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Related Experiment Videos

Cyclooxygenase-2 and the kidney: functional and pathophysiological implications.

Raymond C Harris1

  • 1George M. O'Brien Kidney and Urologic Diseases Center and Division of Nephrology, Department of Medicine, Vanderbilt University School of Medicine, Department of Veterans Affairs, Nashville, Tennessee 37232, USA. Ray.Harris@mcmail.vanderbilt.edu

Journal of Hypertension. Supplement : Official Journal of the International Society of Hypertension
|April 10, 2003
PubMed
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Cyclooxygenase-2 (COX-2) plays a key role in kidney function, regulating salt handling and blood flow. Its expression in specific kidney cells is influenced by various physiological factors, impacting renal health.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Physiology

Background:

  • Cyclooxygenase-2 (COX-2) is expressed in specific kidney cells like macula densa (MD), cortical thick ascending limb of Henle (cTALH), and medullary interstitial cells (MICs).
  • COX-2 expression in podocytes increases during progressive glomerular injury.
  • COX-2 metabolites are crucial for renal salt handling and medullary blood flow.

Purpose of the Study:

  • To investigate the physiological regulation and functional roles of cyclooxygenase-2 (COX-2) in mammalian kidney function.
  • To explore the impact of various physiological states and signaling molecules on COX-2 expression in different renal cell types.

Main Methods:

  • Analysis of COX-2 expression in adult mammalian kidney tissues and human biopsy specimens.

Related Experiment Videos

  • Investigation of COX-2 regulation by salt balance, hormones (angiotensin II, glucocorticoids, mineralocorticoids), and nitric oxide (NO).
  • Studies on the role of p38 MAP kinase and nuclear factor-kappaB (NFkappaB) in COX-2 regulation in cultured cells and in vivo models.

    • Main Results:

    • COX-2 expression is upregulated in high-renin states and downregulated by angiotensin II, glucocorticoids, and mineralocorticoids in MD/cTALH cells.
    • Nitric oxide (NO) positively modulates COX-2 expression in MD/cTALH cells.
    • High-salt diet and hypertonicity increase COX-2 expression in MICs, mediated partly by NFkappaB activation, and COX-2 inhibition induces MIC apoptosis.

    Conclusions:

    • COX-2 is a significant physiological regulator of kidney function, influencing renin levels, salt handling, and medullary blood flow.
    • Differential regulation of COX-2 in various kidney cell compartments highlights its complex role in maintaining renal homeostasis.
    • Targeting COX-2 may offer therapeutic potential for kidney diseases associated with altered renal function.