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Srivastava T, McCarthy ET, Sharma R, et al. Prostaglandin E(2) is crucial in the response of podocytes to fluid flow shear stress. J Cell Commun Signal. 2010;4(2):79-90doi: 10.1007/s12079-010-0088-9.
Srivastava, T., McCarthy, E. T., Sharma, R., Cudmore, P. A., Sharma, M., Johnson, M. L., & Bonewald, L. F. (2010). Prostaglandin E(2) is crucial in the response of podocytes to fluid flow shear stress. Journal of cell communication and signaling, 4(2), 79-90. https://doi.org/10.1007/s12079-010-0088-9
Srivastava, Tarak, et al. "Prostaglandin E(2) is crucial in the response of podocytes to fluid flow shear stress." Journal of cell communication and signaling vol. 4,2 (2010): 79-90. doi: https://doi.org/10.1007/s12079-010-0088-9
Srivastava T, McCarthy ET, Sharma R, Cudmore PA, Sharma M, Johnson ML, Bonewald LF. Prostaglandin E(2) is crucial in the response of podocytes to fluid flow shear stress. J Cell Commun Signal. 2010 Jun;4(2):79-90. doi: 10.1007/s12079-010-0088-9. Epub 2010 Apr 08. PMID: 20531983; PMCID: PMC2876242.
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J Cell Commun Signal. 2010 Jun;4(2):79-90. doi: 10.1007/s12079-010-0088-9. Epub 2010 Apr 08.

Prostaglandin E(2) is crucial in the response of podocytes to fluid flow shear stress.

Journal of cell communication and signaling

Tarak Srivastava, Ellen T McCarthy, Ram Sharma, Patricia A Cudmore, Mukut Sharma, Mark L Johnson, Lynda F Bonewald

PMID: 20531983 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.

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

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