Autophagy is generally considered a degradation pathway involved in many neurodegenerative processes. It can be observed in different stress conditions such as starvation generally improving cell survival. Our previous results described the occurrence of autophagy in neuronal cultures exposed to the toxic compound trimethyltin (TMT) (1). TMT belongs to a family of organotin compounds with wide industrial and agricultural applications, especially as heat stabilizers in PVC production and as biocides. In the nervous system TMT determines the selective destruction of neurons in specific brain regions such as the olfactory bulb and the hippocampus. When this toxic molecule was administered to glial cells we observed in astrocytes a rapid block of the autophagic flux and a consequent increased expression of LC3 and p62 which can be observed both in cultured astrocytes and in the brain of intoxicated animals. Conversely, in microglia autophagy was not impaired in the same conditions and p62 accumulation was not observed neither in vitro primary cultures, nor in brain sections of TMT-treated rats. The protein p62 (also known as SQTM1) is known to be selectively degraded through autophagy and its accumulation activates the transcription factor Nrf2 by sequestering Keap1 (2). To note the block of autophagy has been reported to exert an immunosopressive effect in macrophages (3). Thus, the impairment of autophagy in astrocytes could be related to their limited production of pro-inflammatory cytokines and nitric oxide respect to microglia observed after TMT treatment.

Autophagy is differently regulated in astrocytes and microglia exposed to environmental toxic molecole / Fabrizi, Cinzia; Pompili, Elena; Ciraci, Viviana; Lenzi, P.; Fornai, F.; Fumagalli, Lorenzo. - In: ITALIAN JOURNAL OF ANATOMY AND EMBRYOLOGY. - ISSN 2038-5129. - STAMPA. - 120:1 (supplement)(2015), pp. 167-167. ((Intervento presentato al convegno 69° Congresso Nazionale della Società Italiana di Anatomia e Istologia tenutosi a Ferrara nel 17-19 settembre 2015 [10.13128/IJAE-17041].

Autophagy is differently regulated in astrocytes and microglia exposed to environmental toxic molecole

FABRIZI, CINZIA;POMPILI, Elena;CIRACI, VIVIANA;FUMAGALLI, Lorenzo
2015

Abstract

Autophagy is generally considered a degradation pathway involved in many neurodegenerative processes. It can be observed in different stress conditions such as starvation generally improving cell survival. Our previous results described the occurrence of autophagy in neuronal cultures exposed to the toxic compound trimethyltin (TMT) (1). TMT belongs to a family of organotin compounds with wide industrial and agricultural applications, especially as heat stabilizers in PVC production and as biocides. In the nervous system TMT determines the selective destruction of neurons in specific brain regions such as the olfactory bulb and the hippocampus. When this toxic molecule was administered to glial cells we observed in astrocytes a rapid block of the autophagic flux and a consequent increased expression of LC3 and p62 which can be observed both in cultured astrocytes and in the brain of intoxicated animals. Conversely, in microglia autophagy was not impaired in the same conditions and p62 accumulation was not observed neither in vitro primary cultures, nor in brain sections of TMT-treated rats. The protein p62 (also known as SQTM1) is known to be selectively degraded through autophagy and its accumulation activates the transcription factor Nrf2 by sequestering Keap1 (2). To note the block of autophagy has been reported to exert an immunosopressive effect in macrophages (3). Thus, the impairment of autophagy in astrocytes could be related to their limited production of pro-inflammatory cytokines and nitric oxide respect to microglia observed after TMT treatment.
69° Congresso Nazionale della Società Italiana di Anatomia e Istologia
04 Pubblicazione in atti di convegno::04d Abstract in atti di convegno
Autophagy is differently regulated in astrocytes and microglia exposed to environmental toxic molecole / Fabrizi, Cinzia; Pompili, Elena; Ciraci, Viviana; Lenzi, P.; Fornai, F.; Fumagalli, Lorenzo. - In: ITALIAN JOURNAL OF ANATOMY AND EMBRYOLOGY. - ISSN 2038-5129. - STAMPA. - 120:1 (supplement)(2015), pp. 167-167. ((Intervento presentato al convegno 69° Congresso Nazionale della Società Italiana di Anatomia e Istologia tenutosi a Ferrara nel 17-19 settembre 2015 [10.13128/IJAE-17041].
File allegati a questo prodotto
File Dimensione Formato  
Fabrizi_Autophagy_2015.pdf

accesso aperto

Tipologia: Versione editoriale (versione pubblicata con il layout dell'editore)
Licenza: Tutti i diritti riservati (All rights reserved)
Dimensione 412.76 kB
Formato Adobe PDF
412.76 kB Adobe PDF Visualizza/Apri PDF

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: https://hdl.handle.net/11573/809073
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus ND
  • ???jsp.display-item.citation.isi??? ND
social impact