Abstract
Osteoblast and adipocyte are derived from common mesenchymal progenitor cells. The bone loss of osteoporosis is associated with altered progenitor differentiation from an osteoblastic to an adipocytic lineage. In this study, a comparative analysis of gene expression profiling using cDNA microarray and realtime-PCR indicated that Zinc finger protein 467 (Zfp467) involved in adipocyte and osteoblast differentiation of cultured adipose derived stem cells (ADSCs). Our results showed that RNA interference for Zfp467 in ADSCs inhibited adipocyte formation and stimulated osteoblast commitment. The mRNA levels of osteogenic and adipogenic markers in ADSCs were regulated by si-Zfp467. Zfp467 RNAi in ADSCs could restore bone function and structure in an ovariectomized (OVX)-induced osteoporotic mouse model. Thus Zfp467 play an important role in ADSCs differentiation to adipocyte and osteoblast. This has relevance to therapeutic interventions in osteoporosis, including si-Zfp467-based therapies currently available, and may be of relevance for the use of adipose-derived stem cells for tissue engineering.
Highlights
Adult bone mass is maintained by an exquisite balance between bone formation by osteoblasts and bone resorption by osteoclasts [1]
The ability of adipose derived stem cells (ADSCs) to differentiate into adipocyte and osteoblast lineages at passage 3 was experimentally confirmed by Oil red O staining (Figure 2B), von Kossa staining (Figure 2E) and the mRNA levels of specific adipogenic (Figure 2C) and osteogenic markers (Figure 2F), respectively
Gene expression profiling changes of adipocyte and osteoblast differentiation from ADSCs we studied the difference of gene expression profile changes between adipocyte and osteoblast differentiation from ADSCs at day 14 and to screen the critical genes in the early differentiation stage by cDNA microarray
Summary
Adult bone mass is maintained by an exquisite balance between bone formation by osteoblasts and bone resorption by osteoclasts [1] Disruption of this delicate equilibrium can lead to osteoporosis (OP), a multifactorial, age-related metabolic bone disease characterized by reduction in bone mass, bone tissue microarchitectural deterioration, and increased fracture risk [2,3]. Interpreting the results of these studies is further complicated by variations in the cell source site, There are emerging evidences linking osteoporosis and stem cell defects, including osteoblast-progenitors (mesenchymal stem cells, MSCs) residing in the bone marrow [9], so it has been hypothesized that such cells from in vitro culture might be infused back to osteopenic subjects in order to replenish their stem cell pool, which would result in a positive bone balance and the regeneration of the osteopenic skeleton. Because of increased cytokines from stromal cells and osteoblasts that regulated osteoclast generation due to estrogen loss, the number of osteoclasts increased and caused the elevated bone resorption [13]
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