Low Chloride Stimulation of Prostaglandin E2Release and Cyclooxygenase-2 Expression in a Mouse Macula Densa Cell Line

Yang, Tianxin; Park, John M.; Arend, Lois J.; Huang, Yuning; Topaloğlu, Rezan; Pasumarthy, Anita; Praetorius, Helle A.; Spring, Kenneth R.; Briggs, Josephine P.; Schnermann, Jürgen

doi:10.1074/jbc.m006218200

Cited by 148 publications

(161 citation statements)

References 42 publications

(48 reference statements)

Supporting

Mentioning

143

Contrasting

Order By: Relevance

“…However, stimulation of calpain and scramblase are not functionally linked as PGE 2 -induced phosphatidylserine exposure is not inhibited by calpain inhibitors I/II. The latter result is in accordance with a previous study demonstrating that ionomycin-induced 33 In a former study, it has been shown that mechanically stressed adult human red blood cells produce PGE 2 . 34 Furthermore, evidence was presented earlier for PGE 2 induced activation of a nonselective cation channel, 22 for PGE 2 stimulated increase in cytosolic free Ca 2 þ concentration, 23 and PGE 2 -induced release of K þ from erythrocytes, which was blunted by inhibitors of Ca 2 þ -dependent K þ channels.…”

Section: Discussionsupporting

confidence: 82%

PGE2 in the regulation of programmed erythrocyte death

et al. 2005

View full text Add to dashboard Cite

Hyperosmotic shock, energy depletion, or removal of extracellular Cl À activates Ca 2 þ -permeable cation channels in erythrocyte membranes. Subsequent Ca 2 þ entry induces erythrocyte shrinkage and exposure of phosphatidylserine (PS) at the erythrocyte surface. PS-exposing cells are engulfed by macrophages. The present study explored the signalling involved. Hyperosmotic shock and Cl À removal triggered the release of prostaglandin E 2 (PGE 2 ). In whole-cell recording, activation of the cation channels by Cl À removal was abolished by the cyclooxygenase inhibitor diclophenac. In FACS analysis, phospholipase-A 2 inhibitors quinacrine and palmitoyltrifluoromethyl-ketone, and cyclooxygenase inhibitors acetylsalicylic acid and diclophenac, blunted the increase of PS exposure following Cl À removal. PGE 2 (but not thromboxane) induced cation channel activation, increase in cytosolic Ca 2 þ concentration, cell shrinkage, PS exposure, calpain activation, and ankyrin-R degradation. The latter was attenuated by calpain inhibitors-I/II, while PGE 2 -induced PS exposure was not. In conclusion, hyperosmotic shock or Cl À removal stimulates erythrocyte PS exposure through PGE 2 formation and subsequent activation of Ca 2+ -permeable cation channels.

show abstract

Section: Discussionsupporting

confidence: 82%

PGE2 in the regulation of programmed erythrocyte death

et al. 2005

View full text Add to dashboard Cite

show abstract

“…The MD cell line was generated by FACS sorting cells from mice transgenic for the SV40 large T antigen, and has been previously characterized (15). By using specific primers for each renal OR, we found that Olfr 90 is expressed in the MD cell line.…”

Section: Ac3 and Golfmentioning

confidence: 99%

“…Because AC3 and G olf localized to the MD by immunohistochemistry, we also performed PCR on a MD cell line (15) to determine whether any of the renal ORs were expressed in the MD. The MD cell line was generated by FACS sorting cells from mice transgenic for the SV40 large T antigen, and has been previously characterized (15).…”

Section: Ac3 and Golfmentioning

confidence: 99%

Functional expression of the olfactory signaling system in the kidney

Pluznick

Zou

Zhang

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

197

215

View full text Add to dashboard Cite

Olfactory-like chemosensory signaling occurs outside of the olfactory epithelium. We find that major components of olfaction, including olfactory receptors (ORs), olfactory-related adenylate cyclase (AC3) and the olfactory G protein (Golf), are expressed in the kidney. AC3 and Golf colocalize in renal tubules and in macula densa (MD) cells which modulate glomerular filtration rate (GFR). GFR is significantly reduced in AC3 ؊/؊ mice, suggesting that AC3 participates in GFR regulation. Although tubuloglomerular feedback is normal in these animals, they exhibit significantly reduced plasma renin levels despite up-regulation of COX-2 expression and nNOS activity in the MD. Furthermore, at least one member of the renal repertoire of ORs is expressed in a MD cell line. Thus, key components of olfaction are expressed in the renal distal nephron and may play a sensory role in the MD to modulate both renin secretion and GFR.adenylate cyclase 3 ͉ glomerular filtration rate ͉ Golf ͉ macula densa ͉ renin

show abstract

“…Could the expression of these two pathways in the juxtaglomerular apparatus (JGA) also reflect the existence of vasodepressor mechanisms that might attenuate afferent arteriolar myogenic reactivity in settings in which distal delivery is impaired? Several investigators have demonstrated that signals reflecting reduced distal delivery, such as reduced osmolality or chloride concentration, trigger the release of NO and PGE 2 from the JGA (121,156,170,173), and direct, microelectrode measurements demonstrate an elevation in distal tubular NO concentration in response to furosemide (95). If severe reductions in distal delivery trigger the combined release of NO and PGE 2 , this would be a powerful vasodilator signal.…”

Section: Interactions Between Myogenic and Tgf Mechanismsmentioning

confidence: 99%

Renal autoregulation: new perspectives regarding the protective and regulatory roles of the underlying mechanisms

Loutzenhiser

Griffin²,

Bidani³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

237

244

View full text Add to dashboard Cite

dani. Renal autoregulation: new perspectives regarding the protective and regulatory roles of the underlying mechanisms. Am J Physiol Regul Integr Comp Physiol 290: R1153-R1167, 2006. doi:10.1152/ajpregu.00402.2005.-When the kidney is subjected to acute increases in blood pressure (BP), renal blood flow (RBF) and glomerular filtration rate (GFR) are observed to remain relatively constant. Two mechanisms, tubuloglomerular feedback (TGF) and the myogenic response, are thought to act in concert to achieve a precise moment-by-moment regulation of GFR and distal salt delivery. The current view is that this mechanism insulates renal excretory function from fluctuations in BP. Indeed, the concept that renal autoregulation is necessary for normal renal function and volume homeostasis has long been a cornerstone of renal physiology. This article presents a very different view, at least regarding the myogenic component of this response. We suggest that its primary purpose is to protect the kidney against the damaging effects of hypertension. The arguments advanced take into consideration the unique properties of the afferent arteriolar myogenic response that allow it to protect against the oscillating systolic pressure and the accruing evidence that when this response is impaired, the primary consequence is not a disturbed volume homeostasis but rather an increased susceptibility to hypertensive injury. It is suggested that redundant and compensatory mechanisms achieve volume regulation, despite considerable fluctuations in distal delivery, and the assumed moment-by-moment regulation of renal hemodynamics is questioned. Evidence is presented suggesting that additional mechanisms exist to maintain ambient levels of RBF and GFR within normal range, despite chronic alterations in BP and severely impaired acute responses to pressure. Finally, the implications of this new perspective on the divergent roles of the myogenic response to pressure vs. the TGF response to changes in distal delivery are considered, and it is proposed that in addition to TGF-induced vasoconstriction, vasodepressor responses to reduced distal delivery may play a critical role in modulating afferent arteriolar reactivity to integrate the regulatory and protective functions of the renal microvasculature. renal microcirculation; afferent arteriole; myogenic; tubuloglomerular feedback ONE OF THE MOST STRIKING CHARACTERISTICS of the renal circulation is the ability of the kidney to maintain a constant renal blood flow (RBF) and glomerular filtration rate (GFR) as renal perfusion pressure is altered. The dual regulation of both RBF and GFR is achieved by proportionate changes in the preglomerular resistance and is believed to be mediated by two mechanisms, tubuloglomerular feedback (TGF) and the renal myogenic response. TGF involves a flow-dependent signal that is sensed at the macula densa and alters tone in the adjacent segment of the afferent arteriole via a mechanism that remains controversial but likely involves adenosine and/or ATP (30,80,144). The myo...

show abstract

Low Chloride Stimulation of Prostaglandin E2Release and Cyclooxygenase-2 Expression in a Mouse Macula Densa Cell Line

Cited by 148 publications

References 42 publications

PGE2 in the regulation of programmed erythrocyte death

PGE2 in the regulation of programmed erythrocyte death

Functional expression of the olfactory signaling system in the kidney

Renal autoregulation: new perspectives regarding the protective and regulatory roles of the underlying mechanisms

Contact Info

Product

Resources

About