NDLI: Relative sensitivity of undifferentiated and cyclic adenosine 3′, 5′-monophosphate-induced differentiated neuroblastoma cells to cyclosporin A: potential role of β-amyloid and ubiquitin in neurotoxicity

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Relative sensitivity of undifferentiated and cyclic adenosine 3′, 5′-monophosphate-induced differentiated neuroblastoma cells to cyclosporin A: potential role of β-amyloid and ubiquitin in neurotoxicity

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In Vitro Cellular & Developmental Biology - Animal : Volume 36, Issue 1, January 2000

In Vitro Cellular & Developmental Biology - Animal : Volume 35

In Vitro Cellular & Developmental Biology - Animal : Volume 34

In Vitro Cellular & Developmental Biology - Animal : Volume 33

Relative sensitivity of undifferentiated and cyclic adenosine 3′, 5′-monophosphate-induced differentiated neuroblastoma cells to cyclosporin A: potential role of β-amyloid and ubiquitin in neurotoxicity

Content Provider	Springer Nature Link
Author	Kumar, Arun Hovland, Alicia R. Rosa, Francisco G. Cole, William C. Prasad, Judith E. Prasad, Kedar N.
Copyright Year	2000
Abstract	Cyclosporin A is routinely used in transplant therapy following allogeneic or xenogeneic tissue transplantation to prevent rejection. This immunosuppressive drug is also neurotoxic; however, its mechanisms of action for neurotoxicity are poorly understood. Undifferentiated and cyclic adenosine 3′, 5′-monophosphate (cAMP)-induced differentiated neuroblastoma (NB) cells were used as an experimental model to study the toxicity of cyclosporin A. Results showed that cyclosporin A promoted the outgrowth of neurites and inhibited the growth of undifferentiated NB cells. When cyclosporin A was added simultaneously with RO20-1724, an inhibitor of cyclic nucleotide phosphodiesterase, or with prostaglandin E$_{1}$, a stimulator of adenylate cyclase, it markedly enhanced the growth inhibitory and differentiation effects of these cAMP-stimulating agents. In addition, cyclosporin A added to cAMP-induced differentiated NB cells caused dose-dependent degeneration of these cells as evidenced by the vacuolization of cytoplasm and the fragmentation of nuclear and cytoplasmic materials; however, neurites remained intact. Cyclosporin A alone did not alter the intensity of cell immunostaining for ubiquitin or β-amyloid peptide (amino acids 1–14) (Aβ$_{1–14}$); however, it enhanced the intensity of staining for both ubiquitin and Aß in cells that were treated with cAMP-stimulating agents. The intensity of staining of amyloid precursor protein (amino acids 44–63) (APP$_{44–63}$) did not change in any treated group, suggesting that the increase in Aß staining is due to increased processing of APP to Aß. We propose that one of the mechanisms of cyclosporin A-induced neurotoxicity involves increased levels of Aß and ubiquitin.
Starting Page	81
Ending Page	87
Page Count	7
File Format	PDF
ISSN	10712690
Journal	In Vitro Cellular & Developmental Biology - Animal
Volume Number	36
Issue Number	2
e-ISSN	1543706X
Language	English
Publisher	Springer-Verlag
Publisher Date	2000-01-01
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Cyclosporine A differentiated neuroblastoma cells undifferentiated neuroblastoma cells cAMP beta-amyloid ubiquitin degeneration Cell Biology Developmental Biology Animal Genetics and Genomics Animal Biochemistry Animal Physiology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Developmental Biology Medicine

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