Senile Osteoporosis: The Involvement of Differentiation and Senescence of Bone Marrow Stromal Cells

Qadir, Abdul; Liang, Shujing; Wu, Zixiang; Chen, Zhihao; Hu, Lifang; Qian, Airong

doi:10.3390/ijms21010349

Cited by 169 publications

(96 citation statements)

References 160 publications

(177 reference statements)

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“…An additional factor playing a role in the lower osteogenic potential of osteoporotic MSCs is that in senile osteoporosis, MSCs undergo cellular senescence resulting in a growth arrest [57].…”

Section: Mscs As a Potential Stem Cell Therapy For Bone Degenerationmentioning

confidence: 99%

Impact of 3D cell culture on bone regeneration potential of mesenchymal stromal cells

2021

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As populations age across the world, osteoporosis and osteoporosis-related fractures are becoming the most prevalent degenerative bone diseases. More than 75 million patients suffer from osteoporosis in the USA, the EU and Japan. Furthermore, it is anticipated that the number of patients affected by osteoporosis will increase by a third by 2050. Although conventional therapies including bisphosphonates, calcitonin and oestrogen-like drugs can be used to treat degenerative diseases of the bone, they are often associated with serious side effects including the development of oesophageal cancer, ocular inflammation, severe musculoskeletal pain and osteonecrosis of the jaw.The use of autologous mesenchymal stromal cells/mesenchymal stem cells (MSCs) is a possible alternative therapeutic approach to tackle osteoporosis while overcoming the limitations of traditional treatment options. However, osteoporosis can cause a decrease in the numbers of MSCs, induce their senescence and lower their osteogenic differentiation potential.Three-dimensional (3D) cell culture is an emerging technology that allows a more physiological expansion and differentiation of stem cells compared to cultivation on conventional flat systems.This review will discuss current understanding of the effects of different 3D cell culture systems on proliferation, viability and osteogenic differentiation, as well as on the immunomodulatory and anti-inflammatory potential of MSCs.

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Section: Mscs As a Potential Stem Cell Therapy For Bone Degenerationmentioning

confidence: 99%

Impact of 3D cell culture on bone regeneration potential of mesenchymal stromal cells

2021

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“…Osteogenesis and cellular senescence of BMSCs play great roles in bone formation (Qadir et al, 2020). In this study, our data showed ASPH longest isoform promoting the osteogenesis while inhibiting cellular senescence, indicating it potentially results in an elevated capacity of bone formation.…”

Section: Discussionmentioning

confidence: 49%

ASPH Regulates Osteogenic Differentiation and Cellular Senescence of BMSCs

Peng

Guo

Xiao

et al. 2020

Front. Cell Dev. Biol.

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Osteogenesis and senescence of BMSCs play great roles in age-related bone loss. However, the causes of these dysfunctions remain unclear. In this study, we identified a differentially expressed ASPH gene in middle-aged and elderly aged groups which were obtained from GSE35955. Subsequent analysis in various databases, such as TCGA, GTEx, and CCLE, revealed that ASPH had positive correlations with several osteogenic markers. The depletion of mouse Asph suppressed the capacity of osteogenic differentiation in bone marrow mesenchymal stem cells (BMSCs). Notably, the expression of ASPH in vitro decreased during aging and senescence. The deficiency of Asph accelerated cellular senescence in BMSCs. Conversely, the overexpression of Asph enhanced the capacity of osteogenic differentiation and inhibited cellular senescence. Mechanistically, ASPH regulated Wnt signaling mediated by Gsk3β. Taken together, our data established that ASPH was potentially involved in the pathogenesis of age-related bone loss through regulating cellular senescence and osteogenic differentiation, which provides some new insights to treat age-related bone loss.

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“…Several data confirm that aging is characterized by the reduction of bone tissue which is replaced by bone marrow adipose tissue, as a consequence of decreased osteoblastogenesis and a concomitant enhanced adipogenesis from BMSCs [59] (Table 2). It has been shown that the changes in BMSC proliferation and the switch of differentiation toward the adipogenic lineage is one of the main physio-pathological mechanisms of senile osteoporosis [60,61]. BMSCs deriving from elderly subjects present a decline of osteoblastogenesis and a tendency for adipogenic differentiation [62].…”

Section: Bmscsmentioning

confidence: 99%

Molecular Basis of Bone Aging

Corrado

Cici

Rotondo

et al. 2020

IJMS

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A decline in bone mass leading to an increased fracture risk is a common feature of age-related bone changes. The mechanisms underlying bone senescence are very complex and implicate systemic and local factors and are the result of the combination of several changes occurring at the cellular, tissue and structural levels; they include alterations of bone cell differentiation and activity, oxidative stress, genetic damage and the altered responses of bone cells to various biological signals and to mechanical loading. The molecular mechanisms responsible for these changes remain greatly unclear and many data derived from in vitro or animal studies appear to be conflicting and heterogeneous, probably due to the different experimental approaches; nevertheless, understanding the main physio-pathological processes that cause bone senescence is essential for the development of new potential therapeutic options for treating age-related bone loss. This article reviews the current knowledge concerning the molecular mechanisms underlying the pathogenesis of age-related bone changes.

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Senile Osteoporosis: The Involvement of Differentiation and Senescence of Bone Marrow Stromal Cells

Cited by 169 publications

References 160 publications

Impact of 3D cell culture on bone regeneration potential of mesenchymal stromal cells

Impact of 3D cell culture on bone regeneration potential of mesenchymal stromal cells

ASPH Regulates Osteogenic Differentiation and Cellular Senescence of BMSCs

Molecular Basis of Bone Aging

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