scholarly journals The osteo-inductive activity of bone-marrow-derived mononuclear cells resides within the CD14+ population and is independent of the CD34+ population

2018 ◽  
Vol 35 ◽  
pp. 165-177 ◽  
Author(s):  
D Henrich ◽  
◽  
C Seebach ◽  
R Verboket ◽  
A Schaible ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mononuclear Cells ◽  
Inductive Activity

scholarly journals Bone Marrow Homeostasis Is Impaired via JAK/STAT and Glucocorticoid Signaling in Cancer Cachexia Model

Cancers ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1059
Author(s):  
Jinyeong Yu ◽  
Sanghyuk Choi ◽  
Aran Park ◽  
Jungbeom Do ◽  
Donghyun Nam ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Animal Model ◽  
Bone Loss ◽  
Cancer Cachexia ◽  
Mononuclear Cells ◽  
Bone Homeostasis ◽  
Bone Marrow Mscs ◽  
Hematopoietic Stem ◽  
Glucocorticoid Signaling

Cancer cachexia is a multifactorial systemic inflammation disease caused by complex interactions between the tumor and host tissues via soluble factors. However, whether cancer cachexia affects the bone marrow, in particular the hematopoietic stem cells (HSCs) and mesenchymal stem cells (MSCs), remains unclear. Here, we investigated the bone marrow and bone in a cancer cachexia animal model generated by transplanting Lewis lung carcinoma cells. The number of bone marrow mononuclear cells (BM-MNCs) started to significantly decrease in the cancer cachectic animal model prior to the discernable loss of muscle and fat. This decrease in BM-MNCs was associated with myeloid skewing in the circulation and the expansion of hematopoietic progenitors in the bone marrow. Bone loss occurred in the cancer cachexia animal model and accompanied the decrease in the bone marrow MSCs that play important roles in both supporting HSCs and maintaining bone homeostasis. Glucocorticoid signaling mediated the decrease in bone marrow MSCs in the cancer cachectic environment. The cancer cachexia environment also skewed the differentiation of the bone marrow MSCs toward adipogenic fate via JAK/STAT as well as glucocorticoid signaling. Our results suggest that the bone loss induced in cancer cachexia is associated with the depletion and the impaired differentiation capacity of the bone marrow MSCs.

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