High glucose induces an early and transient cytoprotective autophagy in retinal Müller cells.


Journal

Endocrine
ISSN: 1559-0100
Titre abrégé: Endocrine
Pays: United States
ID NLM: 9434444

Informations de publication

Date de publication:
08 2022
Historique:
received: 24 03 2022
accepted: 11 05 2022
pubmed: 26 5 2022
medline: 29 7 2022
entrez: 25 5 2022
Statut: ppublish

Résumé

We investigated the autophagic response of rat Müller rMC-1 cells during a short-term high glucose challenge. rMC-1 cells were maintained in 5 mM glucose (LG) or exposed to 25 mM glucose (HG). Western blot analysis was used to evaluate the expression levels of markers of autophagy (LC3-II, p62) and glial activation (AQP4), as well as the activation of TRAF2/JNK, ERK and AKT pathways. Autophagic flux assessment was performed using the autophagy inhibitor chloroquine. ROS levels were measured by flow cytometry using dichlorofluorescein diacetate. ERK involvement in autophagy induction was addressed using the ERK inhibitor FR180204. The effect of autophagy inhibition on cell viability was evaluated by SRB assay. Activation of autophagy was observed in the first 2-6 h of HG exposure. This early autophagic response was transient, not accompanied by an increase in AQP4 or in the phospho-activation of JNK, a key mediator of cellular response to oxidative stress, and required ERK activity. Cells exposed to HG had a lower viability upon autophagy inhibition by chloroquine, as compared to those maintained in LG. A short-term HG challenge triggers in rMC-1 cells a process improving the ability to cope with stressful conditions, which involves ERK and an early and transient autophagy activation.

Identifiants

pubmed: 35612691
doi: 10.1007/s12020-022-03079-8
pii: 10.1007/s12020-022-03079-8
pmc: PMC9325829
doi:

Substances chimiques

Chloroquine 886U3H6UFF
Glucose IY9XDZ35W2

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

221-230

Informations de copyright

© 2022. The Author(s).

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Auteurs

A Mecchia (A)

IRCCS-G.B. Bietti Foundation, Rome, Italy.

C Palumbo (C)

Department of Clinical Sciences and Translational Medicine, University of Rome Tor Vergata, Rome, Italy.

A De Luca (A)

Department of Biology, University of Rome Tor Vergata, Rome, Italy.

D Sbardella (D)

IRCCS-G.B. Bietti Foundation, Rome, Italy.

A Boccaccini (A)

IRCCS-G.B. Bietti Foundation, Rome, Italy.

L Rossi (L)

Department of Biology, University of Rome Tor Vergata, Rome, Italy.

M Parravano (M)

IRCCS-G.B. Bietti Foundation, Rome, Italy.

M Varano (M)

IRCCS-G.B. Bietti Foundation, Rome, Italy.

A M Caccuri (AM)

Department of Chemical Sciences and Technologies, University of Rome Tor Vergata, Rome, Italy. caccuri@uniroma2.it.
The NAST Centre for Nanoscience and Nanotechnology and Innovative Instrumentation, University of Rome Tor Vergata, Rome, Italy. caccuri@uniroma2.it.

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