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Changes in extracellular matrix composition regulate cyclooxygenase-2 expression in human mesangial cells

AuthorsAlique, Matilde; Calleros, Laura; Luengo, Alicia; Griera, Mercedes; Íñiguez, Miguel Ángel ; Punzón, Carmen ; Fresno, Manuel ; Rodríguez-Puyol, Manuel; Rodríguez-Puyol, Diego
Glomerular diseases
Issue Date2011
PublisherAmerican Physiological Society
CitationAmerican Journal of Physiology - Cell Physiology 300 (4): C907-C918 (2011)
AbstractGlomerular diseases are characterized by a sustained synthesis and accumulation of abnormal extracellular matrix proteins, such as collagen type I. The extracellular matrix transmits information to cells through interactions with membrane components, which directly activate many intracellular signaling events. Moreover, accumulating evidence suggests that eicosanoids derived from cyclooxygenase (COX)-2 participate in a number of pathological processes in immune-mediated renal diseases, and it is known that protein kinase B (AKT) may act through different transcription factors in the regulation of the COX-2 promoter. The present results show that progressive accumulation of collagen I in the extracellular medium induces a significant increase of COX-2 expression in human mesangial cells, resulting in an enhancement in PGE(2) production. COX-2 overexpression is due to increased COX-2 mRNA levels. The study of the mechanism implicated in COX-2 upregulation by collagen I showed focal adhesion kinase (FAK) activation. Furthermore, we observed that the activation of the phosphatidylinositol 3-kinase (PI3K)/AKT pathway by collagen I and collagen I-induced COX-2 overexpression was abolished by PI3K and AKT inhibitors. Additionally, we showed that the cAMP response element (CRE) transcription factor is implicated. Finally, we studied COX-2 expression in an animal model, N(G)-nitro-l-arginine methyl ester hypertensive rats. In renal tissue and vascular walls, COX-2 and collagen type I content were upregulated. In summary, our results provide evidence that collagen type I increases COX-2 expression via the FAK/PI3K/AKT/cAMP response element binding protein signaling pathway.
Publisher version (URL)http://dx.doi.org/10.​1152/​ajpcell.​00176.​2010
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