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J. Wu, C. C. Luna, G. Li, I. D. Navarro, D. L. Epstein, P. Gonzalez; Changes in MicroRNA Expression Induced by Cyclic Mechanical Stress in Trabecular Meshwork Cells. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5988.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate whether cyclic mechanical stress (CMS) induced changes in microRNA expression that could be involved in the responses of human trabecular meshwork cells (HTM) to mechanical forces.
For CMS, 3 primary HTM cell lines were incubated on flexible bottom plates and subjected to cyclic mechanical stress (20% stretching, 1 cycle per second). Non-stress parallel control cultures were incubated in similar plates under identical conditions. Small RNAs were isolated after 3 hours of CMS and changes in microRNA expression were evaluated using the MAH-001 Human Genome RT2 miRNA PCR Array from SABiosciences, which includes 88 microRNA and 8 controls.
Seven of the 88 microRNAs analyzed showed significant (p<0.05) up-regulation after CMS in all the three HTM cell lines tested, and nine were significantly up-regulated in two of the three cell lines (Table 1). The microRNAs consistently up-regulated in the three cell lines included three members of the miR-23b cluster (miR-27b, miR-24, and miR-26a) that collectively down-regulate TGFbeta signaling through direct targeting of Smads; miR-27b that shares similar predicted targets with its paralog miR-27b; MiR-16, a regulator of apoptosis; miR-7, known to regulate ERK 1/2; and let-7f, which regulates the MAP kinase, G protein-coupled receptor kinase-2, and NF-kappaB signaling cascades.
The microRNAS up-regulated by CMS have the potential to contribute to the biological responses induced by mechanical stimuli in HTM cells and exert effects on aqueous humor outflow facility though regulation of signaling pathways such as TGFbeta, NF-kappaB, and MAP kinases.
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