Experimental study on the regulation of the cholinergic pathway in renal macrophages by microRNA-132 to alleviate inflammatory response

Experimental study on the regulation of the cholinergic pathway in renal macrophages by... AbstractMicroRNA-132 (miR-132) is correlated with inflammatory response regulation, although its effect on acute kidney injury to provide protection against hemorrhagic shock remains currently unknown. AChE in macrophages of the kidney subjected under hemorrhagic shock is presumed to be regulated by miR-132 after its transcription to alleviate the inflammatory response accordingly. Antagonists such as acetylcholine (Ach) (concentration 10−4mol/L) and galanthamine (Gal) (concentration 10μmol/L) were added into separate groups 1 hour after the macrophages in the kidney were isolated and cultured to induce injury under oxygen and glucose deprivation (OGD) and then cultured for 24 hours. To analyze the effect of miR-132, we placed the renal epithelial cells transfected with miR-132 plasmids with stable expression over the renal macrophages to create a double cell culture system. The expression levels of inflammatory factors and apoptosis under OGD were significantly higher in renal macrophages than in other experimental groups. Moreover, the expression of miR-132 in macrophages of the double cell culture system showing stable expression of miR-132 increased, whereas that of several inflammatory factors was significantly inhibited. The expression levels of AChE mRNA and protein in the macrophages significantly decreased. The cholinergic antiinflammatory pathway in renal macrophages is regulated by miR-132 via inhibition of the hydrolytic activity of cholinesterase to alleviate inflammatory response, which may play a role in the prevention and treatment of kidney injury caused by hemorrhagic shock. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Open Chemistry de Gruyter

Experimental study on the regulation of the cholinergic pathway in renal macrophages by microRNA-132 to alleviate inflammatory response

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Publisher
De Gruyter
Copyright
© 2018 Ming Wu et al., published by De Gruyter
ISSN
2391-5420
eISSN
2391-5420
D.O.I.
10.1515/chem-2018-0019
Publisher site
See Article on Publisher Site

Abstract

AbstractMicroRNA-132 (miR-132) is correlated with inflammatory response regulation, although its effect on acute kidney injury to provide protection against hemorrhagic shock remains currently unknown. AChE in macrophages of the kidney subjected under hemorrhagic shock is presumed to be regulated by miR-132 after its transcription to alleviate the inflammatory response accordingly. Antagonists such as acetylcholine (Ach) (concentration 10−4mol/L) and galanthamine (Gal) (concentration 10μmol/L) were added into separate groups 1 hour after the macrophages in the kidney were isolated and cultured to induce injury under oxygen and glucose deprivation (OGD) and then cultured for 24 hours. To analyze the effect of miR-132, we placed the renal epithelial cells transfected with miR-132 plasmids with stable expression over the renal macrophages to create a double cell culture system. The expression levels of inflammatory factors and apoptosis under OGD were significantly higher in renal macrophages than in other experimental groups. Moreover, the expression of miR-132 in macrophages of the double cell culture system showing stable expression of miR-132 increased, whereas that of several inflammatory factors was significantly inhibited. The expression levels of AChE mRNA and protein in the macrophages significantly decreased. The cholinergic antiinflammatory pathway in renal macrophages is regulated by miR-132 via inhibition of the hydrolytic activity of cholinesterase to alleviate inflammatory response, which may play a role in the prevention and treatment of kidney injury caused by hemorrhagic shock.

Journal

Open Chemistryde Gruyter

Published: Mar 20, 2018

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