Atorvastatin prevents glomerular extracellular matrix formation by interfering with the PKC signaling pathway.
Mol Med Rep
; 17(5): 6441-6448, 2018 05.
Article
en En
| MEDLINE
| ID: mdl-29532876
ABSTRACT
Platelet-activating factor (PAF) promotes glomerular extracellular matrix (ECM) deposition, primarily through activation of the protein kinase C (PKC) pathway. The present study was designed to investigate whether atorvastatin, which mediates a protective effect against glomerular ECM deposition and diabetic neuropathy, may interfere with the PKCtransforming growth factorß1 (TGFß1) pathway in a model of human mesangial cells (HMCs) exposed to a high glucose (HG) and lysophosphatidylcholine (LPC) environment. HMCs were divided into three treatment groups Control, high glucose and lysophosphatidylcholine (HG+LPC), and HG+LPC+atorvastatin. Cells were cultured for 24 h. The levels of the ECMassociated molecules collagen IV (Col IV) and fibronectin (Fn) in the supernatant were detected using an ELISA kit. PKCß1, TGFß1 and PAFreceptor gene expression was detected by reverse transcriptionquantitative polymerase chain reaction. PKCß1 and TGFß1 protein expression was detected by western blotting, and the subcellular localization of PKCß1 was assessed using immunofluorescence. The results indicated that atorvastatin may reduce the secretion of ECM components (Fn and Col IV) in HMCs in a HG and LPC environment, by inhibiting the increase in PAF secretion and the activation of the PKCTGFß1 signaling pathway.
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Texto completo:
1
Base de datos:
MEDLINE
Asunto principal:
Transducción de Señal
/
Matriz Extracelular
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Proteína Quinasa C beta
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Atorvastatina
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Mesangio Glomerular
Tipo de estudio:
Prognostic_studies
Idioma:
En
Revista:
Mol Med Rep
Año:
2018
Tipo del documento:
Article