Fluid flow shear stress upregulates prostanoid receptor EP2 but not EP4 in murine podocytes. Prostaglandins Other Lipid Mediat 2013;104-105:49-57
Date
12/25/2012Pubmed ID
23262148DOI
10.1016/j.prostaglandins.2012.11.001Scopus ID
2-s2.0-84879689638 (requires institutional sign-in at Scopus site) 23 CitationsAbstract
Podocytes in the glomerular filtration barrier regulate the passage of plasma proteins into urine. Capillary pressure and ultrafiltration impact the structure and function of podocytes. The mechanism of podocyte injury by fluid flow shear stress (FFSS) from hyperfiltration in chronic kidney disease (CKD) is not completely understood. Recently, we demonstrated increased synthesis of prostaglandin E2 in podocytes exposed to FFSS. Here, we determine the effect of FFSS on prostanoid receptors EP1-EP4 in cultured podocytes and in Os/+ mouse kidney, a model of hyperfiltration. Results of RT-PCR, qRT-PCR, immunoblotting and immunofluorescence studies indicate that cultured podocytes express EP1, EP2 and EP4 but not EP3. FFSS resulted in upregulated expression of only EP2 in podocytes. Kidney immunostaining showed significantly increased expression of EP2 in Os/+ mice compared with littermate controls. These novel results suggest that EP2 may be responsible for mediating podocyte injury from hyperfiltration-induced augmented FFSS in CKD.
Author List
Srivastava T, McCarthy ET, Sharma R, Kats A, Carlton CG, Alon US, Cudmore PA, El-Meanawy A, Sharma MAuthor
Ashraf El-Meanawy MD, PhD Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsCell Line
Diffusion Chambers, Culture
Dinoprostone
Fluorescent Antibody Technique
Gene Expression Regulation
Mice
Mice, Transgenic
Podocytes
Real-Time Polymerase Chain Reaction
Receptors, Prostaglandin E, EP1 Subtype
Receptors, Prostaglandin E, EP2 Subtype
Receptors, Prostaglandin E, EP4 Subtype
Stress, Mechanical
