Pax2 is essential for proliferation and osteogenic differentiation of mouse mesenchymal stem cells via Runx2
- Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, 140 Hanzhong Road, Nanjing 210029 (China)
- Department of Medical Genetics, Nanjing Medical University, Longmian Road 101, Nanjing 211166 (China)
Highlights: • Knock-down of Pax2 inhibits the osteogenesis of mouse MSCs in vitro and in vivo. • Pax2 promotes the proliferation of mouse MSCs. • Pax2 enhances transcriptional activity of Runx2 and activates MAPK pathways. • Pax2 promotes the osteogenesis of mouse MSCs and may serve as a target for future clinical treatment. Mesenchymal stem cells (MSCs) have been widely studied in the field of regenerative medicine with the potential to solve osteoporosis. Paired box 2 (Pax2), as a transcription factor, is the master regulator of embryogenesis and oncogenesis. However, the function of Pax2 in osteogenesis is unknown. Here, we reported for the first time that the expression of Pax2 gradually increased during osteogenic differentiation of mouse MSCs, and osteoprogenitor cells. However, detected in osteoblastic cells of mouse tibia, the expression of Pax2 in the embryonic stage was higher than that in adulthood. In C3H/10/T1/2 cells and compact bone-derived mouse MSCs (mMSCs), Pax2 knock-down inhibited the proliferation of these cells, down-regulated the expression of osteogenic marker genes, as well as repressed the ALP activity and mineralization. In addition, Pax2 enhanced the transcriptional activity of Runx2, and activated the MAPK pathway genes (ERK, JNK and p38). Furthermore, knock-down of Pax2 repressed the mMSCs-mediated bone regeneration in an ectopic bone formation model. In conclusion, Pax2 promotes osteogenesis of mouse MSCs, suggesting that Pax2 has a role in the pathophysiology of bone related diseases, and has potential application in bone tissue regeneration.
- OSTI ID:
- 23082569
- Journal Information:
- Experimental Cell Research, Vol. 371, Issue 2; Other Information: Copyright (c) 2018 Elsevier Inc. All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0014-4827
- Country of Publication:
- United States
- Language:
- English
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