The Multistage Antimalarial Compound Calxinin Modulates Calcium Homeostasis Targeting a Unique Calcium Channel Involved in Subcellular Calcium Storage in P. falciparum

2022 ◽  
Author(s):  
Yash Gupta ◽  
Neha Sharma ◽  
Snigdha Singh ◽  
Jesus G. Romero ◽  
Vinoth Rajendran ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Calcium Homeostasis ◽  
Calcium Storage

scholarly journals Bipolar-associated miR-499-5p controls neuroplasticity by downregulating the Cav1.2 L-type voltage gated calcium channel subunit CACNB2

2021 ◽  
Author(s):  
Helena Caria Martins ◽  
Oezge A Sungur ◽  
Carlotta Gilardi ◽  
Michael Pelzl ◽  
Silvia Bicker ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Calcium Homeostasis ◽  
Childhood Maltreatment ◽  
Molecular Mechanisms ◽  
Short Term Memory ◽  
Surface Expression ◽  
Neurocognitive Dysfunction ◽  
Voltage Gated ◽  
Depressive Episodes

Bipolar disorder (BD) is a chronic mood disorder characterized by alternating manic and depressive episodes, often in conjunction with cognitive deficits. Dysregulation of neuroplasticity and calcium homeostasis as a result of complex genetic environment interactions are frequently observed in BD patients, but the underlying molecular mechanisms are largely unknown. Here, we show that a BD-associated microRNA, miR-499-5p, regulates neuronal dendrite development and cognitive function by downregulating the BD risk gene CACNB2. miR-499-5p expression is increased in peripheral blood of BD patients and healthy subjects at risk of developing the disorder due to a history of childhood maltreatment. This up-regulation is paralleled in the hippocampus of rats which underwent juvenile social isolation. Elevating miR-499-5p levels in rat hippocampal pyramidal neurons impairs dendritogenesis and reduces surface expression and activity of the voltage-gated L-type calcium channel Cav1.2. We further identified CACNB2, which encodes a regulatory β-subunit of Cav1.2, as a direct target of miR-499-5p in neurons. CACNB2 downregulation is required for the miR-499-5p dependent impairment of dendritogenesis, suggesting that CACNB2 is an important downstream target of miR-499-5p in the regulation of neuroplasticity. Finally, elevating miR-499-5p in the hippocampus in vivo is sufficient to induce short-term memory impairments in rats haploinsufficient for the Cav1.2 pore forming subunit Cacna1c. Taken together, we propose that stress-induced upregulation of miR-499-5p contributes to dendritic impairments and deregulated calcium homeostasis in BD, with specific implications for the neurocognitive dysfunction frequently observed in BD patients.

scholarly journals THE L TYPE CALCIUM CHANNEL CA V 1.2 MODULATES MITOCHONDRIAL CALCIUM HOMEOSTASIS AND CELL DEATH

2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Maria Noterman ◽  
Min‐Kyoo Shin ◽  
Edwin Vazquez‐Rosa ◽  
Coral Cintrón‐Pérez ◽  
Anjali Rajadhyaksha ◽  
...  
Keyword(s):  
Cell Death ◽  
Calcium Channel ◽  
Calcium Homeostasis ◽  
Mitochondrial Calcium

Effects of Calcium Channel Blockade on Calcium Homeostasis in Mild to Moderate Essential Hypertension

1990 ◽  
Vol 300 (3) ◽  
pp. 133-137 ◽  
Author(s):  
Raymond Townsend ◽  
Donald J. Dipette ◽  
Robert R. Evans ◽  
Alan Green ◽  
John M. Wallace ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Calcium Channel ◽  
Calcium Homeostasis ◽  
Moderate Essential Hypertension ◽  
Channel Blockade ◽  
Calcium Channel Blockade

Regulation of calcium transport in cardiac cells

1984 ◽  
Vol 62 (1) ◽  
pp. 9-22 ◽  
Author(s):  
Adil E. Shamoo ◽  
Indu S. Ambudkar
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Channel ◽  
Calcium Homeostasis ◽  
Calcium Transport ◽  
Cardiac Cells ◽  
Transport Systems ◽  
Sodium Calcium Exchanger ◽  
Inotropic Effects ◽  
Cellular Calcium ◽  
Sodium Calcium

Calcium transporting systems and the regulatory events accompanying them are pivotal in the function of the cardiac cell. The concerted involvement of the various membranes achieve cellular calcium homeostasis that can also respond to the physiological exigencies of the cell. Three membrane systems are primarily involved; the sarcolemma, sarcoplasmic reticulum, and the mitochondria. The various Ca2+ transport systems that have been described in these membranes are as follows: the calcium channel, Ca2+-ATPase, Ca2+–Mg2+ ATPase, and sodium–calcium exchanger in the sarcolemma; the Ca2+–Mg2+ ATPase and a possible calcium channel in the sarcoplasmic reticulum; and the sodium–calcium exchanger and electrophoretic calcium uniporter in the mitochondrial inner membrane. These systems mediate calcium fluxes to maintain physiological cytosolic calcium concentrations. β-Adrenergic hormones regulate calcium transport systems in sarcolemma and sarcoplasmic reticulum, while α-adrenergic hormones modulate those in the mitochondria and probably in the sarcolemma. The response to these hormones is initiated at the sarcolemma, which contains the specific receptors. Intracellularly the effects are propagated by secondary messengers, e.g., cAMP, calcium, and lipid changes. Specific proteins are also involved in these events. Phospholamban, a 22 000 dalton protein, is involved in mediating the cAMP-dependent inotropic effects, by activating the Ca2+–Mg2+ ATPase of the sarcoplasmic reticulum. Alterations in any one of the systems involved in the regulation of calcium transport or in the calcium transport systems per se, would then result in drastic alterations in the cellular calcium homeostasis. Such effects could be of significance in cellular dysfunction during cardiac disease.

scholarly journals Diabetes-induced changes in calcium homeostasis and the effects of calcium channel blockers in rat and mice nociceptive neurons

Diabetologia ◽  
2001 ◽  
Vol 44 (10) ◽  
pp. 1302-1309 ◽  
Author(s):  
E. Kostyuk ◽  
N. Voitenko ◽  
I. Kruglikov ◽  
A. Shmigol ◽  
V. Shishkin ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Calcium Homeostasis ◽  
Calcium Channel Blockers ◽  
Channel Blockers ◽  
Nociceptive Neurons ◽  
Induced Changes
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