In Vitro Characteristics and In Vivo Immunosuppressive Activity of Compact Bone-Derived Murine Mesenchymal Progenitor Cells

Guo, Zi-Kuan; Li, Hong; Li, Xiu-Sen; Yu, Xiaodan; Wang, Heng-Xiang; Tang, Pei-Hsien; Mao, Ning

doi:10.1634/stemcells.2005-0224

Cited by 95 publications

(76 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Because SDF-1 is reportedly regulated by a hypoxia-specific transcriptional factor, hypoxia-inducible factor 1, the expression of SDF-1 may increase rapidly after the blood supply is stopped in those models (25). However, any trophic vasculature was not apparently affected in our live bone graft model (33). Furthermore, it can be expected that infiltration from the neighboring bone marrow retains the blood supply to the graft bone to some extent.…”

Section: Discussionmentioning

confidence: 84%

Stromal cell–derived factor 1/CXCR4 signaling is critical for the recruitment of mesenchymal stem cells to the fracture site during skeletal repair in a mouse model

Kitaori¹,

Ito²,

Schwarz³

et al. 2009

Arthritis & Rheumatism

512

443

View full text Add to dashboard Cite

Objective. Stromal cell-derived factor 1 (SDF-1; CXCL12/pre-B cell growth-stimulating factor) is a dominant chemokine in bone marrow and is known to be involved in inflammatory diseases, including rheumatoid arthritis. However, its role in bone repair remains unknown. The purpose of this study was to investigate the role of SDF-1 and its receptor, CXCR4, in bone healing.Methods. The expression of SDF-1 during the repair of a murine structural femoral bone graft was examined by real-time polymerase chain reaction and immunohistochemical analysis. The bone graft model was treated with anti-SDF-1 neutralizing antibody or TF14016, an antagonist for CXCR4, and evaluated by histomorphometry. The functional effect of SDF-1 on primary mesenchymal stem cells was determined by in vitro and in vivo migration assays. New bone formation in an exchanging-graft model was compared with that in the autograft models, using mice partially lacking SDF-1 (SDF-1 ؉/؊ ) or CXCR4 (CXCR4 ؉/؊ ).Results. The expression of SDF1 messenger RNA was increased during the healing of live bone grafts but was not increased in dead grafts. High expression of SDF-1 protein was observed in the periosteum of the live graft. New bone formation was inhibited by the administration of anti-SDF-1 antibody or TF14016. SDF-1 increased mesenchymal stem cell chemotaxis in vitro in a dose-dependent manner. The in vivo migration study demonstrated that mesenchymal stem cells recruited by SDF-1 participate in endochondral bone repair. Bone formation was decreased in SDF-1 ؉/؊ and CXCR4 ؉/؊ mice and was restored by the graft bones from CXCR4 ؉/؊ mice transplanted into the SDF-1 ؉/؊ femur, but not vice versa.Conclusion. SDF-1 is induced in the periosteum of injured bone and promotes endochondral bone repair by recruiting mesenchymal stem cells to the site of injury.

show abstract

Section: Discussionmentioning

confidence: 84%

Stromal cell–derived factor 1/CXCR4 signaling is critical for the recruitment of mesenchymal stem cells to the fracture site during skeletal repair in a mouse model

Kitaori¹,

Ito²,

Schwarz³

et al. 2009

Arthritis & Rheumatism

512

443

View full text Add to dashboard Cite

show abstract

“…4A). Mature macrophages were also observed in bone explant cultures (data not shown), another common means of obtaining human and rodent primary osteoblasts (23,24). Immunocytochemical analysis was used to locate TNF and showed that F4/80 ϩ mature macrophages are the cellular source of TNF within these cultures (data not shown).…”

Section: Macrophages Are the Lps-responsive Cell Within Primary Osteomentioning

confidence: 94%

Osteal Tissue Macrophages Are Intercalated throughout Human and Mouse Bone Lining Tissues and Regulate Osteoblast Function In Vitro and In Vivo

Chang

Raggatt

Alexander

et al. 2008

The Journal of Immunology

618

646

View full text Add to dashboard Cite

Resident macrophages are an integral component of many tissues and are important in homeostasis and repair. This study examines the contribution of resident tissue macrophages to bone physiology. Using immunohistochemistry, we showed that a discrete population of resident macrophages, OsteoMacs, was intercalated throughout murine and human osteal tissues. OsteoMacs were distributed among other bone lining cells within both endosteum and periosteum. Furthermore, OsteoMacs were coisolated with osteoblasts in murine bone explant and calvarial preparations. OsteoMacs made up 15.9% of calvarial preparations and persisted throughout standard osteoblast differentiation cultures. Contrary to previous studies, we showed that it was OsteoMacs and not osteoblasts within these preparations that responded to pathophysiological concentrations of LPS by secreting TNF. Removal of OsteoMacs from calvarial cultures significantly decreased osteocalcin mRNA induction and osteoblast mineralization in vitro. In a Transwell coculture system of enriched osteoblasts and macrophages, we demonstrated that macrophages were required for efficient osteoblast mineralization in response to the physiological remodeling stimulus, elevated extracellular calcium. Notably, OsteoMacs were closely associated with areas of bone modeling in situ, forming a distinctive canopy structure covering >75% of mature osteoblasts on diaphyseal endosteal surfaces in young growing mice. Depletion of OsteoMacs in vivo using the macrophage-Fas-induced apoptosis (MAFIA) mouse caused complete loss of osteoblast bone-forming surface at this modeling site. Overall, we have demonstrated that OsteoMacs are an integral component of bone tissues and play a novel role in bone homeostasis through regulating osteoblast function. These observations implicate OsteoMacs, in addition to osteoclasts and osteoblasts, as principal participants in bone dynamics.

show abstract

“…Then the chips were incubated in 1 mg/ml of type II collagenase (Sigma-Aldrich) at 37 C for 2 hr with shaking. After wash with a-MEM for three times, bone fragments were cultured in a-MEM containing 10% selected FBS at 37 C in 5% CO 2 for cell expansion (Guo et al, 2006).…”

Section: Isolation and Expansion Of Mscs From Compact Bonementioning

confidence: 99%

Migration of dorsal aorta mesenchymal stem cells induced by mouse embryonic circulation

Yan

Lan

Wang³

et al. 2010

Developmental Dynamics

Self Cite

View full text Add to dashboard Cite

Mesenchymal stem cells (MSCs) represent powerful tools for regenerative medicine for their differentiation and migration capacity. However, ontogeny and migration of MSCs in mammalian mid-gestation conceptus is poorly understood. We identified canonical MSCs in the mouse embryonic day (E) 11.5 dorsal aorta (DA). They possessed homogenous immunophenotype (CD45 2 CD31 2 Flk-1 2 CD44 1 CD29 1 ), expressed perivascular markers (a-SMA 1 NG2 1 PDGFRb 1 PDGFRa 1 ), and had tri-lineage differentiation potential (osteoblasts, adipocytes, and chondrocytes). Of interest, MSCs were also detected in E12.5-E13.5 embryonic circulation, 24 hr later than in DA, suggesting migration like hematopoietic stem cells. Functionally, E12.5 embryonic blood could trigger efficient migration of DA-MSCs through platelet-derived growth factor (PDGF) receptor-, transforming growth factor-beta receptor-, but not basic fibroblast growth factor receptor-mediated signaling. Moreover, downstream JNK and AKT signaling pathway played important roles in embryonic blood-or PDGF-mediated migration of DA-derived MSCs. Taken together, these results revealed that clonal MSCs developed in the mouse DA. More importantly, the embryonic circulation, in addition to its conventional transporting roles, could modulate migration of MSC during early embryogenesis. Developmental Dynamics 240:65-74,

show abstract

In Vitro Characteristics and In Vivo Immunosuppressive Activity of Compact Bone-Derived Murine Mesenchymal Progenitor Cells

Cited by 95 publications

References 51 publications

Stromal cell–derived factor 1/CXCR4 signaling is critical for the recruitment of mesenchymal stem cells to the fracture site during skeletal repair in a mouse model

Stromal cell–derived factor 1/CXCR4 signaling is critical for the recruitment of mesenchymal stem cells to the fracture site during skeletal repair in a mouse model

Osteal Tissue Macrophages Are Intercalated throughout Human and Mouse Bone Lining Tissues and Regulate Osteoblast Function In Vitro and In Vivo

Migration of dorsal aorta mesenchymal stem cells induced by mouse embryonic circulation

Contact Info

Product

Resources

About