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  • Deen, Peter M. T.  (2)
  • Schweer, Horst  (2)
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  • 1
    Online Resource
    Online Resource
    Lithium reduces aquaporin-2 transcription independent of prostaglandins
    American Physiological Society ; 2012
    In:  American Journal of Physiology-Cell Physiology Vol. 302, No. 1 ( 2012-01), p. C131-C140
    Details
    In: American Journal of Physiology-Cell Physiology, American Physiological Society, Vol. 302, No. 1 ( 2012-01), p. C131-C140
    Abstract: Vasopressin (AVP)-stimulated translocation and transcription of aquaporin-2 (AQP2) water channels in renal principal cells is essential for urine concentration. Twenty percent of patients treated with lithium develop nephrogenic diabetes insipidus (NDI), a disorder in which the kidney is unable to concentrate urine. In vivo and in mouse collecting duct (mpkCCD) cells, lithium treatment coincides with decreased AQP2 abundance and inactivation of glycogen synthase kinase (Gsk) 3β. This is paralleled in vivo by an increased renal cyclooxygenase 2 (COX-2) expression and urinary prostaglandin PGE 2 excretion. PGE 2 reduces AVP-stimulated water reabsorption, but its precise role in lithium-induced downregulation of AQP2 is unclear. Using mpkCCD cells, we here investigated whether prostaglandins contribute to lithium-induced downregulation of AQP2. In these cells, lithium application reduced AQP2 abundance, which coincided with Gsk3β inactivation and increased COX-2 expression. Inhibition of COX by indomethacin, leading to reduced PGE 2 and PGF 2α levels, or dexamethasone-induced downregulation of COX-2 both increased AQP2 abundance, while PGE 2 addition reduced AQP2 abundance. However, lithium did not change the prostaglandin levels, and indomethacin and dexamethasone did not prevent lithium-induced AQP2 downregulation. Further analysis revealed that lithium decreased AQP2 protein abundance, mRNA levels and transcription, while PGE 2 reduced AQP2 abundance by increasing its lysosomal degradation, but not by reducing AQP2 gene transcription. In conclusion, our data reveal that in mpkCCD cells, prostaglandins decrease AQP2 protein stability by increasing its lysosomal degradation, indicating that in vivo paracrine-produced prostaglandins might have a role in lithium-induced NDI via this mechanism. However, lithium affects also AQP2 gene transcription, which is prostaglandin independent.
    Type of Medium: Online Resource
    ISSN: 0363-6143 , 1522-1563
    URL: Article
    DOI: 10.1152/ajpcell.00197.2011
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2012
    detail.hit.zdb_id: 1477334-X
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    A Vasopressin-Induced Change in Prostaglandin Receptor Subtype Expression Explains the Differential Effect of PGE2 on AQP2 Expression
    Frontiers Media SA ; 2022
    In:  Frontiers in Physiology Vol. 12 ( 2022-1-21)
    Details
    In: Frontiers in Physiology, Frontiers Media SA, Vol. 12 ( 2022-1-21)
    Abstract: Arginine vasopressin (AVP) stimulates the concentration of renal urine by increasing the principal cell expression of aquaporin-2 (AQP2) water channels. Prostaglandin E 2 (PGE 2 ) and prostaglandin 2α (PGF 2α ) increase the water absorption of the principal cell without AVP, but PGE 2 decreases it in the presence of AVP. The underlying mechanism of this paradoxical response was investigated here. Mouse cortical collecting duct (mkpCCD c14 ) cells mimic principal cells as they endogenously express AQP2 in response to AVP. PGE 2 increased AQP2 abundance without desmopressin (dDAVP), while in the presence of dDAVP, PGE 2 , and PGF 2α reduced AQP2 abundance. dDAVP increased the cellular PGD 2 and PGE 2 release and decreased the PGF 2α release. MpkCCD cells expressed mRNAs for the receptors of PGE 2 (EP1/EP4), PGF 2 (FP), and TxB 2 (TP). Incubation with dDAVP increased the expression of EP1 and FP but decreased the expression of EP4. In the absence of dDAVP, incubation of mpkCCD cells with an EP4, but not EP1/3, agonist increased AQP2 abundance, and the PGE 2 -induced increase in AQP2 was blocked with an EP4 antagonist. Moreover, in the presence of dDAVP, an EP1/3, but not EP4, agonist decreased the AQP2 abundance, and the addition of EP1 antagonists prevented the PGE 2 -mediated downregulation of AQP2. Our study shows that in mpkCCD c14 cells, reduced EP4 receptor and increased EP1/FP receptor expression by dDAVP explains the differential effects of PGE 2 and PGF 2α on AQP2 abundance with or without dDAVP. As the V2R and EP4 receptor, but not the EP1 and FP receptor, can couple to Gs and stimulate the cyclic adenosine monophosphate (cAMP) pathway, our data support a view that cells can desensitize themselves for receptors activating the same pathway and sensitize themselves for receptors of alternative pathways.
    Type of Medium: Online Resource
    ISSN: 1664-042X
    URL: Article
    DOI: 10.3389/fphys.2021.787598
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2564217-0
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