For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
2
views
59
references
 Top references
cited by
8
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      506
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Glucocorticoid stimulation increases cardiac contractility by SGK1-dependent SOCE-activation in rat cardiac myocytes

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Aims

          Glucocorticoid (GC) stimulation has been shown to increase cardiac contractility by elevated intracellular [Ca] but the sources for Ca entry are unclear. This study aims to determine the role of store-operated Ca entry (SOCE) for GC-mediated inotropy.

          Methods and results

          Dexamethasone (Dex) pretreatment significantly increased cardiac contractile force ex vivo in Langendorff-perfused Sprague-Dawley rat hearts (2 mg/kg BW i.p. Dex 24 h prior to experiment). Moreover, Ca transient amplitude as well as fractional shortening were significantly enhanced in Fura-2-loaded isolated rat ventricular myocytes exposed to Dex (1 mg/mL Dex, 24 h). Interestingly, these Dex-dependent effects could be abolished in the presence of SOCE-inhibitors SKF-96356 (SKF, 2 μM) and BTP2 (5 μM). Ca transient kinetics (time to peak, decay time) were not affected by SOCE stimulation. Direct SOCE measurements revealed a negligible magnitude in untreated myocytes but a dramatic increase in SOCE upon Dex-pretreatment. Importantly, the Dex-dependent stimulation of SOCE could be blocked by inhibition of serum and glucocorticoid-regulated kinase 1 (SGK1) using EMD638683 (EMD, 50 μM). Dex preincubation also resulted in increased mRNA expression of proteins involved in SOCE (stromal interaction molecule 2, STIM2, and transient receptor potential cation channels 3/6, TRPC 3/6), which were also prevented in the presence of EMD.

          Conclusion

          Short-term GC-stimulation with Dex improves cardiac contractility by a SOCE-dependent mechanism, which appears to involve increased SGK1-dependent expression of the SOCE-related proteins. Since Ca transient kinetics were unaffected, SOCE appears to influence Ca cycling more by an integrated response across multiple cardiac cycles but not on a beat-to-beat basis.

          Related collections

          Most cited references59

          • Record: found
          • Abstract: found
          • Article: not found

          Store-operated calcium channels.

          Anant B. Parekh, James W. Putney (2005)
          In electrically nonexcitable cells, Ca(2+) influx is essential for regulating a host of kinetically distinct processes involving exocytosis, enzyme control, gene regulation, cell growth and proliferation, and apoptosis. The major Ca(2+) entry pathway in these cells is the store-operated one, in which the emptying of intracellular Ca(2+) stores activates Ca(2+) influx (store-operated Ca(2+) entry, or capacitative Ca(2+) entry). Several biophysically distinct store-operated currents have been reported, but the best characterized is the Ca(2+) release-activated Ca(2+) current, I(CRAC). Although it was initially considered to function only in nonexcitable cells, growing evidence now points towards a central role for I(CRAC)-like currents in excitable cells too. In spite of intense research, the signal that relays the store Ca(2+) content to CRAC channels in the plasma membrane, as well as the molecular identity of the Ca(2+) sensor within the stores, remains elusive. Resolution of these issues would be greatly helped by the identification of the CRAC channel gene. In some systems, evidence suggests that store-operated channels might be related to TRP homologs, although no consensus has yet been reached. Better understood are mechanisms that inactivate store-operated entry and hence control the overall duration of Ca(2+) entry. Recent work has revealed a central role for mitochondria in the regulation of I(CRAC), and this is particularly prominent under physiological conditions. I(CRAC) therefore represents a dynamic interplay between endoplasmic reticulum, mitochondria, and plasma membrane. In this review, we describe the key electrophysiological features of I(CRAC) and other store-operated Ca(2+) currents and how they are regulated, and we consider recent advances that have shed insight into the molecular mechanisms involved in this ubiquitous and vital Ca(2+) entry pathway.
          Article 0 comments Cited 428 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            STIM proteins: dynamic calcium signal transducers.

            Jonathan Soboloff, Brad Rothberg, Muniswamy Madesh … (2012)
            Stromal interaction molecule (STIM) proteins function in cells as dynamic coordinators of cellular calcium (Ca(2+)) signals. Spanning the endoplasmic reticulum (ER) membrane, they sense tiny changes in the levels of Ca(2+) stored within the ER lumen. As ER Ca(2+) is released to generate primary Ca(2+) signals, STIM proteins undergo an intricate activation reaction and rapidly translocate into junctions formed between the ER and the plasma membrane. There, STIM proteins tether and activate the highly Ca(2+)-selective Orai channels to mediate finely controlled Ca(2+) signals and to homeostatically balance cellular Ca(2+). Details are emerging on the remarkable organization within these STIM-induced junctional microdomains and the identification of new regulators and alternative target proteins for STIM.
            Article 0 comments Cited 223 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The CRAC channel activator STIM1 binds and inhibits L-type voltage-gated calcium channels.

              Chan Young Park, Aleksandr Shcheglovitov, Ricardo Dolmetsch (2010)
              Voltage- and store-operated calcium (Ca(2+)) channels are the major routes of Ca(2+) entry in mammalian cells, but little is known about how cells coordinate the activity of these channels to generate coherent calcium signals. We found that STIM1 (stromal interaction molecule 1), the main activator of store-operated Ca(2+) channels, directly suppresses depolarization-induced opening of the voltage-gated Ca(2+) channel Ca(V)1.2. STIM1 binds to the C terminus of Ca(V)1.2 through its Ca(2+) release-activated Ca(2+) activation domain, acutely inhibits gating, and causes long-term internalization of the channel from the membrane. This establishes a previously unknown function for STIM1 and provides a molecular mechanism to explain the reciprocal regulation of these two channels in cells.
              Article 0 comments Cited 114 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Michael Wester: Role: ConceptualizationRole: Data curationRole: Formal analysisRole: InvestigationRole: MethodologyRole: Writing – original draft
                Anton Heller: Role: Data curation
                Michael Gruber:
                ORCID: http://orcid.org/0000-0002-5509-9760
                Role: MethodologyRole: Resources
                Lars S. Maier: Role: ConceptualizationRole: Funding acquisitionRole: ResourcesRole: Writing – review & editing
                Christian Schach: Role: ConceptualizationRole: Data curationRole: Formal analysisRole: Funding acquisitionRole: InvestigationRole: MethodologyRole: Project administrationRole: ResourcesRole: SupervisionRole: Writing – original draftRole: Writing – review & editing
                Stefan Wagner:
                ORCID: http://orcid.org/0000-0002-9471-1166
                Role: ConceptualizationRole: Formal analysisRole: Funding acquisitionRole: MethodologyRole: Project administrationRole: ResourcesRole: SupervisionRole: Writing – review & editing
                Xun Ai: Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (iso-abbrev): PLoS ONE
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, CA USA )
                ISSN (Electronic): 1932-6203
                Publication date (Electronic): 9 September 2019
                Publication date Collection: 2019
                Volume: 14
                Issue: 9
                Electronic Location Identifier: e0222341
                Affiliations
                [1 ] University Heart Center Regensburg, University Hospital Regensburg, Regensburg, Germany
                [2 ] Clinic for Anesthesiology, University Hospital Regensburg, Regensburg, Germany
                Rush University Medical Center, UNITED STATES
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Author information
                http://orcid.org/0000-0002-5509-9760
                http://orcid.org/0000-0002-9471-1166
                Article
                Publisher ID: PONE-D-19-12032
                DOI: 10.1371/journal.pone.0222341
                PMC ID: 6733454
                PubMed ID: 31498847
                SO-VID: 2cb72694-a468-4b4b-86c0-ce18ace96ab9
                Copyright © © 2019 Wester et al
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 28 April 2019
                Date accepted : 27 August 2019
                Page count
                Figures: 5, Tables: 0, Pages: 17
                Funding
                Funded by: funder-id http://dx.doi.org/10.13039/501100001659, Deutsche Forschungsgemeinschaft;
                Award ID: WA 2539/5-1
                Award Recipient :
                ORCID: http://orcid.org/0000-0002-9471-1166
                Funded by: University of Regensburg
                Award ID: ReForM-B-Programm
                Award Recipient :
                Funded by: Deutsche Forschungsgemeinschaft (DE)
                Award ID: WA 2539/4-1
                Award Recipient :
                ORCID: http://orcid.org/0000-0002-9471-1166
                Funded by: Deutsche Forschungsgemeinschaft (DE)
                Award ID: WA 2539/7-1
                Award Recipient :
                ORCID: http://orcid.org/0000-0002-9471-1166
                Funded by: Deutsche Forschungsgemeinschaft (DE)
                Award ID: MA 1982/5-1
                Award Recipient :
                Funded by: Deutsche Forschungsgemeinschaft (DE)
                Award ID: MA 1982/7-1
                Award Recipient :
                Funded by: Deutsche Forschungsgemeinschaft (DE)
                Award ID: SFB 1350, Project Number 387509280, TPA6
                Award Recipient :
                ORCID: http://orcid.org/0000-0002-9471-1166
                Funded by: Deutsche Forschungsgemeinschaft (DE)
                Award ID: SFB 1350, Project Number 387509280, TPA6
                Award Recipient :
                Funded by: Deutsches Zentrum für Herz-Kreislaufforschung (DE)
                Award Recipient :
                ORCID: http://orcid.org/0000-0002-9471-1166
                Funded by: funder-id http://dx.doi.org/10.13039/501100005626, Universität Regensburg;
                Award ID: ReForM-C-Program
                Award Recipient :
                Funded by: Universität Regensburg (DE)
                Award ID: ReForM-C-Program
                Award Recipient :
                ORCID: http://orcid.org/0000-0002-9471-1166
                Funded by: Deutsches Zentrum für Herz-Kreislaufforschung (DE)
                Award Recipient :
                SW is funded by DFG grants WA 2539/4-1, 5-1 and 7-1. LSM is funded by DFG grants MA 1982/5-1 and 7-1. SW and LSM are also funded by the DFG SFB 1350 grant (Project Number 387509280, TPA6), are supported by the ReForM C program of the faculty and funded by the DZHK (Deutsches Zentrum für Herz-Kreislauf-Forschung; German Center for Cardiovascular Research). CS was funded by the ReForM program of the faculty.
                Categories
                Subject: Research Article
                Subject: Biology and Life Sciences
                Subject: Cell Biology
                Subject: Cellular Types
                Subject: Animal Cells
                Subject: Muscle Cells
                Subject: Biology and Life Sciences
                Subject: Anatomy
                Subject: Biological Tissue
                Subject: Muscle Tissue
                Subject: Muscle Cells
                Subject: Medicine and Health Sciences
                Subject: Anatomy
                Subject: Biological Tissue
                Subject: Muscle Tissue
                Subject: Muscle Cells
                Subject: Biology and Life Sciences
                Subject: Cell Biology
                Subject: Cellular Types
                Subject: Animal Cells
                Subject: Muscle Cells
                Subject: Cardiomyocytes
                Subject: Biology and Life Sciences
                Subject: Anatomy
                Subject: Biological Tissue
                Subject: Muscle Tissue
                Subject: Muscle Cells
                Subject: Cardiomyocytes
                Subject: Medicine and Health Sciences
                Subject: Anatomy
                Subject: Biological Tissue
                Subject: Muscle Tissue
                Subject: Muscle Cells
                Subject: Cardiomyocytes
                Subject: Biology and Life Sciences
                Subject: Anatomy
                Subject: Cardiovascular Anatomy
                Subject: Heart
                Subject: Medicine and Health Sciences
                Subject: Anatomy
                Subject: Cardiovascular Anatomy
                Subject: Heart
                Subject: Biology and Life Sciences
                Subject: Biophysics
                Subject: Ion Channels
                Subject: Calcium Channels
                Subject: Physical Sciences
                Subject: Physics
                Subject: Biophysics
                Subject: Ion Channels
                Subject: Calcium Channels
                Subject: Biology and Life Sciences
                Subject: Physiology
                Subject: Electrophysiology
                Subject: Ion Channels
                Subject: Calcium Channels
                Subject: Medicine and Health Sciences
                Subject: Physiology
                Subject: Electrophysiology
                Subject: Ion Channels
                Subject: Calcium Channels
                Subject: Biology and Life Sciences
                Subject: Physiology
                Subject: Electrophysiology
                Subject: Neurophysiology
                Subject: Ion Channels
                Subject: Calcium Channels
                Subject: Medicine and Health Sciences
                Subject: Physiology
                Subject: Electrophysiology
                Subject: Neurophysiology
                Subject: Ion Channels
                Subject: Calcium Channels
                Subject: Biology and Life Sciences
                Subject: Neuroscience
                Subject: Neurophysiology
                Subject: Ion Channels
                Subject: Calcium Channels
                Subject: Biology and Life Sciences
                Subject: Biochemistry
                Subject: Proteins
                Subject: Ion Channels
                Subject: Calcium Channels
                Subject: Biology and Life Sciences
                Subject: Cell Biology
                Subject: Cellular Types
                Subject: Animal Cells
                Subject: Muscle Cells
                Subject: Myofibrils
                Subject: Sarcomeres
                Subject: Biology and Life Sciences
                Subject: Anatomy
                Subject: Biological Tissue
                Subject: Muscle Tissue
                Subject: Muscle Cells
                Subject: Myofibrils
                Subject: Sarcomeres
                Subject: Medicine and Health Sciences
                Subject: Anatomy
                Subject: Biological Tissue
                Subject: Muscle Tissue
                Subject: Muscle Cells
                Subject: Myofibrils
                Subject: Sarcomeres
                Subject: Medicine and Health Sciences
                Subject: Surgical and Invasive Medical Procedures
                Subject: Functional Electrical Stimulation
                Subject: Physical Sciences
                Subject: Chemistry
                Subject: Chemical Compounds
                Subject: Alkaloids
                Subject: Caffeine
                Subject: Biology and Life Sciences
                Subject: Molecular Biology
                Subject: Molecular Biology Techniques
                Subject: Molecular Biology Assays and Analysis Techniques
                Subject: Gene Expression and Vector Techniques
                Subject: Protein Expression
                Subject: Research and Analysis Methods
                Subject: Molecular Biology Techniques
                Subject: Molecular Biology Assays and Analysis Techniques
                Subject: Gene Expression and Vector Techniques
                Subject: Protein Expression
                Custom metadata
                Data Availability The data underlying the results presented in the study are available from http://doi.org/10.5283/epub.40422.

                ScienceOpen disciplines: Uncategorized
                Data availability:
                ScienceOpen disciplines: Uncategorized

                Comments

                Comment on this article

                scite_

                Similar content506

                See all similar

                Cited by8

                See all cited by

                Most referenced authors714

                See all reference authors