An altered polyamine system has been suggested to play a key role in mood disorders and suicide, a hypothesis corroborated by the evidence that lithium inhibits the polyamine mediated stress response in the rat brain. Recent post-mortem studies have shown that spermidine/spermine N1-acetyltransferase (SAT1), the key regulator of cellular polyamine content, is under-expressed in brains from suicide victims compared to controls. In our study we tested the effect of in vitro lithium treatment on SAT1 gene and protein expression in B lymphoblastoid cell lines (BLCLs) from bipolar disorder (BD) patients who committed suicide (and for which BLCLs were collected prior to their death), BD patients with high and low risk of suicide and a sample of non-psychiatric controls. Baseline mRNA levels were similar in the four groups of subjects (p > 0.05). Lithium had no effect in suicide completers (p > 0.05) while it significantly increased SAT1 expression in the high risk (p < 0.001) and low risk (p < 0.01) groups as well as in controls (p < 0.001). Protein and mRNA levels were not correlated; lithium significantly reduced protein levels only in the control sample (p < 0.05). Our findings suggest that SAT1 transcription is influenced by lithium and that this effect is altered in BD patients who completed suicide, further supporting a role for polyamines in suicide.

Differential effect of lithium on spermidine/spermine N1-acetyltransferase expression in suicidal behaviour / A. Squassina, M. Manchia, C. Chillotti, V. Deiana, D. Congiu, F. Paribello, P. Roncada, A. Soggiu, C. Piras, A. Urbani, G.S. Robertson, P. Keddy, G. Turecki, G.A. Rouleau, M. Alda, M. Del Zompo. - In: INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY. - ISSN 1461-1457. - 16:10(2013 Jun 17), pp. 2209-2218. [10.1017/S1461145713000655]

Differential effect of lithium on spermidine/spermine N1-acetyltransferase expression in suicidal behaviour

A. Soggiu;C. Piras;
2013-06-17

Abstract

An altered polyamine system has been suggested to play a key role in mood disorders and suicide, a hypothesis corroborated by the evidence that lithium inhibits the polyamine mediated stress response in the rat brain. Recent post-mortem studies have shown that spermidine/spermine N1-acetyltransferase (SAT1), the key regulator of cellular polyamine content, is under-expressed in brains from suicide victims compared to controls. In our study we tested the effect of in vitro lithium treatment on SAT1 gene and protein expression in B lymphoblastoid cell lines (BLCLs) from bipolar disorder (BD) patients who committed suicide (and for which BLCLs were collected prior to their death), BD patients with high and low risk of suicide and a sample of non-psychiatric controls. Baseline mRNA levels were similar in the four groups of subjects (p > 0.05). Lithium had no effect in suicide completers (p > 0.05) while it significantly increased SAT1 expression in the high risk (p < 0.001) and low risk (p < 0.01) groups as well as in controls (p < 0.001). Protein and mRNA levels were not correlated; lithium significantly reduced protein levels only in the control sample (p < 0.05). Our findings suggest that SAT1 transcription is influenced by lithium and that this effect is altered in BD patients who completed suicide, further supporting a role for polyamines in suicide.
bipolar disorder; lymphoblasts; polyamines; SAT1; suicide
Settore MED/25 - Psichiatria
Settore VET/05 - Malattie Infettive degli Animali Domestici
Settore BIO/10 - Biochimica
Settore VET/04 - Ispezione degli Alimenti di Origine Animale
INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY
Article (author)
File in questo prodotto:
File Dimensione Formato  
Differential effect of lithium on spermidine-spermine N1-acetyltransferase expression in suicidal behaviour.pdf

non disponibili

188.6 kB Adobe PDF   Visualizza/Apri   Richiedi una copia
Pubblicazioni consigliate

Caricamento pubblicazioni consigliate

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2434/221934
Citazioni
  • ???jsp.display-item.citation.pmc??? 6
  • Scopus 17
  • ???jsp.display-item.citation.isi??? 14
social impact