Taken together, our results show that circulating miR-19b plays an important role in enhancing osteoblastogenesis, possibly through regulation of the PTEN/pAKT/Runx2 pathway, and may be a useful therapeutic target in bone loss disorders, such as osteoporosis.
The probable positive effects of photobiomodulation therapy (PBMT) and oxytocin (OT) treatments together or alone were evaluated on cell viability along with the changes in the gene expression of Osteocalcin (OC), Osteoprotegerin (OPG), and Runt-related transcription factor 2 (Runx2) levels of sham (healthy)-Bone marrow mesenchymal stem cell(BMMSC) and ovariectomy-induced osteoporosis (OVX)-BMMSC.
Overexpression of GAS5 promotes osteogenic differentiation of hMSCs through regulating microRNA-498 to up-regulate RUNX2 expression, thus alleviating the development of osteoporosis.
There were abnormal changes in the protein expressions of Bmp-2, Smad1, Smad5 and Runx2 in bone tissue, which may be an important mechanism underlying the development of kidney deficiency osteoporosis.
All of the above indicate that oral administration of icariin can prevent diabetic osteoporosis; the effect is mainly related to its ability to reduce blood glucose, inhibit bone turnover and bone marrow adipogenesis, as well as up-regulate bone RUNX 2, and OPG expression.
Taken together, these results suggest that miR-135a-5p may serve a role in osteoporosis progression by regulating osteogenic differentiation via RUNX2.
Chromatin immunoprecipitation showed that higher methylation was associated with reduced SP7, RUNX2, and ERα binding to the <i>SOST</i> promoter in patients with osteoporosis.
Cleidocranial dysplasia (CCD) in humans is an autosomal-dominant skeletal dysplasia caused by heterozygous mutations of the runt-related transcription factor 2 (RUNX2) and significantly increases the risk of osteoporosis.
The present results suggested that miR‑488 is a negative regulator of psoralen‑induced BMSC osteogenic differentiation by targeting Runx2, providing a possible therapeutic target for osteoporosis.
However, MSC-based therapy for osteoporosis in CCD patients is difficult due to a reduction in the ability of MSCs to differentiate into osteoblasts resulting from impaired RUNX2 function.
Moreover, caudal vein injection of agomir-23b notably caused severe osteoporosis in mice, and forced expression of runx2 by combined injecting Ad-runx2 attenuated the bone loss induced by miR-23b.
Plausibly, homeostatic feedback loops that rely on Runx2 activation to compensate for bone loss in GIO are thwarted, exacerbating disease progression through stimulation of Wif1..
Taken together, these data implied that miR-221 played an important part in osteoporosis through regulating RUNX2 expression and osteoblast differentiation.
Four of these candidate variants (one each in CXXC1 and RUNX2 and two in LRP5) had a >70% derived allele frequency in East Asians, but were present at lower (20-60%) frequency in Europeans as well, suggesting that the adaptation might have been part of a common response to climatic and dietary changes as humans expanded out of Africa, with implications for their role in vitamin D-dependent bone mineralization and osteoporosis insurgence.
Oxidative stress is implicated in osteoporosis; furthermore the osteoblast transcriptional factor RUNX2 is reported to play a protective role against osteoporosis in postmenopausal women.
The A allele was associated with increased BMD and was protective against a common form of osteoporotic fracture, suggesting that RUNX2 variants may be related to genetic effects on BMD and osteoporosis.