Document Type

Article

Publication Date

6-1-2010

Identifier

PMCID: PMC2876242 DOI: 10.1007/s12079-010-0088-9

Abstract

Podocytes play a key role in maintaining and modulating the filtration barrier of the glomerulus. Because of their location, podocytes are exposed to mechanical strain in the form of fluid flow shear stress (FFSS). Several human diseases are characterized by glomerular hyperfiltration, such as diabetes mellitus and hypertension. The response of podocytes to FFSS at physiological or pathological levels is not known. We exposed cultured podocytes to FFSS, and studied changes in actin cytoskeleton, prostaglandin E(2) (PGE(2)) production and expression of cyclooxygenase-1 and-2 (COX-1, COX-2). FFSS caused a reduction in transversal F-actin stress filaments and the appearance of cortical actin network in the early recovery period. Cells exhibited a pattern similar to control state by 24 h following FFSS without significant loss of podocytes or apoptosis. FFSS caused increased levels of PGE(2) as early as 30 min after onset of shear stress, levels that increased over time. PGE(2) production by podocytes at post-2 h and post-24 h was also significantly increased compared to control cells (p < 0.039 and 0.012, respectively). Intracellular PGE(2) synthesis and expression of COX-2 was increased at post-2 h following FFSS. The expression of COX-1 mRNA was unchanged. We conclude that podocytes are sensitive and responsive to FFSS, exhibiting morphological and physiological changes. We believe that PGE(2) plays an important role in mechanoperception in podocytes.

Journal Title

J Cell Commun Signal

Volume

4

Issue

2

First Page

79

Last Page

90

MeSH Keywords

Podocytes; Dinoprostone; Stress, Mechanical

Keywords

Actin; Cyclooxygenase; Mechanical strain; Prostaglandin E2; Shear stress

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