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Laboratory of Molecular Endocrinology
   
András Spät, MD, PhD, DSc
    Professor, Member of the Hungarian Academy of Sciences

We have been studying the formation and effects of cytosolic Ca2+ signal for 25 years. After examining phosphoinositide metabolism, the formation of inositol trisphosphate (IP3) in glomerulosa cells  and  the description of its receptor (1986), our attention shifted to the participation of mitochondria in the process of Ca2+ signalling. We were the first to describe the effect of cytosolic Ca2+ signal on the Ca2+-dependent activation of mitochondrial dehydrogenases in intact cells (1992). In later studies we focused on the control of mitochondrial Ca2+ uptake. Although some of our data was compatible with the general view that high-Ca2+ microdomains are formed between the IP3 receptor-channel in the endoplasmic reticulum and apposing mitochondria and these microdomains facilitate Ca2+ accumulation by mitochondria, we have also provided evidence that the low submicromolar Ca2+ signals can also induce net Ca2+ uptake by mitochondria in adrenal glomerulosa. Later we extended this observation to ovarian luteal and insulin producing tumour cells. Moreover, we observed that angiotensin II, a Ca2+ mobilising hormone, in addition to inducing mitochondrial Ca2+ signal via primarily inducing cytosolic Ca2+ signal, also exerts an inhibitory action on mitochondrial Ca2+ uptake. This inhibition is brought about by the simultaneous activation of p38 MAPK and a novel-type protein kinase C.  The significance of this negative feed-back mechanism is presumably the protection of mitochondria from calcium overload that could otherwise result in apoptosis of the cell.  Presently we are analysing the details of this inhibition.

Besides providing driving force for Ca2+ uptake mitochondrial oxidases are also sources of free radicals. To better understand the biophysical properties of such electron transfer systems, we use the phagocyte NADPH oxidase in electrophysiological measurements, focusing on the direct demonstration of reversed electron flow across oxidases. 		   
   
        
   
   
KEYWORD(S): calcium, signalling, mitochondria, aldosterone, glomerulosa, 
   
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  KEYWORD UNIVERSE: CO2-sensitivity, GTPase activating proteins - GAPs, NADPH oxidase - NOX2, NADPH oxidase, Neutrophilic granulocytes, TASK, TRESK, aging, apoptosis, asthma, autonomic neuropathy, autoregulation, avian, bioinformatics, blood-brain barrier, c, calcineurin, calcium, cancer, cell biology, cell fusion, cerebral blood flow, cerebral blood volume, complement, dendritic cells, diabetes, dopamine, duplikation, early restenosis, embryo, embryomanipulation, endoplasmic reticulum, endothelium, enviroment, epidemiology, exercise, gene expression, gene, genetics, hydrogen peroxide, hypothalamus, immunology, in vitro fertilization, inflammation, ischemia-reperfusion, liver, lupus nephritis, lymphoid tissue, medicinal chemistry, metabolic bone disease, mitochondria, molecular biology, neuronal plasticity, neuroprotection, oral biology, oxidative stress, pathology, pathophysiology, peroxidase, phagocytes, pharmacokinetics, physiology, potassium channel, reactive oxygen species, receptors redox homeostasis, regulation, signal transduction, small GTPases, stem cell, stress, stroke, superoxide, tetrasomi, tissue engineering, transplantation,  
     Research Areas     

Behavioural sciences

  

Biochemistry, cell biology, biophysics

  

Dental sciences

  

Experimental and clinical immunology and genetics

  

Experimental and clinical oncology

  

Internal medicine and pediatrics

  

Medicine of sensory organs

  

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Molecular biology, microbiology

  

Morphological sciences (anatomy, pathology, forensic medicine)

  

Neurosciences

  

Pharmaceutical sciences, pharmacology

  

Physiology, pathophysiology

  

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Sport sciences

  

Surgery (operative sciences)

  
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