| Title |
Identification of novel microRNA inhibiting actin cytoskeletal rearrangement thereby suppressing osteoblast differentiation
|
|---|---|
| Published in |
Journal of Molecular Medicine, March 2018
|
| DOI | 10.1007/s00109-018-1624-y |
| Pubmed ID | |
| Authors |
Aijaz A. John, Ravi Prakash, Jyoti Kureel, Divya Singh |
| Abstract |
We report the role of miR-1187 in regulation of osteoblast functions. Over-expression of miR-1187 inhibited osteoblast differentiation. Target prediction analysis tools and experimental validation by luciferase 3' UTR reporter assay identified BMPR-II and ArhGEF-9 as direct targets of miR-1187. ArhGEF-9 activates Cdc42 which has a major role in actin reorganization. BMP-2 also induces actin polymerization. Role of miR-1187 in actin reorganization was determined by western blotting, immunofluorescence, and in vivo gene silencing studies. Reduced protein levels of BMPR-II, activated Cdc42, and downstream signaling molecules were observed in miR-1187-transfected osteoblasts. miR-1187 over-expression resulted in decreased actin polymerization. Additionally, P-cofilin, which does not bind F-actin, was decreased in miR-1187-transfected cells. These results were corroborated by administration of BMPR-II exogenously in miR-1187-transfected osteoblasts. Silencing of miR-1187 in neonatal mice mitigated all the inhibitory effects of miR-1187 on actin cytoskeletal rearrangement. Importantly, in vivo treatment of miR-1187 inhibitor to ovariectomized BALB/c mice led to significant improvement in trabecular bone microarchitecture. Overall, miR-1187 functions as a negative regulator of osteogenesis by repressing BMPR-II and ArhGEF-9 expression thus suppressing non-Smad BMP2/Cdc42 signaling pathway and inhibiting actin reorganization. miR-1187 functions as a negative regulator of osteogenesis by repressing BMPR-II expression, which in turn, suppresses non-Smad BMP2/Cdc42 signaling pathway, thus inhibiting actin cytoskeletal rearrangement. Silencing of miR-1187 significantly improves trabecular bone microarchitecture. As miR-1187 exerts a negative regulatory role in osteoblasts function, hence, we propose that therapeutic approaches targeting miR-1187 could be useful in enhancing the bone formation and treatment of pathological conditions of bone loss. |
X Demographics
The data shown below were collected from the profiles of 2 X users who shared this research output. Click here to find out more about how the information was compiled.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 2 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Practitioners (doctors, other healthcare professionals) | 1 | 50% |
| Members of the public | 1 | 50% |
Mendeley readers
The data shown below were compiled from readership statistics for 17 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 17 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Master | 4 | 24% |
| Student > Ph. D. Student | 3 | 18% |
| Researcher | 2 | 12% |
| Student > Doctoral Student | 1 | 6% |
| Unknown | 7 | 41% |
| Readers by discipline | Count | As % |
|---|---|---|
| Biochemistry, Genetics and Molecular Biology | 4 | 24% |
| Pharmacology, Toxicology and Pharmaceutical Science | 2 | 12% |
| Agricultural and Biological Sciences | 2 | 12% |
| Medicine and Dentistry | 1 | 6% |
| Unknown | 8 | 47% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 12 March 2018.
All research outputs
#17,933,348
of 23,026,672 outputs
Outputs from Journal of Molecular Medicine
#1,223
of 1,554 outputs
Outputs of similar age
#241,663
of 332,332 outputs
Outputs of similar age from Journal of Molecular Medicine
#6
of 11 outputs
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