“Plasma Membrane Calcium ATPase downregulation in dopaminergic neurons alters cellular physiology and motor behavior in Drosophila melanogaster”

2021 ◽  
Author(s):  
Brenda Erhardt ◽  
María Silvina Marcora ◽  
Lía Frenkel ◽  
Pablo Alejandro Bochicchio ◽  
Diego Hernán Bodin ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Plasma Membrane ◽  
Dopaminergic Neurons ◽  
Motor Behavior ◽  
Calcium Atpase ◽  
Plasma Membrane Calcium Atpase ◽  
Cellular Physiology

scholarly journals “Plasma Membrane Calcium Atpase downregulation in dopaminergic neurons alters cellular physiology and behavior in Drosophila melanogaster”

2019 ◽  
Author(s):  
Brenda Erhardt ◽  
María Celeste Leal ◽  
María Silvina Marcora ◽  
Lía Frenkel ◽  
Pablo Alejandro Bochicchio ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Drosophila Melanogaster ◽  
Plasma Membrane ◽  
Cytosolic Calcium ◽  
Calcium Atpase ◽  
Plasma Membrane Calcium Atpase ◽  
Mitochondrial Oxidative Stress ◽  
And Behavior ◽  
Cellular Dysfunction

AbstractAccumulation of calcium is proposed to account for selective dopaminergic neuron (DN) dysfunctionality, a characteristic of Parkinson’s Disease (PD). To test the in vivo impact of calcium increment in DN physiology we downregulated the Plasma Membrane Calcium ATPase (PMCA), a bomb that extrudes cytosolic calcium, in those neurons in Drosophila melanogaster. Using th-GAL4>PMCARNAi, PMCA was selectively reduced, leading to increased cytosolic calcium and mitochondrial oxidative stress with no neurodegeneration. In the eye, PMCARNAi expression provoked a subtle disorganization, suggesting scarce toxicity. Interestingly, we observed several locomotor alterations and a higher level of dopamine in brains. Finally, flies presented a reduction of lifespan and a perimortem non-motor phenotype characterized by abdominal swelling, possibly due to constipation. We conclude that elevated cytosolic calcium in DN could trigger cellular dysfunction generating mitochondrial oxidative stress and motor and non-motor symptoms, typical of PD.

Plasma Membrane Calcium ATPase Gene Expression in Bovine Lens Epithelium

2000 ◽  
Vol 32 (2-3) ◽  
pp. 100-105 ◽  
Author(s):  
Lijun Bian ◽  
Junwen Zeng ◽  
Douglas Borchman ◽  
Christopher A. Paterson
Keyword(s):  
Gene Expression ◽  
Plasma Membrane ◽  
Calcium Atpase ◽  
Lens Epithelium ◽  
Plasma Membrane Calcium Atpase ◽  
Bovine Lens ◽  
Atpase Gene

scholarly journals A NOVEL ROLE OF PLASMA MEMBRANE CALCIUM ATPASE 4 AS A NEGATIVE-REGULATOR OF VEGF-INDUCED ANGIOGENESIS

Heart ◽  
2014 ◽  
Vol 100 (Suppl 4) ◽  
pp. A17.1-A17
Author(s):  
RR Baggott ◽  
A Alfranca ◽  
MD López-Maderuelo ◽  
TMA Mohamed ◽  
A Escolano ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Calcium Atpase ◽  
Negative Regulator ◽  
Plasma Membrane Calcium Atpase

scholarly journals Plasma Membrane Calcium ATPase Regulates Stoichiometry of CD4+ T-Cell Compartments

2021 ◽  
Vol 12 ◽  
Author(s):  
Maylin Merino-Wong ◽  
Barbara A. Niemeyer ◽  
Dalia Alansary
Keyword(s):  
Plasma Membrane ◽  
T Cell ◽  
Immune Responses ◽  
Chromatin Immunoprecipitation ◽  
Expression Patterns ◽  
Calcium Atpase ◽  
Cd4 T Cell ◽  
Plasma Membrane Calcium Atpase ◽  
Cell Compartments

Immune responses involve mobilization of T cells within naïve and memory compartments. Tightly regulated Ca2+ levels are essential for balanced immune outcomes. How Ca2+ contributes to regulating compartment stoichiometry is unknown. Here, we show that plasma membrane Ca2+ ATPase 4 (PMCA4) is differentially expressed in human CD4+ T compartments yielding distinct store operated Ca2+ entry (SOCE) profiles. Modulation of PMCA4 yielded a more prominent increase of SOCE in memory than in naïve CD4+ T cell. Interestingly, downregulation of PMCA4 reduced the effector compartment fraction and led to accumulation of cells in the naïve compartment. In silico analysis and chromatin immunoprecipitation point towards Ying Yang 1 (YY1) as a transcription factor regulating PMCA4 expression. Analyses of PMCA and YY1 expression patterns following activation and of PMCA promoter activity following downregulation of YY1 highlight repressive role of YY1 on PMCA expression. Our findings show that PMCA4 adapts Ca2+ levels to cellular requirements during effector and quiescent phases and thereby represent a potential target to intervene with the outcome of the immune response.

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