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Phosphorylation of p62 by AMP-activated protein kinase mediates autophagic cell death in adult hippocampal neural stem cells

Ha, Shinwon, Jeong, Seol-Hwa, Yi, Kyungrim, Chung, Kyung Min, Hong, Caroline Jeeyeon, Kim, Seong Who, Kim, Eun-Kyoung, Yu, Seong-Woon·2017·Journal of Biological Chemistry
DOI 10.1074/jbc.m117.780874
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Figure 1 AMPK activation is required for ACD in I( H11546 ) HCN cells. A , time-course analysis of AMPK activation and autophagy induction following insulin withdrawal. Blots shown are representative of three independent experiments, which yielded similar results. B , pharmacological inhibition of AMPK with CC (0.5 𝛍 M) decreased cell death ( n = 5). C , administration of CC attenuated autophagy. The levels of LC3-II and p62 were measured 5 h after insulin withdrawal. D , quantification of LC3-II and p62 after normalization to 𝛃 -actin ( n = 5). E , HCN cells were transfected with the GFP-LC3 plasmid, and LC3 puncta were visualized after insulin withdrawal for 5 h. F , analysis of E . Quantification of the puncta from three independent experiments ( n = 40) is shown. G , AMPK 𝛂 2 knock-out decreased cell death following insulin withdrawal. Cell death of AMPK 𝛂 2 KO ( Sg-AMPK 𝛂 2 ) and control ( Sg-con ) HCN cells was measured at the indicated time points following insulin withdrawal ( n = 4). H , autophagy flux following insulin withdrawal (5 h) was abrogated in AMPK 𝛂 2KOHCNcells.BafA1 (20 nM) was added 1 h before sampling. I , quantification of LC3-II and p62 after normalization to 𝛃 -actin ( n = 4). Error bars represent ± S.D. from independent assays. *, p < 0.05; **, p < 0.01; ***, p < 0.001. Scale bar , 10 𝛍 m. p-AMPK , phospho-AMPK; t-AMPK , total AMPK.
Figure 1 AMPK activation is required for ACD in I( H11546 ) HCN cells. A , time-course analysis of AMPK activation and autophagy induction following insulin withdrawal. Blots shown are representative of three independent experiments, which yielded similar results. B , pharmacological inhibition of AMPK with CC (0.5 𝛍 M) decreased cell death ( n = 5). C , administration of CC attenuated autophagy. The levels of LC3-II and p62 were measured 5 h after insulin withdrawal. D , quantification of LC3-II and p62 after normalization to 𝛃 -actin ( n = 5). E , HCN cells were transfected with the GFP-LC3 plasmid, and LC3 puncta were visualized after insulin withdrawal for 5 h. F , analysis of E . Quantification of the puncta from three independent experiments ( n = 40) is shown. G , AMPK 𝛂 2 knock-out decreased cell death following insulin withdrawal. Cell death of AMPK 𝛂 2 KO ( Sg-AMPK 𝛂 2 ) and control ( Sg-con ) HCN cells was measured at the indicated time points following insulin withdrawal ( n = 4). H , autophagy flux following insulin withdrawal (5 h) was abrogated in AMPK 𝛂 2KOHCNcells.BafA1 (20 nM) was added 1 h before sampling. I , quantification of LC3-II and p62 after normalization to 𝛃 -actin ( n = 4). Error bars represent ± S.D. from independent assays. *, p < 0.05; **, p < 0.01; ***, p < 0.001. Scale bar , 10 𝛍 m. p-AMPK , phospho-AMPK; t-AMPK , total AMPK.CC-BY · From the PDF
Figure2 GeneticactivationofAMPKenhancesACDinI( H11546 ) HCNcells. A , overexpression of AMPK-CA increased the level of LC3-II and decreased that of p62 but did not activate caspase-3 following insulin withdrawal for 5 h. STS (0.5 𝛍 M for 8 h) was used as a positive control for apoptosis. C-cas3 , cleaved caspase-3. B , quantification of LC3-II and p62 after normalization to 𝛃 -actin ( n = 4). C , AMPK-CA increased cell death more than did I( -) alone. Z-VAD (20 𝛍 M) failed to reduce cell death induced by AMPK-CA but efficiently reduced STS-induced apoptosis ( n = 5). D , AMPK-CA increased autophagic flux in I( -) HCN cells. Insulin was withdrawn for 5 h, and BafA1 (20 nM) was added 1 h before sampling. E , quantification of LC3-II and p62 after normalization to 𝛃 -actin ( n = 5). F , AMPK-CA ( CA ) increased autophagic flux. Autophagic flux was measured using tandem mRFP-GFP-LC3 after 5-h insulin withdrawal. G , analysis of F . The red and yellow puncta were counted from three independent experiments ( n = 29). H , Atg7 knockdown abrogated AMPK-CA-triggered cell death. Cell death was measured 24 h after insulin withdrawal ( n = 6). I , Atg7 knockdown abrogated AMPK-CA-triggered autophagic flux. AMPK-CA failed to affect LC3-II or p62 in Sh-Atg7 HCN cells analyzed 5 h after insulin withdrawal. J , quantification of LC3-II and p62 after normalization to 𝛃 -actin ( n = 9). Error bars represent ± S.D. from independent assays. *, p < 0.05; **, p < 0.01; ***, p < 0.001; ns , not significant. Scale bar , 10 𝛍 m. EV , empty vector; con , control.
Figure2 GeneticactivationofAMPKenhancesACDinI( H11546 ) HCNcells. A , overexpression of AMPK-CA increased the level of LC3-II and decreased that of p62 but did not activate caspase-3 following insulin withdrawal for 5 h. STS (0.5 𝛍 M for 8 h) was used as a positive control for apoptosis. C-cas3 , cleaved caspase-3. B , quantification of LC3-II and p62 after normalization to 𝛃 -actin ( n = 4). C , AMPK-CA increased cell death more than did I( -) alone. Z-VAD (20 𝛍 M) failed to reduce cell death induced by AMPK-CA but efficiently reduced STS-induced apoptosis ( n = 5). D , AMPK-CA increased autophagic flux in I( -) HCN cells. Insulin was withdrawn for 5 h, and BafA1 (20 nM) was added 1 h before sampling. E , quantification of LC3-II and p62 after normalization to 𝛃 -actin ( n = 5). F , AMPK-CA ( CA ) increased autophagic flux. Autophagic flux was measured using tandem mRFP-GFP-LC3 after 5-h insulin withdrawal. G , analysis of F . The red and yellow puncta were counted from three independent experiments ( n = 29). H , Atg7 knockdown abrogated AMPK-CA-triggered cell death. Cell death was measured 24 h after insulin withdrawal ( n = 6). I , Atg7 knockdown abrogated AMPK-CA-triggered autophagic flux. AMPK-CA failed to affect LC3-II or p62 in Sh-Atg7 HCN cells analyzed 5 h after insulin withdrawal. J , quantification of LC3-II and p62 after normalization to 𝛃 -actin ( n = 9). Error bars represent ± S.D. from independent assays. *, p < 0.05; **, p < 0.01; ***, p < 0.001; ns , not significant. Scale bar , 10 𝛍 m. EV , empty vector; con , control.CC-BY · From the PDF
Figure 3 p62 is required for ACD in I( H11546 ) HCN cells. A , schematic representation of the functional domains and predicted AMPK 𝛂 2 phosphorylation sites of p62. B , knockdown of p62 abrogated an increase in LC3-II following insulin withdrawal. C , quantification of LC3-II after normalization to 𝛃 -actin ( n = 3). D , p62 knockdown attenuated the AMPK-CA-induced increase in cell death I( -) HCN cells ( n = 6). E , p62 knockdown attenuated the AMPK-CAinduced increase in LC3-II in I( -) HCN cells. F , quantification of LC3-II after normalization to 𝛃 -actin ( n = 6). Error bars represent ± S.D. from independent assays. ***, p < 0.001. con , control; ZZ , ZZ-type zinc finger domain; LIR , LC3interacting region; UBA , ubiquitin-associated domain; KIR , Keap1-interacting region.
Figure 3 p62 is required for ACD in I( H11546 ) HCN cells. A , schematic representation of the functional domains and predicted AMPK 𝛂 2 phosphorylation sites of p62. B , knockdown of p62 abrogated an increase in LC3-II following insulin withdrawal. C , quantification of LC3-II after normalization to 𝛃 -actin ( n = 3). D , p62 knockdown attenuated the AMPK-CA-induced increase in cell death I( -) HCN cells ( n = 6). E , p62 knockdown attenuated the AMPK-CAinduced increase in LC3-II in I( -) HCN cells. F , quantification of LC3-II after normalization to 𝛃 -actin ( n = 6). Error bars represent ± S.D. from independent assays. ***, p < 0.001. con , control; ZZ , ZZ-type zinc finger domain; LIR , LC3interacting region; UBA , ubiquitin-associated domain; KIR , Keap1-interacting region.CC-BY · From the PDF
Figure 5 Serine phosphorylation at a novel site in p62 is mediated by AMPK. A , endogenous p62 was phosphorylated in an AMPK-dependent manner in HCN cells. Insulin withdrawal for 5 h induced phosphorylation of p62 Ser-293, which was detected by using a phosphospecific antibody. CC (0.5 𝛍 M) reduced Ser-293 phosphorylation. B , quantification of p62 Ser-293 phosphorylation ( p-p62 ) after normalization to total p62 ( t-p62 ) following CC treatment ( n = 6). C , AMPK 𝛂 2KOreducedSer-293phosphorylation. D , quantification of p62 Ser-293 phosphorylation ( p-p62 ) after normalization to total p62( t-p62 ) in AMPK 𝛂 2 KO HCN cells ( n = 6). E , hp62-WT, but not hp62-S294A mutant( SA ), was phosphorylated in vitro bytheenrichedAMPKimmunecomplex. Phosphorylation was detected by Western blotting with phosphospecific antibody. F , quantification of in vitro kinase assay results ( n = 4). G , treatment of the AMPK immune complex with CC (1 𝛍 M) for 1 h abolished p62 phosphorylation. H , quantification of in vitro kinase assay results with CC ( n = 3). Error bars represent ± S.D. from independent assays. *, p < 0.05; **, p < 0.01; ***, p < 0.001.
Figure 5 Serine phosphorylation at a novel site in p62 is mediated by AMPK. A , endogenous p62 was phosphorylated in an AMPK-dependent manner in HCN cells. Insulin withdrawal for 5 h induced phosphorylation of p62 Ser-293, which was detected by using a phosphospecific antibody. CC (0.5 𝛍 M) reduced Ser-293 phosphorylation. B , quantification of p62 Ser-293 phosphorylation ( p-p62 ) after normalization to total p62 ( t-p62 ) following CC treatment ( n = 6). C , AMPK 𝛂 2KOreducedSer-293phosphorylation. D , quantification of p62 Ser-293 phosphorylation ( p-p62 ) after normalization to total p62( t-p62 ) in AMPK 𝛂 2 KO HCN cells ( n = 6). E , hp62-WT, but not hp62-S294A mutant( SA ), was phosphorylated in vitro bytheenrichedAMPKimmunecomplex. Phosphorylation was detected by Western blotting with phosphospecific antibody. F , quantification of in vitro kinase assay results ( n = 4). G , treatment of the AMPK immune complex with CC (1 𝛍 M) for 1 h abolished p62 phosphorylation. H , quantification of in vitro kinase assay results with CC ( n = 3). Error bars represent ± S.D. from independent assays. *, p < 0.05; **, p < 0.01; ***, p < 0.001.CC-BY · From the PDF
Figure 6 AMPK induces mitophagy in I( H11546 ) HCN cells. A , transfection of HCN cells with the plasmids encoding GFP-LC3 and DsRed2-Mito. Mitophagy was assessed as the overlap of LC3 and DsRed2-Mito signals and was greatly enhanced following insulin withdrawal (5 h) and prevented by CC. Inset , a highmagnification image of the boxed area. B , analysis of A . Quantification of mitochondrial localization of GFP-LC3 ( n = 8) is shown. C , fluorescence signal of mt-mKeima.Cellsexpressingmt-mKeimawereexcited( Ex. ) at two wavelengths (458 and 561 nm), and the emission signal was collected at 620 nm after insulin withdrawal for 5 h. D , analysis of C . The relative intensity ratio as an index of mitophagy ( n = 10) is shown. E , insulin withdrawal-induced mitophagy was abrogated in AMPK 𝛂 2 KO HCN cells. F , analysis of E . The relative intensity ratio as an index of mitophagy is shown. CCCP (5 𝛍 M for 5 h) was added to I( + ) HCN cells to induce mitophagy as a positive control ( n = 8). ns , not significant; G , the amount of mitochondria in HCN cells following insulin withdrawal for 12 h and treatment with CC (5 𝛍 Mfor 12 h) was determined by FACS using MitoTracker Green ( x axis ). FSC , forward scatter. H , analysis of G . The relative 𝚫 MitoTracker (%) as an index of mitophagic degradation of mitochondria is shown. CCCP (10 𝛍 Mfor 12 h) was used as a positive control ( n = 5). Error bars represent ± S.D. from independent assays. *, p < 0.05; **, p < 0.01; ***, p < 0.001; ns , not significant. Scale bar , 10 𝛍 m.
Figure 6 AMPK induces mitophagy in I( H11546 ) HCN cells. A , transfection of HCN cells with the plasmids encoding GFP-LC3 and DsRed2-Mito. Mitophagy was assessed as the overlap of LC3 and DsRed2-Mito signals and was greatly enhanced following insulin withdrawal (5 h) and prevented by CC. Inset , a highmagnification image of the boxed area. B , analysis of A . Quantification of mitochondrial localization of GFP-LC3 ( n = 8) is shown. C , fluorescence signal of mt-mKeima.Cellsexpressingmt-mKeimawereexcited( Ex. ) at two wavelengths (458 and 561 nm), and the emission signal was collected at 620 nm after insulin withdrawal for 5 h. D , analysis of C . The relative intensity ratio as an index of mitophagy ( n = 10) is shown. E , insulin withdrawal-induced mitophagy was abrogated in AMPK 𝛂 2 KO HCN cells. F , analysis of E . The relative intensity ratio as an index of mitophagy is shown. CCCP (5 𝛍 M for 5 h) was added to I( + ) HCN cells to induce mitophagy as a positive control ( n = 8). ns , not significant; G , the amount of mitochondria in HCN cells following insulin withdrawal for 12 h and treatment with CC (5 𝛍 Mfor 12 h) was determined by FACS using MitoTracker Green ( x axis ). FSC , forward scatter. H , analysis of G . The relative 𝚫 MitoTracker (%) as an index of mitophagic degradation of mitochondria is shown. CCCP (10 𝛍 Mfor 12 h) was used as a positive control ( n = 5). Error bars represent ± S.D. from independent assays. *, p < 0.05; **, p < 0.01; ***, p < 0.001; ns , not significant. Scale bar , 10 𝛍 m.CC-BY · From the PDF
Image 6
CC-BY · From the PDF
Figure 8 Phosphorylated p62 mediates AMPK-induced mitophagy in I( H11546 ) HCN cells. A , co-transfection of Sh-rp62 HCN cells with plasmids encoding mt-mKeima and HA-tagged hp62-WT, -S294A, or -S294E. Cells expressing hp62-WT or hp62-S294E underwent mitophagy, whereas the expression of hp62-S294Amutantpreventedmitophagy. Ex , excitation. B , analysis of A . The relative intensity ratio as an index of mitophagy ( n = 8) is shown. C , a schematic diagram illustrating p62 phosphorylation by AMPK and subsequent mitophagy and ACD in HCN cells following insulin withdrawal. Error bars represent ± S.D. from independent assays. *, p < 0.05; ***, p < 0.001. Scale bar , 10 𝛍 m.
Figure 8 Phosphorylated p62 mediates AMPK-induced mitophagy in I( H11546 ) HCN cells. A , co-transfection of Sh-rp62 HCN cells with plasmids encoding mt-mKeima and HA-tagged hp62-WT, -S294A, or -S294E. Cells expressing hp62-WT or hp62-S294E underwent mitophagy, whereas the expression of hp62-S294Amutantpreventedmitophagy. Ex , excitation. B , analysis of A . The relative intensity ratio as an index of mitophagy ( n = 8) is shown. C , a schematic diagram illustrating p62 phosphorylation by AMPK and subsequent mitophagy and ACD in HCN cells following insulin withdrawal. Error bars represent ± S.D. from independent assays. *, p < 0.05; ***, p < 0.001. Scale bar , 10 𝛍 m.CC-BY · From the PDF

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Metadata

Authors
Ha, S., Jeong, S.-H., Yi, K., Chung, K. M., Hong, C. J., Kim, S. W., Kim, E.-K., & Yu, S.-W.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2017-08
Volume
292
Issue
33
Pages
13795-13808
ISSN
0021-9258
DOI
10.1074/jbc.m117.780874
Cited by
61
References
10
Language
en
Licence
Funders
  • National Research Foundation of Korea (2012M3A9C6049935, 2013M3C7A1056099)
  • Ministry of Science ICT and Future Planning (17-BD-04)
  • Ministry of Science, ICT and Future Planning (17-BR-04)

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