CALL FOR PAPERS Novel Mechanisms and Roles of Glomerular Podocytes Cyclooxygenase-2, prostaglandin E2, and prostanoid receptor EP2 in fluid flow shear stress-mediated injury in the solitary kidney

نویسندگان

  • Tarak Srivastava
  • Uri S. Alon
  • Patricia A. Cudmore
  • Belal Tarakji
  • Alexander Kats
  • Robert E. Garola
  • R. Scott Duncan
  • Ellen T. McCarthy
  • Ram Sharma
  • Mark L. Johnson
  • Lynda F. Bonewald
  • Ashraf El-Meanawy
  • Virginia J. Savin
  • Mukut Sharma
چکیده

Tarak Srivastava, Uri S. Alon, Patricia A. Cudmore, Belal Tarakji, Alexander Kats, Robert E. Garola, R. Scott Duncan, Ellen T. McCarthy, Ram Sharma, Mark L. Johnson, Lynda F. Bonewald, Ashraf El-Meanawy, Virginia J. Savin, and Mukut Sharma Section of Nephrology, Children’s Mercy Hospital and University of Missouri-Kansas City, Kansas City, Missouri; Department of Pathology and Laboratory Medicine, Children’s Mercy Hospital and University of Missouri-Kansas City, Kansas City, Missouri; Section of Infectious Diseases, Children’s Mercy Hospital and University of Missouri-Kansas City, Kansas City, Missouri; Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas; Renal Research Laboratory, Research and Development, Kansas City Veterans Affairs Medical Center, Kansas City, Missouri; Department of Oral Biology, University of Missouri-Kansas City School of Dentistry, Kansas City, Missouri; and Division of Nephrology, Medical College of Wisconsin, Milwaukee, Wisconsin

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منابع مشابه

Cyclooxygenase-2, prostaglandin E2, and prostanoid receptor EP2 in fluid flow shear stress-mediated injury in the solitary kidney.

Hyperfiltration subjects podocytes to increased tensile stress and fluid flow shear stress (FFSS). We showed a 1.5- to 2.0-fold increase in FFSS in uninephrectomized animals and altered podocyte actin cytoskeleton and increased synthesis of prostaglandin E2 (PGE2) following in vitro application of FFSS. We hypothesized that increased FFSS mediates cellular changes through specific receptors of ...

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Role of the prostaglandin E2/E-prostanoid 2 receptor signalling pathway in TGFβ-induced mice mesangial cell damage

The prostaglandin E2 receptor, EP2 (E-prostanoid 2), plays an important role in mice glomerular MCs (mesangial cells) damage induced by TGFβ1 (transforming growth factor-β1); however, the molecular mechanisms for this remain unknown. The present study examined the role of the EP2 signalling pathway in TGFβ1-induced MCs proliferation, ECM (extracellular matrix) accumulation and expression of PGE...

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Distinct roles for basal and induced COX-2 in podocyte injury.

Transgenic mice that overexpress cyclooxygenase-2 (COX-2) selectively in podocytes are more susceptible to glomerular injury by adriamycin and puromycin (PAN). To investigate the potential roles of COX-2 metabolites, we studied mice with selective deletion of prostanoid receptors and generated conditionally immortalized podocyte lines from mice with either COX-2 deletion or overexpression. Podo...

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Role of prostaglandin receptor EP2 in the regulations of cancer cell proliferation, invasion, and inflammation.

Population studies, preclinical, and clinical trials suggest a role for cyclooxygenase-2 (COX-2, PTGS2) in tumor formation and progression. The downstream prostanoid receptor signaling pathways involved in tumorigenesis are poorly understood, although prostaglandin E2 (PGE(2)), a major COX-2 metabolite which is usually upregulated in the involved tissues, presumably plays important roles in tum...

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Prostaglandin E2 mediates IL-1beta-related fibroblast mitogenic effects in acute lung injury through differential utilization of prostanoid receptors.

The fibroproliferative response to acute lung injury (ALI) results in severe, persistent respiratory dysfunction. We have reported that IL-1beta is elevated in pulmonary edema fluid in those with ALI and mediates an autocrine-acting, fibroblast mitogenic pathway. In this study, we examine the role of IL-1beta-mediated induction of cyclooxygenase-2 and PGE2, and evaluate the significance of indi...

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تاریخ انتشار 2014