Podocytes maintain high basal levels of autophagy independent of mtor signaling
Identifieur interne : 000239 ( Main/Exploration ); précédent : 000238; suivant : 000240Podocytes maintain high basal levels of autophagy independent of mtor signaling
Auteurs : Tillmann Bork [Allemagne] ; Wei Liang [Allemagne] ; Kosuke Yamahara [Allemagne] ; Philipp Lee [Allemagne] ; Zhejia Tian [Allemagne] ; Shuya Liu [Allemagne] ; Christoph Schell [Allemagne] ; Kathrin Thedieck [Autriche] ; Bjoern Hartleben [Allemagne] ; Ketan Patel [Allemagne] ; Pierre-Louis Tharaux [France] ; Olivia Lenoir [France] ; Tobias Huber [Allemagne]Source :
- Autophagy [ 1554-8627 ] ; 2019-12.
English descriptors
Abstract
While constant basal levels of macroautophagy/autophagy are a prerequisite to preserve long-lived podocytes at the filtration barrier, MTOR regulates at the same time podocyte size and compensatory hypertrophy. Since MTOR is known to generally suppress autophagy, the apparently independent regulation of these two key pathways of glomerular maintenance remained puzzling. We now report that long-term genetic manipulation of MTOR activity does in fact not influence high basal levels of autophagy in podocytes either in vitro or in vivo. Instead we present data showing that autophagy in podocytes is mainly controlled by AMP-activated protein kinase (AMPK) and ULK1 (unc-51 like kinase 1). Pharmacological inhibition of MTOR further shows that the uncoupling of MTOR activity and autophagy is time dependent. Together, our data reveal a novel and unexpected cell-specific mechanism, which permits concurrent MTOR activity as well as high basal autophagy rates in podocytes. Thus, these data indicate manipulation of the AMPK-ULK1 axis rather than inhibition of MTOR as a promising therapeutic intervention to enhance autophagy and preserve podocyte homeostasis in glomerular diseases.Abbreviations: AICAR: 5-aminoimidazole-4-carboxamide ribonucleotide; AMPK: AMP-activated protein kinase; ATG: autophagy related; BW: body weight; Cq: chloroquine; ER: endoplasmic reticulum; ESRD: end stage renal disease; FACS: fluorescence activated cell sorting; GFP: green fluorescent protein; i.p.: intra peritoneal; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MTOR: mechanistic target of rapamycin kinase; NPHS1: nephrosis 1, nephrin; NPHS2: nephrosis 2, podocin; PLA: proximity-ligation assay; PRKAA: 5'-AMP-activated protein kinase catalytic subunit alpha; RPTOR/RAPTOR: regulatory associated protein of MTOR, complex 1; RFP: red fluorescent protein; TSC1: tuberous sclerosis 1; ULK1: unc-51 like kinase 1.
Url:
DOI: 10.1080/15548627.2019.1705007
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream Hal, to step Corpus: 000191
- to stream Hal, to step Curation: 000191
- to stream Hal, to step Checkpoint: 000005
- to stream Main, to step Merge: 000239
- to stream Main, to step Curation: 000239
Le document en format XML
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<author><name sortKey="Huber, Tobias" sort="Huber, Tobias" uniqKey="Huber T" first="Tobias" last="Huber">Tobias Huber</name>
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<idno type="DOI">10.1080/15548627.2019.1705007</idno>
<series><title level="j">Autophagy</title>
<idno type="ISSN">1554-8627</idno>
<imprint><date type="datePub">2019-12</date>
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<profileDesc><textClass><keywords scheme="mix" xml:lang="en"><term>AMPK</term>
<term>LC3</term>
<term>MTOR</term>
<term>Raptor</term>
<term>Tsc1</term>
<term>autophagy</term>
<term>glomerulus</term>
<term>kidney</term>
<term>podocyte</term>
<term>rapamycin</term>
<term>signaling</term>
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<front><div type="abstract" xml:lang="en"> <p>While constant basal levels of macroautophagy/autophagy are a prerequisite to preserve long-lived podocytes at the filtration barrier, MTOR regulates at the same time podocyte size and compensatory hypertrophy. Since MTOR is known to generally suppress autophagy, the apparently independent regulation of these two key pathways of glomerular maintenance remained puzzling. We now report that long-term genetic manipulation of MTOR activity does in fact not influence high basal levels of autophagy in podocytes either in vitro or in vivo. Instead we present data showing that autophagy in podocytes is mainly controlled by AMP-activated protein kinase (AMPK) and ULK1 (unc-51 like kinase 1). Pharmacological inhibition of MTOR further shows that the uncoupling of MTOR activity and autophagy is time dependent. Together, our data reveal a novel and unexpected cell-specific mechanism, which permits concurrent MTOR activity as well as high basal autophagy rates in podocytes. Thus, these data indicate manipulation of the AMPK-ULK1 axis rather than inhibition of MTOR as a promising therapeutic intervention to enhance autophagy and preserve podocyte homeostasis in glomerular diseases.Abbreviations: AICAR: 5-aminoimidazole-4-carboxamide ribonucleotide; AMPK: AMP-activated protein kinase; ATG: autophagy related; BW: body weight; Cq: chloroquine; ER: endoplasmic reticulum; ESRD: end stage renal disease; FACS: fluorescence activated cell sorting; GFP: green fluorescent protein; i.p.: intra peritoneal; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MTOR: mechanistic target of rapamycin kinase; NPHS1: nephrosis 1, nephrin; NPHS2: nephrosis 2, podocin; PLA: proximity-ligation assay; PRKAA: 5'-AMP-activated protein kinase catalytic subunit alpha; RPTOR/RAPTOR: regulatory associated protein of MTOR, complex 1; RFP: red fluorescent protein; TSC1: tuberous sclerosis 1; ULK1: unc-51 like kinase 1.</p>
</div>
</front>
</TEI>
<affiliations><list><country><li>Allemagne</li>
<li>Autriche</li>
<li>France</li>
</country>
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<tree><country name="Allemagne"><noRegion><name sortKey="Bork, Tillmann" sort="Bork, Tillmann" uniqKey="Bork T" first="Tillmann" last="Bork">Tillmann Bork</name>
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<name sortKey="Lee, Philipp" sort="Lee, Philipp" uniqKey="Lee P" first="Philipp" last="Lee">Philipp Lee</name>
<name sortKey="Liang, Wei" sort="Liang, Wei" uniqKey="Liang W" first="Wei" last="Liang">Wei Liang</name>
<name sortKey="Liu, Shuya" sort="Liu, Shuya" uniqKey="Liu S" first="Shuya" last="Liu">Shuya Liu</name>
<name sortKey="Patel, Ketan" sort="Patel, Ketan" uniqKey="Patel K" first="Ketan" last="Patel">Ketan Patel</name>
<name sortKey="Schell, Christoph" sort="Schell, Christoph" uniqKey="Schell C" first="Christoph" last="Schell">Christoph Schell</name>
<name sortKey="Tian, Zhejia" sort="Tian, Zhejia" uniqKey="Tian Z" first="Zhejia" last="Tian">Zhejia Tian</name>
<name sortKey="Yamahara, Kosuke" sort="Yamahara, Kosuke" uniqKey="Yamahara K" first="Kosuke" last="Yamahara">Kosuke Yamahara</name>
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</noRegion>
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