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Physiology and pathophysiology of cyclooxygenase-2 and prostaglandin E2 in the kidney
( Rikke Nørregaard ),( Tae Hwan Kwon ),( Jørgen Frøkiær ) 대한신장학회 2015 Kidney Research and Clinical Practice Vol.34 No.4
The cyclooxygenase (COX) enzyme system is the major pathway catalyzing the conversion of arachidonic acid into prostaglandins (PGs). PGs are lipid mediators implicated in a variety of physiological and pathophysiological processes in the kidney, including renal hemodynamics, body water and sodium balance, and the inflammatory injury characteristic in multiple renal diseases. Since the beginning of 1990s, it has been confirmed that COX exists in 2 isoforms, referred to as COX-1 and COX-2. Even though the 2 enzymes are similar in size and structure, COX-1 and COX- 2 are regulated by different systems and have different functional roles. This review summarizes the current data on renal expression of the 2 COX isoforms and highlights mainly the role of COX-2 and PGE2 in several physiological and pathophysiological processes in the kidney.
Prostaglandin E2 receptors as therapeutic targets in renal fibrosis
Mutsaers Henricus A.M.,Nørregaard Rikke 대한신장학회 2022 Kidney Research and Clinical Practice Vol.41 No.1
Prostaglandin E2 (PGE2), a lipid mediator produced by the cyclooxygenase enzyme system, is the main prostaglandin in the kidney. PGE2 is involved in various physiological and pathophysiological processes in the kidney, including renal hemodynamics, water and salt balance, and renal fibrosis—a key pathological feature of progressive kidney diseases. PGE2 functions by binding to four G-protein-coupled EP receptors (EP1 to EP4), which stimulate different intracellular signaling pathways. The intrarenal distribution of the four EP receptors as well as the different downstream signaling pathways associated with each receptor give rise to the distinct functional consequence of activating each receptor subtype. This review summarizes the current data on the renal expression of the four EP receptors and delineates the role of each receptor in renal fibrosis.
( Martin Skott ),( Rikke Nørregaard ),( Hanne Birke Sørensen ),( Johan Palmfeldt ),( Tae Hwan Kwon ),( Thomas Jonassen ),( Jørgen Frøkiær ),( Søren Nielsen ) 대한신장학회 2014 Kidney Research and Clinical Practice Vol.33 No.2
Background: The primary aim of the study was to investigate the cytokine/chemokine response in the kidney, lung, and liver following acute kidney injury(AKI). The secondary aim was to test whether α-melanocyte-stimulating hormone(α-MSH) could prevent a reduction in organ function, and attenuate the inflammatorycytokine/chemokine response within the kidney, lung, and liver following AKIin rats with or without preexisting chronic kidney disease (CKD). Methods: A two-stage animal model, in which AKI was induced in rats withpreexisting CKD, induced by 5/6 nephrectomy (Nx), was used. Six weeks later, AKIwas induced by intestinal ischemia and reperfusion (IIR). Sham procedures [S(Nx)and S(IIR)] were also performed. Results: Increasing levels of serum creatinine (sCr) demonstrated progressive developmentof CKD in response to Nx, and following IIR sCr levels increased furthersignificantly, except in the S(Nx) group treated with α-MSH. However, no significantdifferences in the fractional increase in sCr were observed between any of the groupsexposed to IIR. In kidney, lung, and liver tissue the levels of interleukin (IL)-1β weresignificantly higher in rats undergoing IIR when compared to the S(IIR) and control rats. The same pattern was observed for the chemokine monocyte chemoattractant protein(MCP)-1 in lung and liver tissue. Furthermore, kidney IL-1β and RANTES levels weresignificantly increased after IIR in the Nx rats compared to the S(Nx) rats. Conclusion: Both the functional parameters and the cytokine/chemokine response areas dramatic when AKI is superimposed onto CKD as onto non-CKD. No convincingprotective effect of α-MSH was detected.