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Review
. 2018 Aug 9;19(8):2343.
doi: 10.3390/ijms19082343.

Mesenchymal Stem Cell Migration during Bone Formation and Bone Diseases Therapy

Peihong Su  1   2   3 , Ye Tian  4   5   6 , Chaofei Yang  7   8   9 , Xiaoli Ma  10   11   12 , Xue Wang  13   14   15 , Jiawei Pei  16   17   18 , Airong Qian  19   20   21
Affiliations
Review

Mesenchymal Stem Cell Migration during Bone Formation and Bone Diseases Therapy

Peihong Su et al. Int J Mol Sci. .

Abstract

During bone modeling, remodeling, and bone fracture repair, mesenchymal stem cells (MSCs) differentiate into chondrocyte or osteoblast to comply bone formation and regeneration. As multipotent stem cells, MSCs were used to treat bone diseases during the past several decades. However, most of these implications just focused on promoting MSC differentiation. Furthermore, cell migration is also a key issue for bone formation and bone diseases treatment. Abnormal MSC migration could cause different kinds of bone diseases, including osteoporosis. Additionally, for bone disease treatment, the migration of endogenous or exogenous MSCs to bone injury sites is required. Recently, researchers have paid more and more attention to two critical points. One is how to apply MSC migration to bone disease therapy. The other is how to enhance MSC migration to improve the therapeutic efficacy of bone diseases. Some considerable outcomes showed that enhancing MSC migration might be a novel trick for reversing bone loss and other bone diseases, such as osteoporosis, fracture, and osteoarthritis (OA). Although plenty of challenges need to be conquered, application of endogenous and exogenous MSC migration and developing different strategies to improve therapeutic efficacy through enhancing MSC migration to target tissue might be the trend in the future for bone disease treatment.

Keywords: bone diseases; bone formation; mesenchymal stem cells; migration; therapy.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Schematic diagram of mesenchymal stem cell (MSC) migration during intramembranous ossification. LL-37, platelet-derived growth factors (PDGFs), and Transforming growth factor-β (TGF-β) released from bone resorption surface and the high expression of Matrix metalloproteinases (MMP) in MSCs promote their migration to the site near bone surface. At the same time, MSCs differentiate into preosteoblast. Bone morphogenetic protein (BMP) and receptor activator of the nuclear factor kappa B ligand RANKL accelerate preosteoblast migration to the bone surface and the high expression of guanosine triphosphatase (GTPase) in preosteoblast promote cell migration. The solid arrows refer to cell migration. The dotted arrows refer to the effect of chemokine on MSC migration.
Figure 2
Figure 2
Schematic diagram of MSC migration during fracture healing. LL-37, PDGFs, and TGE-β from the inflammation area promote MSCs migrate to the site near the bone surface. At the same time, MSCs differentiated into preosteoblasts. SDF-1α and CXCL7 released from the bone injury site enhances preostelast migration to the bone surface. At the same time, preosteoblasts differentiate into osteoblasts. The solid arrows refer to cell migration. The dotted arrows refer to the effect of chemokines on MSC migration.
See this image and copyright information in PMC

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