering of Humanized Bone Marrow Microenvironments in Mouse and Their Visualization by Live Imaging

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Published on: August 1, 2017

Area of Science:

Hematology
Cell Biology
Cancer Biology

Background:

Hematopoiesis relies on hematopoietic stem cells (HSCs) responding to intrinsic and extrinsic signals.
Cell cycle regulation's role in HSC fate decisions, as either intrinsic or extrinsic, remains unclear.
The retinoblastoma protein (RB) is a key cell cycle regulator.

Purpose of the Study:

To investigate the role of the retinoblastoma protein (RB) in hematopoiesis.
To determine if RB's function in HSC fate is intrinsic or extrinsic.

Main Methods:

Inactivation of the RB gene in the murine hematopoietic system.
Analysis of HSC behavior, bone marrow microenvironment interactions, and myeloproliferation.

Main Results:

Widespread RB inactivation led to significant myeloproliferation.
HSCs were lost from the bone marrow due to mobilization and differentiation.
The observed phenotype resulted from RB-dependent interactions between myeloid cells and the microenvironment, not intrinsic HSC defects.

Conclusions:

RB extrinsically regulates HSCs by maintaining the bone marrow microenvironment's supportive capacity.
Perturbed interactions between hematopoietic cells and their niche, influenced by RB, can cause myeloproliferation.
RB is crucial for maintaining normal hematopoiesis and HSCs within the bone marrow niche.