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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

Diabetes impairs hematopoietic stem cell mobilization by altering niche function.

Francesca Ferraro¹, Stefania Lymperi, Simón Méndez-Ferrer

¹Center for Regenerative Medicine, Massachusetts General Hospital, Boston, MA 02114, USA.

Science Translational Medicine

|October 15, 2011

Summary

Diabetes impairs hematopoietic stem and progenitor cell (HSPC) mobilization, crucial for transplantation success. This study reveals diabetes-induced bone marrow changes affecting HSPC egress and suggests a potential therapeutic target for improving mobilization in diabetic patients.

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Analysis of Hematopoietic Stem Progenitor Cell Metabolism

Analysis of Hematopoietic Stem Progenitor Cell Metabolism

Published on: November 9, 2019

Area of Science:

Hematology
Endocrinology
Stem Cell Biology

Background:

Successful autologous hematopoietic stem and progenitor cell (HSPCs) transplantation relies on effective mobilization from the bone marrow using granulocyte colony-stimulating factor (G-CSF).
Some patients exhibit insufficient HSPC mobilization, impacting transplant outcomes.
Retrospective analysis indicated a correlation between diabetes and poor CD34+ HSPC mobilization.

Purpose of the Study:

To investigate the impact of diabetes on HSPC mobilization.
To elucidate the mechanisms underlying impaired HSPC egress in diabetic conditions.
To identify potential therapeutic strategies to enhance HSPC mobilization in diabetic patients.

Main Methods:

Utilized mouse models of type 1 (streptozotocin-induced) and type 2 (db/db) diabetes.
Assessed HSPC mobilization and localization in the bone marrow following G-CSF treatment.
Examined the role of sympathetic nerve termini and mesenchymal stem cell responses to adrenergic stimulation.
Investigated the CXCL12/CXCR4 pathway and its modulation by AMD3100.

Main Results:

Diabetic mice showed impaired HSPC egress from the bone marrow after G-CSF administration.
HSPCs were aberrantly localized within the bone marrow niche of diabetic mice.
Abnormalities in sympathetic nerve termini and mesenchymal stem cell function (nestin+ cells) were observed.
The CXCL12/CXCR4 pathway was implicated, and its inhibition with AMD3100 rescued the HSPC mobilization defect.

Conclusions:

Diabetes induces significant changes in bone marrow microanatomy and physiology, leading to impaired HSPC mobilization.
The sympathetic nervous system and CXCL12/CXCR4 signaling play critical roles in diabetes-associated mobilization defects.
Targeting the CXCL12/CXCR4 axis presents a promising therapeutic approach to improve HSPC collection in diabetic patients undergoing transplantation.