2020
DOI: 10.1016/j.diabres.2020.108121
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miR-221-3p and miR-222-3p downregulation promoted osteogenic differentiation of bone marrow mesenchyme stem cells through IGF-1/ERK pathway under high glucose condition

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Cited by 31 publications
(26 citation statements)
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“…Combined with the negative effect of miR-186 on rat BMSC osteogenesis and the inhibitory action on the final myogenesis differentiation step by influencing myogenin translation, we deduce that miR-186 may be the driving factor in bone-muscle crosstalk during aging (Antoniou et al, 2014;. Furthermore, the increased miR-221 in aged-BMSC may also function in osteosarcopenia, because it was reported that ectopic overexpression of miR-221 in skeletal muscle satellite cells inhibits myotube formation and miR-221 was found to be a negative regulator of bone formation (Zhang et al, 2017;Liu B. et al, 2018;Gan et al, 2020). Xu R. et al (2018) reported aged BMSCs express high levels of miR-31a-5p leading to bias lineage fate of BMSCs to adipocytes through AT-rich sequence binding protein 2 (SATB2), aged BMSCs also release miR-31a-5p enriched EVs to its microenvironment, inducing increase in osteoclast number and function via the RhoA pathway.…”
Section: Ev-micrornas Of Bone Cells Engaged In Bone-muscle Crosstalkmentioning
confidence: 81%
“…Combined with the negative effect of miR-186 on rat BMSC osteogenesis and the inhibitory action on the final myogenesis differentiation step by influencing myogenin translation, we deduce that miR-186 may be the driving factor in bone-muscle crosstalk during aging (Antoniou et al, 2014;. Furthermore, the increased miR-221 in aged-BMSC may also function in osteosarcopenia, because it was reported that ectopic overexpression of miR-221 in skeletal muscle satellite cells inhibits myotube formation and miR-221 was found to be a negative regulator of bone formation (Zhang et al, 2017;Liu B. et al, 2018;Gan et al, 2020). Xu R. et al (2018) reported aged BMSCs express high levels of miR-31a-5p leading to bias lineage fate of BMSCs to adipocytes through AT-rich sequence binding protein 2 (SATB2), aged BMSCs also release miR-31a-5p enriched EVs to its microenvironment, inducing increase in osteoclast number and function via the RhoA pathway.…”
Section: Ev-micrornas Of Bone Cells Engaged In Bone-muscle Crosstalkmentioning
confidence: 81%
“…Upregulating miR-7-5p inhibited the osteogenic differentiation of iPDLSCs and IGF-1R was identified as a direct target of miR-7-5p. Otherwise, Gan et al showed that miR-221-3p and miR-222-3p were up-regulated in the mandibles of diabetic rats and BMSCs cultured in high glucose condition [ 70 ]. Silencing of miR-221-3p or/ and miR-222-3p increased ALP activity and up-regulated osteoblast-related protein levels.…”
Section: Mechanisms Of Action Of the Gh/igfs/igfbps Axis On Dental And Bone Cellsmentioning
confidence: 99%
“…MicroRNA-222 is located within an X-chromosome miRNA cluster, and the miR-222 sequence is highly conserved in pigs, humans, mice, cattle and other species, suggesting that it may be related to male fertility and sperm function and that the effect may be similar across species. As a key regulatory factor, miR-222 has also been reported to be involved in many other biological processes, such as cell proliferation, cell death, autophagy and apoptosis (Wang et al, 2015;Ding et al, 2018;Gan et al, 2020). In the present study, the results suggested that miR-222 can significantly improve sperm motility.…”
Section: Discussionsupporting
confidence: 54%