Vitamin D stimulates (Na<sup>+</sup> + K<sup>+</sup>)‐ATPase activity in chick small intestine

Cross, Heide S.; Peterlik, Meinrad

doi:10.1016/0014-5793(83)80135-5

Cited by 11 publications

(2 citation statements)

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“…Changes in enzymatic antioxidant activity and GPx levels were also prevented by calcitriol. This protective effect of calcitriol on Na+, K + -ATPase activity was previously described by Cross and Peterlik (1983) in peripheral tissues.…”

Section: Discussionsupporting

confidence: 73%

“…Recent studies have demonstrated a neuroprotective role for 1,25-dihydroxyvitamin D3 (calcitriol, the active form of vitamin D3) in experimental models of neurodegenerative diseases (Jang et al, 2014;Jang et al, 2015;Newmark and Newmark, 2007). Others studies have shown that calcitriol improved energy metabolism mainly by affecting Na + , K + -ATPase activity (Cross and Peterlik, 1983;Elstein and Silver, 1986). The specific mechanisms that mediate this effect are unclear; however, calcitriol acts in many pathways, including the following: i) antioxidant pathways, ii) neuronal calcium regulation, iii) immunomodulation and iv) the glutamatergic system (Shinpo et al, 2000;Taniura et al, 2006;Wang et al, 2001).…”

Section: Figmentioning

confidence: 99%

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1,25‐Dihydroxyvitamin D3 exerts neuroprotective effects in an ex vivo model of mild hyperhomocysteinemia

Longoni

Kolling

Santos

et al. 2015

Intl J of Devlp Neuroscience

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Elevated plasma homocysteine (Hcy) levels have been detected in patients with various neurodegenerative conditions. Studies of brain tissue have revealed that hyperhomocysteinemia may impair energy metabolism, resulting in neuronal damage. In addition, new evidence has indicated that vitamin D plays crucial roles in brain development, brain metabolism and neuroprotection. The aim of this study was to investigate the neuroprotective effects of 1,25-dihydroxivitamin D3 (calcitriol) in cerebral cortex slices that were incubated with a mild concentration of Hcy. Cerebral cortex slices from adult rats were first pre-treated for 30 min with one of three different concentrations of calcitriol (50 nM, 100 nM and 250 nM), followed by Hcy for 1h to promote cellular dysfunction. Hcy caused changes in bioenergetics parameters (e.g., respiratory chain enzymes) and mitochondrial functions by inducing changes in mitochondrial mass and swelling. Here, we used flow cytometry to analyze neurons that were double-labelled with Propidium Iodide (PI) and found that Hcy induced an increase in NeuN(+)/PI cells but did not affect GFAP(+)/Pi cells. Hcy also induced oxidative stress by increasing reactive oxygen species generation, lipid peroxidation and protein damage and reducing the activity of antioxidant enzymes (e.g., SOD, CAT and GPx). Calcitriol (50 nM) prevented these alterations by increasing the level of the vitamin D receptor. Our findings suggest that using calcitriol may be a therapeutic strategy for treating the cerebral complications caused by Hcy.

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Section: Discussionsupporting

confidence: 73%

Section: Figmentioning

confidence: 99%

1,25‐Dihydroxyvitamin D3 exerts neuroprotective effects in an ex vivo model of mild hyperhomocysteinemia

Longoni

Kolling

Santos

et al. 2015

Intl J of Devlp Neuroscience

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1,25-dihydroxyvitamin D3 selectively induces increased expression of the Na,K-ATPase β1 subunit in avian myelomonocytic cells without a concomitant change in Na,K-ATPase activity

et al. 1997

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Treatment of avian myelomonocytic cells with 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) results in an approximately two fold increase in levels of Na,K-ATPase beta 1 subunit mRNA and protein (both total and plasma membrane-associated). The changes in beta 1 subunit expression occur in the absence of a detectable increase in expression of any of the three alpha subunit isoforms or in Na,K-ATPase activity. The selective induction of the expression of the beta subunit in avian myelomonocytic cells by 1,25(OH)2D3 reveals a previously unobserved feature of the regulation of Na,K-ATPase expression, while the targeting of beta subunit polypeptides to the plasma membrane in the absence of a corresponding increase in active Na,K-ATPase suggests that, in these cells, transport of the beta subunit to the plasma membrane may be independent of its binding to the alpha subunit.

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Intestinal Phosphate Transport

Peterlik

1985

The Enzymes of Biological Membranes

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Vitamin D stimulates (Na⁺ + K⁺)‐ATPase activity in chick small intestine

Cited by 11 publications

References 20 publications

1,25‐Dihydroxyvitamin D3 exerts neuroprotective effects in an ex vivo model of mild hyperhomocysteinemia

1,25‐Dihydroxyvitamin D3 exerts neuroprotective effects in an ex vivo model of mild hyperhomocysteinemia

1,25-dihydroxyvitamin D3 selectively induces increased expression of the Na,K-ATPase β1 subunit in avian myelomonocytic cells without a concomitant change in Na,K-ATPase activity

Intestinal Phosphate Transport

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Vitamin D stimulates (Na+ + K+)‐ATPase activity in chick small intestine

Cited by 11 publications

References 20 publications

1,25‐Dihydroxyvitamin D3 exerts neuroprotective effects in an ex vivo model of mild hyperhomocysteinemia

1,25‐Dihydroxyvitamin D3 exerts neuroprotective effects in an ex vivo model of mild hyperhomocysteinemia

1,25-dihydroxyvitamin D3 selectively induces increased expression of the Na,K-ATPase β1 subunit in avian myelomonocytic cells without a concomitant change in Na,K-ATPase activity

Intestinal Phosphate Transport

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Vitamin D stimulates (Na⁺ + K⁺)‐ATPase activity in chick small intestine