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Related Experiment Videos

Endoglin regulates cyclooxygenase-2 expression and activity.

Mirjana Jerkic1, Juan V Rivas-Elena, Juan F Santibanez

  • 1Instituto Reina Sofía de Investigación Nefrológica, Departamento de Fisiología & Farmacología, Universidad de Salamanca, Salamanca, Spain.

Circulation Research
|July 15, 2006
PubMed
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Endoglin deficiency in hereditary hemorrhagic telangiectasia (HHT) models increases cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2). Endoglin regulates COX-2, suggesting impaired NO production contributes to COX-2 upregulation in HHT.

Area of Science:

  • Vascular Biology
  • Molecular Medicine
  • Biochemistry

Background:

  • Hereditary hemorrhagic telangiectasia (HHT) is modeled by endoglin heterozygous (Eng(+/-)) mice, exhibiting reduced endothelial NO synthase (eNOS) and impaired activity.
  • Vasomotor function is complex in Eng(+/-) mice, with potential interactions between nitric oxide (NO) and prostaglandin pathways.

Purpose of the Study:

  • To investigate the expression and function of cyclooxygenase (COX) isoforms in the context of endoglin deficiency and HHT.
  • To determine the regulatory role of endoglin in COX-2 expression and activity.

Main Methods:

  • Assessed COX isoform expression and activity in Eng(+/-) and wild-type (Eng(+/+)) mice.
  • Utilized COX-2 inhibition (parecoxib) and NO synthesis inhibition (N(omega)-nitro-l-arginine methyl ester).

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  • Employed gene transfection and silencing techniques in cell models (L6E9 myoblasts, endothelial cells) with endoglin manipulation.

    • Main Results:

    • Eng(+/-) mice showed COX-2 upregulation in vascular endothelium and increased urinary prostaglandin E2 (PGE2).
    • COX-2 inhibition transiently increased arterial pressure in Eng(+/-) mice.
    • Endoglin transfection downregulated COX-2; endoglin levels inversely correlated with COX-2 activity.
    • NO synthesis inhibition increased COX-2 in normal mice but had differential effects in endoglin-manipulated cells.

    Conclusions:

    • Endoglin plays a regulatory role in COX-2 activity.
    • Reduced endoglin levels and impaired NO production contribute to elevated COX-2 expression and activity in HHT models.