Abstract
In the adult bone marrow, osteoblasts and adipocytes share a common precursor called mesenchymal stem cells (MSCs). The plasticity between the two lineages has been confirmed over the past decades, and has important implications in the etiology of bone diseases such as osteoporosis, which involves an imbalance between osteoblasts and adipocytes. The commitment and differentiation of bone marrow (BM) MSCs is tightly controlled by the local environment that maintains a balance between osteoblast lineage and adipocyte. However, pathological conditions linked to osteoporosis can change the BM microenvironment and shift the MSC fate to favor adipocytes over osteoblasts, and consequently decrease bone mass with marrow fat accumulation. This review discusses the changes that occur in the BM microenvironment under pathological conditions, and how these changes affect MSC fate. We suggest that manipulating local environments could have therapeutic implications to avoid bone loss in diseases like osteoporosis.
Highlights
In the adult bone marrow, osteoblasts and adipocytes share a common precursor called mesenchymal stem cells (MSCs)
These findings demonstrated that bone tissue homeostasis is largely regulated and maintained by the bone marrow (BM) microenvironment
The BM microenvironment changes progressively during pathological conditions linked to osteoporosis, and are characterized by increased oxidative stress, chronic inflammation, suppressed osteogenic signals and elevated osteoblastic inhibitors
Summary
Researchers found that age-related osteoporosis can be introduced in normal mice by injection of total BM cells from senile mice directly into the BM cavity of normal recipients [17,18,19]. Transforming growth factor- β1 (TGF-β1), which is one of the most abundant cytokines in the BM, induces the migration of preosteoblasts to bone forming surface [23] This surface provides a stiff, elastic microenvironment that immediately triggers focal adhesion kinase (FAK) pathway in attached pre-osteoblasts leading to cytoskeleton rearrangement and a more spread out cell shape [24, 25]. Adipocytic differentiation of MSCs in physiological BM is restricted Osteogenic signaling factors such as TGF-β1 and Wnt have been reported to inhibit adipogenesis [32,33,34] by repressing the expression and/or activities of key adipogenic transcriptional factors, CCAAT/enhancer binding protein alpha (C/EBPα) and peroxisome proliferator-activated receptor gamma (PPARγ) [32,33,34]
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