Regulation of cyclooxygenase‐2 in renal medulla

Yang, Tianxin

doi:10.1046/j.1365-201x.2003.01102.x

Cited by 26 publications

(20 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Chronic acclimation to seawater results in a suite of morphological and biochemical alterations (including increased NKCC1 and CFTR expression) that assemble the NaCl secretory mechanism (Perry, 1997;Marshall et al, 1999;Katoh and Kaneko, 2003), and we hypothesize that COX2 expression also increases as a fine-tuning negative regulatory mechanism. COX2 expression is also dramatically increased in the mammalian renal medulla by chronic dehydration and salt loading (Yang, 2003). The resulting increased prostaglandin synthesis then inhibits transport in surrounding collecting ducts and promotes salt excretion in urine (Brater, 1999).…”

Section: Chronic Salinity Acclimationmentioning

confidence: 99%

“…Specifically, COX2 is expressed constitutively in the macula densa and the adjacent cortical thick ascending limb of the loop of Henle where it appears to be an important intermediary step in the control of renin secretion by juxtaglomerular cells (Harris and Breyer, 2001). COX2 is also expressed constitutively in medullary interstitial cells where it is important for cell survival during dehydration and for mediating NaCl excretion during salt loading and dehydration (Yang et al, 2002;Yang, 2003).…”

Section: Introductionmentioning

confidence: 99%

“…Systemic osmotic imbalances such as chronic salt loading and hydration stimulate renal prostaglandin production that facilitates salt excretion via complex pathways. One effect of renal prostaglandins is to inhibit salt transport by cells in the cortical thick ascending limb and collecting ducts (Stokes and Kokko, 1977;Stokes, 1979;Guan et al, 1998), another is to facilitate cell survival during acute osmotic stress in medullary interstitial cells (Yang, 2003).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

COX2 in a euryhaline teleost,Fundulus heteroclitus: primary sequence, distribution, localization, and potential function in gills during salinity acclimation

Choe

Havird

Rose

et al. 2006

Journal of Experimental Biology

View full text Add to dashboard Cite

SUMMARY In the kidneys of mammals, cyclooxygenase type 2 (COX2) is expressed in medullary interstitial cells, the macula densa and epithelial cells of the cortical thick ascending limb where it generates prostaglandins that regulate hormone secretion, inhibit ion transport, and support cell survival during salt loading and dehydration. In teleosts, the gills are in direct contact with an aquatic environment and are the dominant site of osmoregulation. During transfers between salinities, specialized cells in the gills (chloride cells) rapidly regulate NaCl secretion for systemic osmoregulation while they simultaneously are exposed to acute osmotic shock. This study was conducted to determine if COX2 is expressed in the gills, and if so, to evaluate its function in cellular and systemic osmoregulation. Degenerate primers, reverse transcription–PCR and rapid amplification of cDNA ends were used to deduce the complete cDNA sequence of a putative COX2 enzyme from the gills of the euryhaline killifish (Fundulus heteroclitus). The 2738 base pair cDNA includes a coding region for a 610 amino acid protein that is over 70%identical to mammalian COX2. A purified antibody generated against a conserved region of mouse COX2 labeled chloride cells, suggesting that the enzyme may control NaCl secretion as an autocrine agent. Real-time PCR was then used to demonstrate that mRNA expression of the COX2 homologue was threefold greater in gills from chronic seawater killifish than in gills from chronic freshwater killifish. Expression of Na+/K+/2Cl–cotransporter and the cystic fibrosis transmembrane conductance regulator were also greater in seawater, suggesting that chronic COX2 expression in the gills is regulated in parallel to the key ion transporters that mediate NaCl secretion. Real-time PCR was also used to demonstrate that acute transfer from seawater to freshwater and from freshwater to seawater led to rapid, transient inductions of COX2 expression. Together with previous physiological evidence,the present molecular and immunological data suggest that constitutive branchial COX2 expression is enhanced in seawater, where prostaglandins can regulate NaCl secretion in chloride cells. Our data also suggest that branchial COX2 expression may play a role in cell survival during acute osmotic shock.

show abstract

Section: Chronic Salinity Acclimationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

COX2 in a euryhaline teleost,Fundulus heteroclitus: primary sequence, distribution, localization, and potential function in gills during salinity acclimation

Choe

Havird

Rose

et al. 2006

Journal of Experimental Biology

View full text Add to dashboard Cite

show abstract

“…Molecular cloning of these COX isoforms provides a novel tool to explore the physiological functions of renal PGs. Within the kidney, both COX isoforms are expressed at substantially higher levels in the inner medulla than in the cortex (3,38,40). Increases in the expression of renal medullary COX-2, but not COX-1, are seen in response to chronic salt loading (8,15,40).…”

mentioning

confidence: 96%

Expression and function of COX isoforms in renal medulla: evidence for regulation of salt sensitivity and blood pressure

Zhang

Hillas

et al. 2006

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

Expression and function of COX isoforms in renal medulla: evidence for regulation of salt sensitivity and blood pressure. Am J Physiol Renal Physiol 290: F542-F549, 2006. First published September 27, 2005; doi:10.1152/ajprenal.00232.2005.-Expression of cyclooxygenase (COX)-2, but not COX-1, in the renal medulla is stimulated by chronic salt loading; yet the functional implication of this phenomenon is incompletely understood. The present study examined the cellular localization and antihypertensive function of high-salt-induced COX-2 expression in the renal medulla, with a parallel assessment of the function of COX-1. COX-2 protein expression in response to high-salt loading, assessed by immunostaining, was found predominantly in inner medullary interstitial cells, whereas COX-1 protein was abundant in collecting duct (CD) and inner medullary interstitial cells and was not affected by high salt. We compared mRNA expressions of COX-1 and COX-2 in CD vs. non-CD cells isolated from aquaporin 2-green fluorescent protein transgenic mice. A low level of COX-2 mRNA, but a high level of COX-1 mRNA, as determined by real-time RT-PCR, was detected in CD compared with non-CD segments. During high-salt intake, chronic infusions of the COX-2 blocker NS-398 and the COX-1 blocker SC-560 into the renal medulla of Sprague-Dawley rats for 5 days induced ϳ30-and 15-mmHg increases in mean arterial pressure, respectively. During similar high-salt intake, COX-1 knockout mice exhibited a gradual, but significant, increase in systolic blood pressure that was associated with a marked suppression of urinary PGE2 excretion. Therefore, we conclude that the two COX isoforms in the renal medulla play a similar role in the stabilization of arterial blood pressure during salt loading.cyclooxygenase-1; cyclooxygenase-2; mean blood pressure; prostaglandins; renal medullary interstitial cells PROSTAGLANDINS (PGs) are important autocrine/paracrine factors that contribute to salt balance and blood pressure (BP) control through mechanisms that primarily involve the regulation of vascular tone and renal excretory function. The vascular endothelium is a rich source of prostacyclin (PGI 2 ) and a potent vasodilator and inhibitor of platelet aggregation (5), whereas platelets produce thromboxane A 2 , a potent vasoconstrictor (9). The PGI 2 -thromboxane A 2 balance is considered to play an important role in the maintenance of normal vascular tone. The kidney is capable of synthesizing all types of PGs, especially PGE 2 and PGI 2 , which influence urinary sodium excretion directly through inhibition of tubular transport function and indirectly through regulation of activity of the reninangiotensin system (4). Within the kidney, the inner medulla has the greatest capacity for PG synthesis. In vitro studies have demonstrated that PGs, such as PGE 2 , can directly inhibit NaCl transport in isolated thick ascending limbs (30) and collecting ducts (CDs) (11, 31). In addition, PGE 1 augments renal medullary blood flow and attenuates the hydroosmotic effect o...

show abstract

“…In contrast, COX-2 is much more restricted in its expression and its abundance is highly inducible by growth factors and cytokines as well as physiological stimuli. In the kidney, COX-2 is constitutively expressed in the macula densa and thick ascending limb cells as well as in renal medullary cells in which the expression undergoes dynamic changes under changing states of sodium and water balance (4,12,39). COX-2 has been shown to influence renin secretion (6,40) and renal hemodynamics (21,22,29,32,33).…”

mentioning

confidence: 99%

Influence of genetic background and gender on hypertension and renal failure in COX-2-deficient mice

Yang

Huang

et al. 2005

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

show abstract

Regulation of cyclooxygenase‐2 in renal medulla

Cited by 26 publications

References 43 publications

COX2 in a euryhaline teleost,Fundulus heteroclitus: primary sequence, distribution, localization, and potential function in gills during salinity acclimation

COX2 in a euryhaline teleost,Fundulus heteroclitus: primary sequence, distribution, localization, and potential function in gills during salinity acclimation

Expression and function of COX isoforms in renal medulla: evidence for regulation of salt sensitivity and blood pressure

Influence of genetic background and gender on hypertension and renal failure in COX-2-deficient mice

Contact Info

Product

Resources

About