Tension-loaded bone marrow stromal cells potentiate the paracrine osteogenic signaling of co-cultured vascular endothelial cells
Autor: | Feng Ting Chu, Guo Hua Tang, Jun Zhao, Yang Yang Jiang, Yu Nan Jiang |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Stromal cell Tivozanib QH301-705.5 VEGF receptors Mrna expression Science General Biochemistry Genetics and Molecular Biology Bone tissue engineering 03 medical and health sciences Paracrine signalling stomatognathic system Conditioned medium medicine Biology (General) Paracrine signaling biology Bone marrow stromal cells Cell biology 030104 developmental biology medicine.anatomical_structure Tension biology.protein Bone marrow Co-culture General Agricultural and Biological Sciences Vascular endothelial cells Research Article medicine.drug |
Zdroj: | Biology Open, Vol 7, Iss 6 (2018) Biology Open |
ISSN: | 2046-6390 |
Popis: | Co-culture of bone marrow stromal cells (BMSCs) and vascular endothelial cells (VECs) is a promising strategy for better osteogenesis and pre-vascularization in bone tissue engineering. Recent reports have shown that mechanical stretching further promotes osteogenesis in BMSC/VEC co-culture systems, but the underlying mechanism of this process remains unclear. In this study, noncontact co-cultures of rat primary BMSCs and VECs were employed to interrogate paracrine cell-to-cell communications in response to tension. Exposure of VECs to 6% tension for 48 h elicited neither ALP activity nor mRNA expression of OCN and OPN in BMSCs incubated in a shared culture medium. Instead, BMSCs subjected to tension induced robust VEGF release, and its conditioned medium enhanced the proliferation and tubular formation of VECs with a concurrent increase in BMP-2 and IGF-1 production. Conditioned medium from activated VECs in turn promoted expression of osteogenic genes in BMSCs, followed by an increase in matrix mineralization. The addition of VEGF-R inhibitor Tivozanib to these systems abrogated the tension-induced paracrine effects on VECs and subsequently impaired BMSC osteogenesis. These results clearly demonstrate that the response of BMSCs to tension potentiates paracrine osteogenic signaling from VECs; this positive feedback loop is initiated by VEGF release. Summary: This present study demonstrates that the response of BMSCs to tension potentiates paracrine osteogenic signaling from co-cultured VECs; this positive feedback loop is initiated by VEGF release. |
Databáze: | OpenAIRE |
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