Mesenchymal progenitors in osteopenias of diverse pathologies: differential characteristics in the common shift from osteoblastogenesis to adipogenesis

RUNX2 Senescence
DOI: 10.1038/srep30186 Publication Date: 2016-07-22T09:19:25Z
ABSTRACT
Abstract Osteoporosis is caused by pathologic factors such as aging, hormone deficiency or excess, inflammation and systemic diseases like diabetes. Bone marrow stromal cells (BMSCs), the mesenchymal progenitors for both osteoblasts adipocytes, are modulated niche signals. In differential states, pathological characteristics of BMSCs to osteoporoses functional differences unknown. Here, we detected that trabecular bone loss co-existed with increased adiposity in 6 osteoporotic models, respectively induced natural accelerated senescence (SAMP6), ovariectomy (OVX), type 1 diabetes (T1D), excessive glucocorticoids (GIOP) orchidectomy (ORX). Of ex vivo BMSCs, colony-forming efficiency proliferation rate SAMP6, OVX, GIOP ORX models decreased. The apoptosis cellular except T1D, up-regulation p53 p16 expression. osteogenesis declined GIOP, corresponding down-regulation Runt-related transcription factor 2 (RUNX2) adipogenesis Peroxisome proliferator activated receptor gamma (PPARγ) These findings revealed a common shift from osteoblastogenesis among different between sexes provide theoretical basis modulation resident regenerative therapy osteoporosis.
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