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PKC-α-dependent augmentation of cAMP and CREB phosphorylation mediates the angiotensin II stimulation of renin in the collecting duct

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Title: PKC-α-dependent augmentation of cAMP and CREB phosphorylation mediates the angiotensin II stimulation of renin in the collecting duct
Authors: Gonzalez, Alexis A., Liu, Liu, Lara, Lucienne S., Bourgeois, Camille R. T., Ibaceta-Gonzalez, Cristobal, Salinas-Parra, Nicolas, Gogulamudi, Venkateswara R., Seth, Dale M., Prieto, Minolfa C.
Source: American Journal of Physiology - Renal Physiology; November 2015, Vol. 309 Issue: 10 pF880-F888, 9p
Abstract: In contrast to the negative feedback of angiotensin II (ANG II) on juxtaglomerular renin, ANG II stimulates renin in the principal cells of the collecting duct (CD) in rats and mice via ANG II type 1 (AT1R) receptor, independently of blood pressure. In vitro data indicate that CD renin is augmented by AT1R activation through protein kinase C (PKC), but the exact mechanisms are unknown. We hypothesize that ANG II stimulates CD renin synthesis through AT1R via PKC and the subsequent activation of cAMP/PKA/CREB pathway. In M-1 cells, ANG II increased cAMP, renin mRNA (3.5-fold), prorenin, and renin proteins, as well as renin activity in culture media (2-fold). These effects were prevented by PKC inhibition with calphostin C, PKC-α dominant negative, and by PKA inhibition. Forskolin-induced increases in cAMP and renin expression were prevented by calphostin C. PKC inhibition and Ca2+depletion impaired ANG II-mediated CREB phosphorylation and upregulation of renin. Adenylate cyclase 6 (AC) siRNA remarkably attenuated the ANG II-dependent upregulation of renin mRNA. Physiological activation of AC with vasopressin increased renin expression in M-1 cells. The results suggest that the ANG II-dependent upregulation of renin in the CD depends on PKC-α, which allows the augmentation of cAMP production and activation of PKA/CREB pathway via AC6. This study defines the intracellular signaling pathway involved in the ANG II-mediated stimulation of renin in the CD. This is a novel mechanism responsible for the regulation of local renin-angiotensin system in the distal nephron.
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  Data: PKC-α-dependent augmentation of cAMP and CREB phosphorylation mediates the angiotensin II stimulation of renin in the collecting duct
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  Data: <searchLink fieldCode="AR" term="%22Gonzalez%2C+Alexis+A%2E%22">Gonzalez, Alexis A.</searchLink><br /><searchLink fieldCode="AR" term="%22Liu%2C+Liu%22">Liu, Liu</searchLink><br /><searchLink fieldCode="AR" term="%22Lara%2C+Lucienne+S%2E%22">Lara, Lucienne S.</searchLink><br /><searchLink fieldCode="AR" term="%22Bourgeois%2C+Camille+R%2E+T%2E%22">Bourgeois, Camille R. T.</searchLink><br /><searchLink fieldCode="AR" term="%22Ibaceta-Gonzalez%2C+Cristobal%22">Ibaceta-Gonzalez, Cristobal</searchLink><br /><searchLink fieldCode="AR" term="%22Salinas-Parra%2C+Nicolas%22">Salinas-Parra, Nicolas</searchLink><br /><searchLink fieldCode="AR" term="%22Gogulamudi%2C+Venkateswara+R%2E%22">Gogulamudi, Venkateswara R.</searchLink><br /><searchLink fieldCode="AR" term="%22Seth%2C+Dale+M%2E%22">Seth, Dale M.</searchLink><br /><searchLink fieldCode="AR" term="%22Prieto%2C+Minolfa+C%2E%22">Prieto, Minolfa C.</searchLink>
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  Data: American Journal of Physiology - Renal Physiology; November 2015, Vol. 309 Issue: 10 pF880-F888, 9p
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: In contrast to the negative feedback of angiotensin II (ANG II) on juxtaglomerular renin, ANG II stimulates renin in the principal cells of the collecting duct (CD) in rats and mice via ANG II type 1 (AT1R) receptor, independently of blood pressure. In vitro data indicate that CD renin is augmented by AT1R activation through protein kinase C (PKC), but the exact mechanisms are unknown. We hypothesize that ANG II stimulates CD renin synthesis through AT1R via PKC and the subsequent activation of cAMP/PKA/CREB pathway. In M-1 cells, ANG II increased cAMP, renin mRNA (3.5-fold), prorenin, and renin proteins, as well as renin activity in culture media (2-fold). These effects were prevented by PKC inhibition with calphostin C, PKC-α dominant negative, and by PKA inhibition. Forskolin-induced increases in cAMP and renin expression were prevented by calphostin C. PKC inhibition and Ca2+depletion impaired ANG II-mediated CREB phosphorylation and upregulation of renin. Adenylate cyclase 6 (AC) siRNA remarkably attenuated the ANG II-dependent upregulation of renin mRNA. Physiological activation of AC with vasopressin increased renin expression in M-1 cells. The results suggest that the ANG II-dependent upregulation of renin in the CD depends on PKC-α, which allows the augmentation of cAMP production and activation of PKA/CREB pathway via AC6. This study defines the intracellular signaling pathway involved in the ANG II-mediated stimulation of renin in the CD. This is a novel mechanism responsible for the regulation of local renin-angiotensin system in the distal nephron.
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RecordInfo BibRecord:
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      – Type: doi
        Value: 10.1152/ajprenal.00155.2015
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      – Code: eng
        Text: English
    PhysicalDescription:
      Pagination:
        PageCount: 9
        StartPage: F880
    Titles:
      – TitleFull: PKC-α-dependent augmentation of cAMP and CREB phosphorylation mediates the angiotensin II stimulation of renin in the collecting duct
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            NameFull: Gonzalez, Alexis A.
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            NameFull: Liu, Liu
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            NameFull: Lara, Lucienne S.
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            NameFull: Bourgeois, Camille R. T.
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            NameFull: Ibaceta-Gonzalez, Cristobal
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            NameFull: Salinas-Parra, Nicolas
      – PersonEntity:
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            NameFull: Gogulamudi, Venkateswara R.
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            NameFull: Seth, Dale M.
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            NameFull: Prieto, Minolfa C.
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          Dates:
            – D: 15
              M: 11
              Text: November 2015
              Type: published
              Y: 2015
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              Value: 309
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              Value: 10
          Titles:
            – TitleFull: American Journal of Physiology - Renal Physiology
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