RT Journal Article
SR Electronic
T1 In Lyl1-/- mice, adipose stem cell vascular niche impairment leads to premature development of fat tissues
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2020.04.24.059683
DO 10.1101/2020.04.24.059683
A1 Abid Hussain
A1 Leila El Kebriti
A1 Virginie Deleuze
A1 Yaël Glasson
A1 Nelly Pirot
A1 Danièle Mathieu
A1 Valérie Pinet
YR 2020
UL http://biorxiv.org/content/early/2020/04/25/2020.04.24.059683.abstract
AB Lymphoblastic leukemia-derived sequence 1 (Lyl1) encodes a hematopoietic- and endothelial-specific transcriptional factor. Lyl1-deficient mice are viable, but they display mild hematopoietic and vascular defects. Here, we report that young Lyl1-/- mice exhibit transient obesity associated with general expansion of adipose tissues and unrelated to food intake. The increased fat tissue development in Lyl1-/- mice resulted from an earlier adipocyte differentiation of adipose stem cells (ASCs) through non-cell autonomous mechanisms. Specifically, we found that in Lyl1-/- mice, the vascular structures of adipose tissues are unstable, more prone to angiogenesis and, consequently, cannot maintain adipose progenitors in the niche vessel wall. Together, our data show that in Lyl1-/- mice, the impaired vascular compartment of the adipose niche promotes uncontrolled ASC activation and differentiation, leading to early adipocyte expansion and premature depletion of ASCs. Our study highlights the major structural role of the adipose tissue vascular niche in coordinating stem cell self-renewal and differentiation into adipocytes.Competing Interest StatementThe authors have declared no competing interest.