Role of intracellular calcium in thermal allodynia and hyperalgesia in diabetic mice

In fura 2-loaded N1E-115 cells, regulation of intracellular Ca2+ concentration ([Ca2+]i) following a Ca2+ load induced by 1 μM thapsigargin and 10 μM carbonylcyanide p-trifluoromethyoxyphenylhydrazone (FCCP) was Na+ dependent and inhibited by 5 mM Ni2+. In cells with normal intracellular Na+ concentration ([Na+]i), removal of bath Na+, which should result in reversal of Na+/Ca2+exchange, did not increase [Ca2+]i unless cell Ca2+ buffer capacity was reduced. When N1E-115 cells were Na+ loaded using 100 μM veratridine and 4 μg/ml scorpion venom, the rate of the reverse mode of the Na+/Ca2+ exchanger was apparently enhanced, since an ∼4- to 6-fold increase in [Ca2+]ioccurred despite normal cell Ca2+ buffering. In SBFI-loaded cells, we were able to demonstrate forward operation of the Na+/Ca2+ exchanger (net efflux of Ca2+) by observing increases (∼ 6 mM) in [Na+]i. These Ni2+ (5 mM)-inhibited increases in [Na+]i could only be observed when a continuous ionomycin-induced influx of Ca2+ occurred. The voltage-sensitive dye bis-(1,3-diethylthiobarbituric acid) trimethine oxonol was used to measure changes in membrane potential. Ionomycin (1 μM) depolarized N1E-115 cells (∼25 mV). This depolarization was Na+dependent and blocked by 5 mM Ni2+ and 250–500 μM benzamil. These data provide evidence for the presence of an electrogenic Na+/Ca2+ exchanger that is capable of regulating [Ca2+]i after release of Ca2+ from cell stores.

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The role of intracellular calcium phosphate in osteoblast-mediated bone apatite formation

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1208916109 ◽

2012 ◽

Vol 109 (35) ◽

pp. 14170-14175 ◽

Cited By ~ 269

Author(s):

S. Boonrungsiman ◽

E. Gentleman ◽

R. Carzaniga ◽

N. D. Evans ◽

D. W. McComb ◽

...

Keyword(s):

Calcium Phosphate ◽

Intracellular Calcium ◽

Apatite Formation ◽

Bone Apatite

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PT681. The protective role of erythropoietin on the cognitive power deficit of the brain and histological changes in the hippocampus of diabetic mice.

The International Journal of Neuropsychopharmacology ◽

10.1093/ijnp/pyw044.681 ◽

2016 ◽

Vol 19 (Suppl_1) ◽

pp. 48-48

Keyword(s):

Protective Role ◽

Diabetic Mice ◽

Histological Changes ◽

Power Deficit ◽

Cognitive Power ◽

The Brain

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Intracellular calcium levels in the Plasmodium berghei ookinete

Parasitology ◽

10.1017/s0031182008004939 ◽

2008 ◽

Vol 135 (12) ◽

pp. 1355-1362 ◽

Cited By ~ 6

Author(s):

I. SIDÉN-KIAMOS ◽

C. LOUIS

Keyword(s):

Intracellular Calcium ◽

Plasmodium Berghei ◽

Calcium Concentration ◽

Insect Cells ◽

Ionophore A23187 ◽

Rodent Malaria Parasite ◽

Calcium Indicators ◽

Intracellular Ca

SUMMARYOokinetes are the motile and invasive stages of Plasmodium parasites in the mosquito host. Here we explore the role of intracellular Ca2+ in ookinete survival and motility as well as in the formation of oocysts in vitro in the rodent malaria parasite Plasmodium berghei. Treatment with the Ca2+ ionophore A23187 induced death of the parasite, an effect that could be prevented if the ookinetes were co-incubated with insect cells before incubation with the ionophore. Treatment with the intracellular calcium chelator BAPTA/AM resulted in increased formation of oocysts in vitro. Calcium imaging in the ookinete using fluorescent calcium indicators revealed that the purified ookinetes have an intracellular calcium concentration in the range of 100 nm. Intracellular calcium levels decreased substantially when the ookinetes were incubated with insect cells and their motility was concomitantly increased. Our results suggest a pleiotropic role for intracellular calcium in the ookinete.

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Role of insulin and IGF-I in activation of muscle protein synthesis after oral feeding

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1996.270.4.e614 ◽

1996 ◽

Vol 270 (4) ◽

pp. E614-E620 ◽

Cited By ~ 16

Author(s):

E. Svanberg ◽

H. Zachrisson ◽

C. Ohlsson ◽

B. M. Iresjo ◽

K. G. Lundholm

Keyword(s):

Protein Synthesis ◽

Skeletal Muscles ◽

Muscle Protein ◽

Muscle Protein Synthesis ◽

Oral Feeding ◽

Myofibrillar Proteins ◽

Diabetic Mice ◽

Igf I ◽

Stimulation Of

The aim was to evaluate the role of insulin and insulin-like growth factor I (IGF-I) in activation of muscle protein synthesis after oral feeding. Synthesis rate of globular and myofibrillar proteins in muscle tissue was quantified by a flooding dose of radioactive phenylalanine. Muscle tissue expression of IGF-I mRNA was measured. Normal (C57 Bl) and diabetic mice (type I and type II) were subjected to an overnight fast (18 h) with subsequent refeeding procedures for 3 h with either oral chow intake or provision of insulin, IGF-I, glucose, and amino acids. Anti-insulin and anti-IGF-I were provided intraperitoneally before oral refeeding in some experiments. An overnight fast reduced synthesis of both globular (38 +/- 3%) and myofibrillar proteins (54 +/- 3%) in skeletal muscles, which was reversed by oral refeeding. Muscle protein synthesis, after starvation/ refeeding, was proportional and similar to changes in skeletal muscle IGF-I mRNA expression. Diabetic mice responded quantitatively similarly to starvation/refeeding in muscle protein synthesis compared with normal mice (C57 Bl). Both anti-insulin and anti-IGF-I attenuated significantly the stimulation of muscle protein synthesis in response to oral feeding, whereas exogenous provision of either insulin or IGF-I to overnight-starved and freely fed mice did not clearly stimulate protein synthesis in skeletal muscles. Our results support the suggestion that insulin and IGF-I either induce or facilitate the protein synthesis machinery in skeletal muscles rather than exerting a true stimulation of the biosynthetic process during feeding.

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