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MicroRNA-132/212 family enhances arteriogenesis after hindlimb ischaemia through modulation of the Ras-MAPK pathway.

Lei Z, van Mil A, Brandt MM, Grundmann S, Hoefer I, Smits M, El Azzouzi H, Fukao T, Cheng C, Doevendans PA, Sluijter JP - J. Cell. Mol. Med. (2015)

Bottom Line: Moreover, in in vitro pericyte-endothelial co-culture cell assays, overexpression of miR-132 and mir-212 in endothelial cells results in enhanced vascularization, as shown by an increase in tubular structures and junctions.Our results suggested that miR-132/212 may exert their effects by enhancing the Ras-Mitogen-activated protein kinases MAPK signalling pathway through direct inhibition of Rasa1, and Spred1.The miR-132/212 cluster promotes arteriogenesis by modulating Ras-MAPK signalling via direct targeting of its inhibitors Rasa1 and Spred1.

View Article: PubMed Central - PubMed

Affiliation: Division Heart and Lungs, Department of Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands.

No MeSH data available.


Related in: MedlinePlus

miR-132/212 expression after hind-limb ischaemia. (A) miR-132 expression as measured by qPCR assays. N = 5, values in the graph are shown as mean ± SEM, *P < 0.05; **P < 0.01. (B) miR-212 expression as measured by qPCR assays. N = 5, values in the graph are shown as mean ± SEM, **P < 0.01; ***P < 0.001.
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fig01: miR-132/212 expression after hind-limb ischaemia. (A) miR-132 expression as measured by qPCR assays. N = 5, values in the graph are shown as mean ± SEM, *P < 0.05; **P < 0.01. (B) miR-212 expression as measured by qPCR assays. N = 5, values in the graph are shown as mean ± SEM, **P < 0.01; ***P < 0.001.

Mentions: To understand the function of miR-132 and miR-212 in arteriogenesis, we performed hind-limb ischaemia on WT mice and checked the expression of these two microRNAs in the thigh muscle at different time points after hind-limb ischaemia. By qRT-PCR, we found that miR-132 and miR-212 levels were significantly increased on day 4 and day 7 (Fig.1A and B) after hindlimb ischaemia in the adductor muscle.


MicroRNA-132/212 family enhances arteriogenesis after hindlimb ischaemia through modulation of the Ras-MAPK pathway.

Lei Z, van Mil A, Brandt MM, Grundmann S, Hoefer I, Smits M, El Azzouzi H, Fukao T, Cheng C, Doevendans PA, Sluijter JP - J. Cell. Mol. Med. (2015)

miR-132/212 expression after hind-limb ischaemia. (A) miR-132 expression as measured by qPCR assays. N = 5, values in the graph are shown as mean ± SEM, *P < 0.05; **P < 0.01. (B) miR-212 expression as measured by qPCR assays. N = 5, values in the graph are shown as mean ± SEM, **P < 0.01; ***P < 0.001.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4549050&req=5

fig01: miR-132/212 expression after hind-limb ischaemia. (A) miR-132 expression as measured by qPCR assays. N = 5, values in the graph are shown as mean ± SEM, *P < 0.05; **P < 0.01. (B) miR-212 expression as measured by qPCR assays. N = 5, values in the graph are shown as mean ± SEM, **P < 0.01; ***P < 0.001.
Mentions: To understand the function of miR-132 and miR-212 in arteriogenesis, we performed hind-limb ischaemia on WT mice and checked the expression of these two microRNAs in the thigh muscle at different time points after hind-limb ischaemia. By qRT-PCR, we found that miR-132 and miR-212 levels were significantly increased on day 4 and day 7 (Fig.1A and B) after hindlimb ischaemia in the adductor muscle.

Bottom Line: Moreover, in in vitro pericyte-endothelial co-culture cell assays, overexpression of miR-132 and mir-212 in endothelial cells results in enhanced vascularization, as shown by an increase in tubular structures and junctions.Our results suggested that miR-132/212 may exert their effects by enhancing the Ras-Mitogen-activated protein kinases MAPK signalling pathway through direct inhibition of Rasa1, and Spred1.The miR-132/212 cluster promotes arteriogenesis by modulating Ras-MAPK signalling via direct targeting of its inhibitors Rasa1 and Spred1.

View Article: PubMed Central - PubMed

Affiliation: Division Heart and Lungs, Department of Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands.

No MeSH data available.


Related in: MedlinePlus