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Abstract #92458 Published in IGR 22-1

MiR-137 promotes cell growth and inhibits extracellular matrix protein expression in HO-induced human trabecular meshwork cells by targeting Src

Wang L; Tian Y; Cao Y; Ma Q; Zhao S
Neuroscience Letters 2021; 755: 135902

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Glaucoma is a progressive optic neuropathy in more than 25 % of cases in patients with permanent blindness. The microRNA is implicated in modulating the cellular function of the trabecular meshwork (TM). The aim of this study is to investigate the role of miR-137 in glaucoma and illustrate the potential molecular mechanisms. We show that miR-137 was down-regulated in HO-induced human trabecular meshwork cells (HTMCs), and overexpression of miR-137 attenuated HO-induced cell growth inhibition, apoptosis and elevated extracellular matrix (ECM) protein expression. In addition, miR-137 blocked the activation of YAP/TAZ by directly targeting src. Overexpression of src or activation of the YAP/TAZ pathway partly abrogated the effects of miR-137 on HO-induced cell viability and apoptosis and dampened the inhibition effect on ECM protein expression. In conclusion, miR-137 promotes cell growth and inhibits extracellular matrix protein expression in HO-induced human trabecular meshwork cells via the YAP/TAZ pathway by targeting src. Hence, miR-137 might be used as a novel therapeutic target to treat glaucoma.

Department of Ophthalmology, Xi'an NO.1 Hospital, Xi'an, 710002, China.

Full article

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Classification:

3.6 Cellular biology (Part of: 3 Laboratory methods)
11.14 Investigational drugs; pharmacological experiments (Part of: 11 Medical treatment)
3.5 Molecular biology incl. SiRNA (Part of: 3 Laboratory methods)

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