Activation of Non-Canonical Autophagic Pathway through Inhibition of Non-Integrin Laminin Receptor in Neuronal Cells

To fight neurodegenerative diseases, several therapeutic strategies have been proposed that, to date, are either ineffective or at the early preclinical stages. Intracellular protein aggregates represent the cause of about 70% of neurodegenerative disorders, such as Alzheimer’s disease. Thus, autoph...
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Autor*in:	Adriana Limone [verfasserIn] Iolanda Veneruso [verfasserIn] Antonella Izzo [verfasserIn] Maurizio Renna [verfasserIn] Raffaella Bonavita [verfasserIn] Silvia Piscitelli [verfasserIn] Gaetano Calì [verfasserIn] Sergio De Nicola [verfasserIn] Patrizia Riccio [verfasserIn] Valeria D’Argenio [verfasserIn] Antonio Lavecchia [verfasserIn] Daniela Sarnataro [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	non-canonical autophagy m-TOR-independent autophagy 37/67 kDa laminin receptor (LR) ribosomal protein SA (RPSA) 37/67 kDa LR inhibitor endocytic pathway

Übergeordnetes Werk:	In: Cells - MDPI AG, 2012, 11(2022), 3, p 466
Übergeordnetes Werk:	volume:11 ; year:2022 ; number:3, p 466

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/cells11030466

Katalog-ID:	DOAJ070763879

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allfields	10.3390/cells11030466 doi (DE-627)DOAJ070763879 (DE-599)DOAJc69d8e02f08c457bb35dbce20539ebfe DE-627 ger DE-627 rakwb eng QH573-671 Adriana Limone verfasserin aut Activation of Non-Canonical Autophagic Pathway through Inhibition of Non-Integrin Laminin Receptor in Neuronal Cells 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier To fight neurodegenerative diseases, several therapeutic strategies have been proposed that, to date, are either ineffective or at the early preclinical stages. Intracellular protein aggregates represent the cause of about 70% of neurodegenerative disorders, such as Alzheimer’s disease. Thus, autophagy, i.e., lysosomal degradation of macromolecules, could be employed in this context as a therapeutic strategy. Searching for a compound that stimulates this process led us to the identification of a 37/67kDa laminin receptor inhibitor, NSC48478. We have analysed the effects of this small molecule on the autophagic process in mouse neuronal cells and found that NSC48478 induces the conversion of microtubule-associated protein 1A/1B-light chain 3 (LC3-I) into the LC3-phosphatidylethanolamine conjugate (LC3-II). Interestingly, upon NSC48478 treatment, the contribution of membranes to the autophagic process derived mainly from the non-canonical m-TOR-independent endocytic pathway, involving the Rab proteins that control endocytosis and vesicle recycling. Finally, qRT-PCR analysis suggests that, while the expression of key genes linked to canonical autophagy was unchanged, the main genes related to the positive regulation of endocytosis (pinocytosis and receptor mediated), along with genes regulating vesicle fusion and autolysosomal maturation, were upregulated under NSC48478 conditions. These results strongly suggest that 37/67 kDa inhibitor could be a useful tool for future studies in pathological conditions. non-canonical autophagy m-TOR-independent autophagy 37/67 kDa laminin receptor (LR) ribosomal protein SA (RPSA) 37/67 kDa LR inhibitor endocytic pathway Cytology Iolanda Veneruso verfasserin aut Antonella Izzo verfasserin aut Maurizio Renna verfasserin aut Raffaella Bonavita verfasserin aut Silvia Piscitelli verfasserin aut Gaetano Calì verfasserin aut Sergio De Nicola verfasserin aut Patrizia Riccio verfasserin aut Valeria D’Argenio verfasserin aut Antonio Lavecchia verfasserin aut Daniela Sarnataro verfasserin aut In Cells MDPI AG, 2012 11(2022), 3, p 466 (DE-627)718622081 (DE-600)2661518-6 20734409 nnns volume:11 year:2022 number:3, p 466 https://doi.org/10.3390/cells11030466 kostenfrei https://doaj.org/article/c69d8e02f08c457bb35dbce20539ebfe kostenfrei https://www.mdpi.com/2073-4409/11/3/466 kostenfrei https://doaj.org/toc/2073-4409 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2022 3, p 466
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allfieldsGer	10.3390/cells11030466 doi (DE-627)DOAJ070763879 (DE-599)DOAJc69d8e02f08c457bb35dbce20539ebfe DE-627 ger DE-627 rakwb eng QH573-671 Adriana Limone verfasserin aut Activation of Non-Canonical Autophagic Pathway through Inhibition of Non-Integrin Laminin Receptor in Neuronal Cells 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier To fight neurodegenerative diseases, several therapeutic strategies have been proposed that, to date, are either ineffective or at the early preclinical stages. Intracellular protein aggregates represent the cause of about 70% of neurodegenerative disorders, such as Alzheimer’s disease. Thus, autophagy, i.e., lysosomal degradation of macromolecules, could be employed in this context as a therapeutic strategy. Searching for a compound that stimulates this process led us to the identification of a 37/67kDa laminin receptor inhibitor, NSC48478. We have analysed the effects of this small molecule on the autophagic process in mouse neuronal cells and found that NSC48478 induces the conversion of microtubule-associated protein 1A/1B-light chain 3 (LC3-I) into the LC3-phosphatidylethanolamine conjugate (LC3-II). Interestingly, upon NSC48478 treatment, the contribution of membranes to the autophagic process derived mainly from the non-canonical m-TOR-independent endocytic pathway, involving the Rab proteins that control endocytosis and vesicle recycling. Finally, qRT-PCR analysis suggests that, while the expression of key genes linked to canonical autophagy was unchanged, the main genes related to the positive regulation of endocytosis (pinocytosis and receptor mediated), along with genes regulating vesicle fusion and autolysosomal maturation, were upregulated under NSC48478 conditions. These results strongly suggest that 37/67 kDa inhibitor could be a useful tool for future studies in pathological conditions. non-canonical autophagy m-TOR-independent autophagy 37/67 kDa laminin receptor (LR) ribosomal protein SA (RPSA) 37/67 kDa LR inhibitor endocytic pathway Cytology Iolanda Veneruso verfasserin aut Antonella Izzo verfasserin aut Maurizio Renna verfasserin aut Raffaella Bonavita verfasserin aut Silvia Piscitelli verfasserin aut Gaetano Calì verfasserin aut Sergio De Nicola verfasserin aut Patrizia Riccio verfasserin aut Valeria D’Argenio verfasserin aut Antonio Lavecchia verfasserin aut Daniela Sarnataro verfasserin aut In Cells MDPI AG, 2012 11(2022), 3, p 466 (DE-627)718622081 (DE-600)2661518-6 20734409 nnns volume:11 year:2022 number:3, p 466 https://doi.org/10.3390/cells11030466 kostenfrei https://doaj.org/article/c69d8e02f08c457bb35dbce20539ebfe kostenfrei https://www.mdpi.com/2073-4409/11/3/466 kostenfrei https://doaj.org/toc/2073-4409 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2022 3, p 466
allfieldsSound	10.3390/cells11030466 doi (DE-627)DOAJ070763879 (DE-599)DOAJc69d8e02f08c457bb35dbce20539ebfe DE-627 ger DE-627 rakwb eng QH573-671 Adriana Limone verfasserin aut Activation of Non-Canonical Autophagic Pathway through Inhibition of Non-Integrin Laminin Receptor in Neuronal Cells 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier To fight neurodegenerative diseases, several therapeutic strategies have been proposed that, to date, are either ineffective or at the early preclinical stages. Intracellular protein aggregates represent the cause of about 70% of neurodegenerative disorders, such as Alzheimer’s disease. Thus, autophagy, i.e., lysosomal degradation of macromolecules, could be employed in this context as a therapeutic strategy. Searching for a compound that stimulates this process led us to the identification of a 37/67kDa laminin receptor inhibitor, NSC48478. We have analysed the effects of this small molecule on the autophagic process in mouse neuronal cells and found that NSC48478 induces the conversion of microtubule-associated protein 1A/1B-light chain 3 (LC3-I) into the LC3-phosphatidylethanolamine conjugate (LC3-II). Interestingly, upon NSC48478 treatment, the contribution of membranes to the autophagic process derived mainly from the non-canonical m-TOR-independent endocytic pathway, involving the Rab proteins that control endocytosis and vesicle recycling. Finally, qRT-PCR analysis suggests that, while the expression of key genes linked to canonical autophagy was unchanged, the main genes related to the positive regulation of endocytosis (pinocytosis and receptor mediated), along with genes regulating vesicle fusion and autolysosomal maturation, were upregulated under NSC48478 conditions. These results strongly suggest that 37/67 kDa inhibitor could be a useful tool for future studies in pathological conditions. non-canonical autophagy m-TOR-independent autophagy 37/67 kDa laminin receptor (LR) ribosomal protein SA (RPSA) 37/67 kDa LR inhibitor endocytic pathway Cytology Iolanda Veneruso verfasserin aut Antonella Izzo verfasserin aut Maurizio Renna verfasserin aut Raffaella Bonavita verfasserin aut Silvia Piscitelli verfasserin aut Gaetano Calì verfasserin aut Sergio De Nicola verfasserin aut Patrizia Riccio verfasserin aut Valeria D’Argenio verfasserin aut Antonio Lavecchia verfasserin aut Daniela Sarnataro verfasserin aut In Cells MDPI AG, 2012 11(2022), 3, p 466 (DE-627)718622081 (DE-600)2661518-6 20734409 nnns volume:11 year:2022 number:3, p 466 https://doi.org/10.3390/cells11030466 kostenfrei https://doaj.org/article/c69d8e02f08c457bb35dbce20539ebfe kostenfrei https://www.mdpi.com/2073-4409/11/3/466 kostenfrei https://doaj.org/toc/2073-4409 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2022 3, p 466
language	English
source	In Cells 11(2022), 3, p 466 volume:11 year:2022 number:3, p 466
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author	Adriana Limone
spellingShingle	Adriana Limone misc QH573-671 misc non-canonical autophagy misc m-TOR-independent autophagy misc 37/67 kDa laminin receptor (LR) misc ribosomal protein SA (RPSA) misc 37/67 kDa LR inhibitor misc endocytic pathway misc Cytology Activation of Non-Canonical Autophagic Pathway through Inhibition of Non-Integrin Laminin Receptor in Neuronal Cells
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topic_title	QH573-671 Activation of Non-Canonical Autophagic Pathway through Inhibition of Non-Integrin Laminin Receptor in Neuronal Cells non-canonical autophagy m-TOR-independent autophagy 37/67 kDa laminin receptor (LR) ribosomal protein SA (RPSA) 37/67 kDa LR inhibitor endocytic pathway
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topic_unstemmed	misc QH573-671 misc non-canonical autophagy misc m-TOR-independent autophagy misc 37/67 kDa laminin receptor (LR) misc ribosomal protein SA (RPSA) misc 37/67 kDa LR inhibitor misc endocytic pathway misc Cytology
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title	Activation of Non-Canonical Autophagic Pathway through Inhibition of Non-Integrin Laminin Receptor in Neuronal Cells
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title_sort	activation of non-canonical autophagic pathway through inhibition of non-integrin laminin receptor in neuronal cells
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title_auth	Activation of Non-Canonical Autophagic Pathway through Inhibition of Non-Integrin Laminin Receptor in Neuronal Cells
abstract	To fight neurodegenerative diseases, several therapeutic strategies have been proposed that, to date, are either ineffective or at the early preclinical stages. Intracellular protein aggregates represent the cause of about 70% of neurodegenerative disorders, such as Alzheimer’s disease. Thus, autophagy, i.e., lysosomal degradation of macromolecules, could be employed in this context as a therapeutic strategy. Searching for a compound that stimulates this process led us to the identification of a 37/67kDa laminin receptor inhibitor, NSC48478. We have analysed the effects of this small molecule on the autophagic process in mouse neuronal cells and found that NSC48478 induces the conversion of microtubule-associated protein 1A/1B-light chain 3 (LC3-I) into the LC3-phosphatidylethanolamine conjugate (LC3-II). Interestingly, upon NSC48478 treatment, the contribution of membranes to the autophagic process derived mainly from the non-canonical m-TOR-independent endocytic pathway, involving the Rab proteins that control endocytosis and vesicle recycling. Finally, qRT-PCR analysis suggests that, while the expression of key genes linked to canonical autophagy was unchanged, the main genes related to the positive regulation of endocytosis (pinocytosis and receptor mediated), along with genes regulating vesicle fusion and autolysosomal maturation, were upregulated under NSC48478 conditions. These results strongly suggest that 37/67 kDa inhibitor could be a useful tool for future studies in pathological conditions.
abstractGer	To fight neurodegenerative diseases, several therapeutic strategies have been proposed that, to date, are either ineffective or at the early preclinical stages. Intracellular protein aggregates represent the cause of about 70% of neurodegenerative disorders, such as Alzheimer’s disease. Thus, autophagy, i.e., lysosomal degradation of macromolecules, could be employed in this context as a therapeutic strategy. Searching for a compound that stimulates this process led us to the identification of a 37/67kDa laminin receptor inhibitor, NSC48478. We have analysed the effects of this small molecule on the autophagic process in mouse neuronal cells and found that NSC48478 induces the conversion of microtubule-associated protein 1A/1B-light chain 3 (LC3-I) into the LC3-phosphatidylethanolamine conjugate (LC3-II). Interestingly, upon NSC48478 treatment, the contribution of membranes to the autophagic process derived mainly from the non-canonical m-TOR-independent endocytic pathway, involving the Rab proteins that control endocytosis and vesicle recycling. Finally, qRT-PCR analysis suggests that, while the expression of key genes linked to canonical autophagy was unchanged, the main genes related to the positive regulation of endocytosis (pinocytosis and receptor mediated), along with genes regulating vesicle fusion and autolysosomal maturation, were upregulated under NSC48478 conditions. These results strongly suggest that 37/67 kDa inhibitor could be a useful tool for future studies in pathological conditions.
abstract_unstemmed	To fight neurodegenerative diseases, several therapeutic strategies have been proposed that, to date, are either ineffective or at the early preclinical stages. Intracellular protein aggregates represent the cause of about 70% of neurodegenerative disorders, such as Alzheimer’s disease. Thus, autophagy, i.e., lysosomal degradation of macromolecules, could be employed in this context as a therapeutic strategy. Searching for a compound that stimulates this process led us to the identification of a 37/67kDa laminin receptor inhibitor, NSC48478. We have analysed the effects of this small molecule on the autophagic process in mouse neuronal cells and found that NSC48478 induces the conversion of microtubule-associated protein 1A/1B-light chain 3 (LC3-I) into the LC3-phosphatidylethanolamine conjugate (LC3-II). Interestingly, upon NSC48478 treatment, the contribution of membranes to the autophagic process derived mainly from the non-canonical m-TOR-independent endocytic pathway, involving the Rab proteins that control endocytosis and vesicle recycling. Finally, qRT-PCR analysis suggests that, while the expression of key genes linked to canonical autophagy was unchanged, the main genes related to the positive regulation of endocytosis (pinocytosis and receptor mediated), along with genes regulating vesicle fusion and autolysosomal maturation, were upregulated under NSC48478 conditions. These results strongly suggest that 37/67 kDa inhibitor could be a useful tool for future studies in pathological conditions.
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title_short	Activation of Non-Canonical Autophagic Pathway through Inhibition of Non-Integrin Laminin Receptor in Neuronal Cells
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Activation of Non-Canonical Autophagic Pathway through Inhibition of Non-Integrin Laminin Receptor in Neuronal Cells

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