Background: Limited homing capability of human mesenchymal stem cells (MSCs) is the key obstacle
in MSC-based cellular therapy. It is believed that chemokine/chemokine receptor interactions,
especially the SDF1/CXCR4 axis, play key roles in cellular processes associated to
migration. Meanwhile, human adipose-derived MSCs express a very low level of CXCR4
on the surface and they even lose these receptors after few passages resulting to
a reduction in their therapeutic efficiency. WHIM (warts, hypogammaglobulinemia, infections,
and myelokatexis) syndrome is a rare immunodeficiency syndrome linked to heterozygous
mutations of the chemokine receptor CXCR4 resulting in truncation of its cytoplasmic
tail. We propose that decreased internalization of WHIM-associated mutant CXCR4 leads
to prolongation of signaling in response to SDF1 and increasing its function. In the
present study, WHIM-type CXCR4 (CXCR4R334X) was overexpressed in adipose-derived MSCs to evaluate its impact on their level
of migration.
To read this article in full you will need to make a payment
Purchase one-time access:
Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online accessOne-time access price info
- For academic or personal research use, select 'Academic and Personal'
- For corporate R&D use, select 'Corporate R&D Professionals'
Subscribe:
Subscribe to CytotherapyAlready a print subscriber? Claim online access
Already an online subscriber? Sign in
Register: Create an account
Institutional Access: Sign in to ScienceDirect
