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Mitochondrial p53 interacted with <t>SLC25A28</t> to trigger iron accumulation in BRD7-enhanced HSC ferroptosis. The mutant p53 or p53 KD HSC-LX2 cells were transfected with BRD7 plasmid, and were exposed to erastin (10 μM) for 24 h. (A) Mitochondrial iron levels were determined by iron assay kit (n = 3 in every group, **P < 0.01, N·S., not significant). (B) SLC25A28 expression was determined by real-time PCR (n = 3 in every group, **P < 0.01, ***P < 0.001, N·S., not significant). HSC-LX2 cells were transfected with BRD7 plasmid, and then were exposed to erastin (10 μM) for 24 h. (C) The combination of p53 and SLC25A28 was examined by immunocoprecipitation (n = 3 in every group). (D) The co-localization of p53 (red fluorescence), SLC25A28 (green fluorescence), and mitochondria (mitotracker blue) was determined by confocal imaging. Scale bars are 100 μm. Representative photographs were shown (n = 3 in every group). (E) HSC-LX2 cells were transfected with p53 plasmid, and were exposed to erastin (10 μM) with or without cycloheximide (CHX, 20 μg/ml) for 24 h. The levels of SLC25A28 were evaluated 0, 4, 8, and 12 h after the end of cell exposure to erastin and CHX (n = 3 in every group). (F) The indicated cells were transfected with p53 plasmid, and were exposed to erastin (10 μM) for 24 h. The SLC25A28 activity was examined as the rate of mitochondrial iron uptake (n = 3 in every group, *P < 0.05, **P < 0.01). (G, H) HSC-LX2 cells were transfected with BRD7 plasmid and SLC25A28 shRNA, and were exposed to erastin (10 μM) for 24 h. Cell death and the levels of mitochondrial iron, lipid ROS, GSH, and MDA were determined by commercial kits (n = 3 in every group, *P < 0.05, **P < 0.01,***P < 0.001, N·S., not significant). (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
Slc25a28 Shrna, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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IRP2-associated mitochondrial iron loading and CS. ( a ) Representative Perls’ stained lung sections (n=3 mice per group) (left) ( n = 2 technical replicates) with quantification (middle) ( n = 10 images per mouse, n = 3 per group) and non-heme iron levels (right, n = 4 mice per group, n = 4 technical replicates) in WT mice exposed to RA or CS (1–6 months). Scale bars, 50 μm. Arrows indicate staining. n.c.; negative control. ( b ) Representative immunoblot (n=3 experiments) (left) with quantification (right) of transferrin and ferritin expression ( n = 5 per group, n = 2 technical replicates), ( c ) total non-heme iron (left, n = 5 mice per group , n = 4 technical replicates) and fold change mitochondrial (RA n = 11; CS 1 month n = 6, 4 months n = 8, 6 months n = 9) and cytosolic non-heme (RA n = 6; CS 1 month n = 11, 4 months n = 3, 6 months n = 5) iron (right) in WT mouse lungs exposed to RA or CS, n = 2 technical replicates. ( d ) Fold change non-heme iron (left, WT and Irp2 −/− ; RA n = 13, CS 1 and 6 months n =5, CS 4 months n =3) and heme-iron (right , WT and Irp2 −/− ; RA n = 10, CS 1–6 months n =5) in mitochondrial fractions from WT mouse lungs exposed to RA or CS, n = 2 technical replicates. ( e ) <t>Mitoferrin</t> <t>2</t> (WT and Irp2 −/− ; RA n = 8; CS 1 month n = 3, 4 months n = 6), ( f ) frataxin expression (WT RA n = 5; CS n = 3; Irp2 −/− RA n = 6; CS n = 6) in whole lung of mice exposed to RA or CS. ( g ) Mitochondrial non-heme (left , n = 4 per group), mitochondrial heme iron (right , n = 4 per group), ( h ) 3 hour 99m Tc-SC clearance (left) and IL-6 protein concentrations (right , n = 4 per group) in the lungs of WT and Fxn ki/ko mice exposed to RA or CS (1 month). ( i ) Schematic of mitochondrial iron loading regulated by Irp2. All data are mean ± s.e.m. * P < 0.05. ** P < 0.01, *** P < 0.005 by one-way ANOVA followed by Bonferroni correction. # P < 0.05 by student’s unpaired t -test.
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item number designation 90800  (Velcro Industries BV)
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Velcro Industries BV item number designation 90800
IRP2-associated mitochondrial iron loading and CS. ( a ) Representative Perls’ stained lung sections (n=3 mice per group) (left) ( n = 2 technical replicates) with quantification (middle) ( n = 10 images per mouse, n = 3 per group) and non-heme iron levels (right, n = 4 mice per group, n = 4 technical replicates) in WT mice exposed to RA or CS (1–6 months). Scale bars, 50 μm. Arrows indicate staining. n.c.; negative control. ( b ) Representative immunoblot (n=3 experiments) (left) with quantification (right) of transferrin and ferritin expression ( n = 5 per group, n = 2 technical replicates), ( c ) total non-heme iron (left, n = 5 mice per group , n = 4 technical replicates) and fold change mitochondrial (RA n = 11; CS 1 month n = 6, 4 months n = 8, 6 months n = 9) and cytosolic non-heme (RA n = 6; CS 1 month n = 11, 4 months n = 3, 6 months n = 5) iron (right) in WT mouse lungs exposed to RA or CS, n = 2 technical replicates. ( d ) Fold change non-heme iron (left, WT and Irp2 −/− ; RA n = 13, CS 1 and 6 months n =5, CS 4 months n =3) and heme-iron (right , WT and Irp2 −/− ; RA n = 10, CS 1–6 months n =5) in mitochondrial fractions from WT mouse lungs exposed to RA or CS, n = 2 technical replicates. ( e ) <t>Mitoferrin</t> <t>2</t> (WT and Irp2 −/− ; RA n = 8; CS 1 month n = 3, 4 months n = 6), ( f ) frataxin expression (WT RA n = 5; CS n = 3; Irp2 −/− RA n = 6; CS n = 6) in whole lung of mice exposed to RA or CS. ( g ) Mitochondrial non-heme (left , n = 4 per group), mitochondrial heme iron (right , n = 4 per group), ( h ) 3 hour 99m Tc-SC clearance (left) and IL-6 protein concentrations (right , n = 4 per group) in the lungs of WT and Fxn ki/ko mice exposed to RA or CS (1 month). ( i ) Schematic of mitochondrial iron loading regulated by Irp2. All data are mean ± s.e.m. * P < 0.05. ** P < 0.01, *** P < 0.005 by one-way ANOVA followed by Bonferroni correction. # P < 0.05 by student’s unpaired t -test.
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Mitochondrial p53 interacted with SLC25A28 to trigger iron accumulation in BRD7-enhanced HSC ferroptosis. The mutant p53 or p53 KD HSC-LX2 cells were transfected with BRD7 plasmid, and were exposed to erastin (10 μM) for 24 h. (A) Mitochondrial iron levels were determined by iron assay kit (n = 3 in every group, **P < 0.01, N·S., not significant). (B) SLC25A28 expression was determined by real-time PCR (n = 3 in every group, **P < 0.01, ***P < 0.001, N·S., not significant). HSC-LX2 cells were transfected with BRD7 plasmid, and then were exposed to erastin (10 μM) for 24 h. (C) The combination of p53 and SLC25A28 was examined by immunocoprecipitation (n = 3 in every group). (D) The co-localization of p53 (red fluorescence), SLC25A28 (green fluorescence), and mitochondria (mitotracker blue) was determined by confocal imaging. Scale bars are 100 μm. Representative photographs were shown (n = 3 in every group). (E) HSC-LX2 cells were transfected with p53 plasmid, and were exposed to erastin (10 μM) with or without cycloheximide (CHX, 20 μg/ml) for 24 h. The levels of SLC25A28 were evaluated 0, 4, 8, and 12 h after the end of cell exposure to erastin and CHX (n = 3 in every group). (F) The indicated cells were transfected with p53 plasmid, and were exposed to erastin (10 μM) for 24 h. The SLC25A28 activity was examined as the rate of mitochondrial iron uptake (n = 3 in every group, *P < 0.05, **P < 0.01). (G, H) HSC-LX2 cells were transfected with BRD7 plasmid and SLC25A28 shRNA, and were exposed to erastin (10 μM) for 24 h. Cell death and the levels of mitochondrial iron, lipid ROS, GSH, and MDA were determined by commercial kits (n = 3 in every group, *P < 0.05, **P < 0.01,***P < 0.001, N·S., not significant). (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

Journal: Redox Biology

Article Title: The BRD7-P53-SLC25A28 axis regulates ferroptosis in hepatic stellate cells

doi: 10.1016/j.redox.2020.101619

Figure Lengend Snippet: Mitochondrial p53 interacted with SLC25A28 to trigger iron accumulation in BRD7-enhanced HSC ferroptosis. The mutant p53 or p53 KD HSC-LX2 cells were transfected with BRD7 plasmid, and were exposed to erastin (10 μM) for 24 h. (A) Mitochondrial iron levels were determined by iron assay kit (n = 3 in every group, **P < 0.01, N·S., not significant). (B) SLC25A28 expression was determined by real-time PCR (n = 3 in every group, **P < 0.01, ***P < 0.001, N·S., not significant). HSC-LX2 cells were transfected with BRD7 plasmid, and then were exposed to erastin (10 μM) for 24 h. (C) The combination of p53 and SLC25A28 was examined by immunocoprecipitation (n = 3 in every group). (D) The co-localization of p53 (red fluorescence), SLC25A28 (green fluorescence), and mitochondria (mitotracker blue) was determined by confocal imaging. Scale bars are 100 μm. Representative photographs were shown (n = 3 in every group). (E) HSC-LX2 cells were transfected with p53 plasmid, and were exposed to erastin (10 μM) with or without cycloheximide (CHX, 20 μg/ml) for 24 h. The levels of SLC25A28 were evaluated 0, 4, 8, and 12 h after the end of cell exposure to erastin and CHX (n = 3 in every group). (F) The indicated cells were transfected with p53 plasmid, and were exposed to erastin (10 μM) for 24 h. The SLC25A28 activity was examined as the rate of mitochondrial iron uptake (n = 3 in every group, *P < 0.05, **P < 0.01). (G, H) HSC-LX2 cells were transfected with BRD7 plasmid and SLC25A28 shRNA, and were exposed to erastin (10 μM) for 24 h. Cell death and the levels of mitochondrial iron, lipid ROS, GSH, and MDA were determined by commercial kits (n = 3 in every group, *P < 0.05, **P < 0.01,***P < 0.001, N·S., not significant). (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

Article Snippet: BRD7 shRNA (sc-92998, sc-141741), p53 shRNA (sc-44218, sc-45917), SLC25A28 shRNA (sc-90800, sc-149448), and control shRNA were obtained from Santa Cruz Biotechnology.

Techniques: Mutagenesis, Transfection, Plasmid Preparation, Iron Assay, Expressing, Real-time Polymerase Chain Reaction, Fluorescence, Imaging, Activity Assay, shRNA

BRD7-P53-SLC25A28 axis disturbed electron transport chain to aggravate lipid peroxidation in BRD7-enhanced HSC ferroptosis. (A) Scheme indicated mitochondrial electron transport chain (ETC) complexes and their inhibitors. HSC-LX2 cells were transfected with SLC25A28 shRNA or SLC25A28 plasmid, and were exposed to erastin (10 μM) for 24 h. (B) Mitochondria mass was determined by plate reader-based quantitation of Mito Tracker (n = 3 in every group, N·S., not significant). (C) mtDNA copy number was examined by real-time PCR (n = 3 in every group, N·S., not significant). (D) The enzymatic activities of mitochondrial complexes were analyzed by commercial kits (n = 3 in every group, *P < 0.05, **P < 0.01, ***P < 0.001). (E) BRD7 knockout or knockin HSC-LX2 cells were exposed to erastin (10 μM) for 24 h. Subunits expression of mitochondrial complexes was detected by real-time PCR (n = 3 in every group, *P < 0.05, **P < 0.01, ***P < 0.001). (F) HSC-LX2 cells were transfected with BRD7 plasmid, and were exposed to erastin (10 μM) with or without ETC inhibitors (rotenone, 10 mM; diethyl butylmalonate (DBM), 2 mM; Antimycin A (Anti A), 50 mM; and NaN 3 , 15 mM) for 24 h. Cell death and the levels of mitochondrial iron, lipid ROS, and MDA were determined by commercial kits (n = 3 in every group, **P < 0.01, ***P < 0.001). (G) HSC-LX2 cells were transfected with SLC25A28 plasmid, and were exposed to erastin (10 μM) with or without ETC inhibitors (rotenone, 10 mM; DBM, 2 mM; Antimycin A (Anti A), 50 mM; and NaN 3 , 15 mM) for 24 h. Cell death and the levels of mitochondrial iron, lipid ROS, and MDA were determined by commercial kits (n = 3 in every group, **P < 0.01, ***P < 0.001).

Journal: Redox Biology

Article Title: The BRD7-P53-SLC25A28 axis regulates ferroptosis in hepatic stellate cells

doi: 10.1016/j.redox.2020.101619

Figure Lengend Snippet: BRD7-P53-SLC25A28 axis disturbed electron transport chain to aggravate lipid peroxidation in BRD7-enhanced HSC ferroptosis. (A) Scheme indicated mitochondrial electron transport chain (ETC) complexes and their inhibitors. HSC-LX2 cells were transfected with SLC25A28 shRNA or SLC25A28 plasmid, and were exposed to erastin (10 μM) for 24 h. (B) Mitochondria mass was determined by plate reader-based quantitation of Mito Tracker (n = 3 in every group, N·S., not significant). (C) mtDNA copy number was examined by real-time PCR (n = 3 in every group, N·S., not significant). (D) The enzymatic activities of mitochondrial complexes were analyzed by commercial kits (n = 3 in every group, *P < 0.05, **P < 0.01, ***P < 0.001). (E) BRD7 knockout or knockin HSC-LX2 cells were exposed to erastin (10 μM) for 24 h. Subunits expression of mitochondrial complexes was detected by real-time PCR (n = 3 in every group, *P < 0.05, **P < 0.01, ***P < 0.001). (F) HSC-LX2 cells were transfected with BRD7 plasmid, and were exposed to erastin (10 μM) with or without ETC inhibitors (rotenone, 10 mM; diethyl butylmalonate (DBM), 2 mM; Antimycin A (Anti A), 50 mM; and NaN 3 , 15 mM) for 24 h. Cell death and the levels of mitochondrial iron, lipid ROS, and MDA were determined by commercial kits (n = 3 in every group, **P < 0.01, ***P < 0.001). (G) HSC-LX2 cells were transfected with SLC25A28 plasmid, and were exposed to erastin (10 μM) with or without ETC inhibitors (rotenone, 10 mM; DBM, 2 mM; Antimycin A (Anti A), 50 mM; and NaN 3 , 15 mM) for 24 h. Cell death and the levels of mitochondrial iron, lipid ROS, and MDA were determined by commercial kits (n = 3 in every group, **P < 0.01, ***P < 0.001).

Article Snippet: BRD7 shRNA (sc-92998, sc-141741), p53 shRNA (sc-44218, sc-45917), SLC25A28 shRNA (sc-90800, sc-149448), and control shRNA were obtained from Santa Cruz Biotechnology.

Techniques: Transfection, shRNA, Plasmid Preparation, Quantitation Assay, Real-time Polymerase Chain Reaction, Knock-Out, Knock-In, Expressing

HSC-specific blockade of BRD7-P53-SLC25A28 axis impaired erastin-mediated HSC ferroptosis in murine liver fibrosis. Mice of 6 groups were treated with Sham, BDL + VA-Lip-Control-shRNA, BDL + VA-Lip-Control-shRNA + erastin, BDL + VA-Lip-BRD7 - shRNA + erastin, BDL + VA-Lip-P53-shRNA + erastin, or BDL + VA-Lip-SLC25A28-shRNA + erastin. (A, B) The fibrotic injury was observed by macroscopic examination and histopathological examination (n = 6 in every group, **P < 0.01, ***P < 0.001). (C) The levels of ACTA2, COL1A1, fibronectin, and desmin were examined by real-time PCR in fibrotic liver tissues (n = 6 in every group, ***P < 0.001). Primary HSCs were also isolated from fibrotic livers. (D) The levels of BRD7 were detected by Western blot (n = 6 in every group). (E) The combination of BRD7 and p53 was examined by immunocoprecipitation (n = 6 in every group). (F) The levels of p53 in mitochondria were detected by Western blot (n = 6 in every group). (G) The combination of SLC25A28 and p53 was examined by immunocoprecipitation (n = 6 in every group). (H) The levels of mitochondrial iron, lipid ROS MDA, and cell death were determined by commercial kits (n = 6 in every group, *P < 0.05, **P < 0.01, ***P < 0.001, N·S., not significant).

Journal: Redox Biology

Article Title: The BRD7-P53-SLC25A28 axis regulates ferroptosis in hepatic stellate cells

doi: 10.1016/j.redox.2020.101619

Figure Lengend Snippet: HSC-specific blockade of BRD7-P53-SLC25A28 axis impaired erastin-mediated HSC ferroptosis in murine liver fibrosis. Mice of 6 groups were treated with Sham, BDL + VA-Lip-Control-shRNA, BDL + VA-Lip-Control-shRNA + erastin, BDL + VA-Lip-BRD7 - shRNA + erastin, BDL + VA-Lip-P53-shRNA + erastin, or BDL + VA-Lip-SLC25A28-shRNA + erastin. (A, B) The fibrotic injury was observed by macroscopic examination and histopathological examination (n = 6 in every group, **P < 0.01, ***P < 0.001). (C) The levels of ACTA2, COL1A1, fibronectin, and desmin were examined by real-time PCR in fibrotic liver tissues (n = 6 in every group, ***P < 0.001). Primary HSCs were also isolated from fibrotic livers. (D) The levels of BRD7 were detected by Western blot (n = 6 in every group). (E) The combination of BRD7 and p53 was examined by immunocoprecipitation (n = 6 in every group). (F) The levels of p53 in mitochondria were detected by Western blot (n = 6 in every group). (G) The combination of SLC25A28 and p53 was examined by immunocoprecipitation (n = 6 in every group). (H) The levels of mitochondrial iron, lipid ROS MDA, and cell death were determined by commercial kits (n = 6 in every group, *P < 0.05, **P < 0.01, ***P < 0.001, N·S., not significant).

Article Snippet: BRD7 shRNA (sc-92998, sc-141741), p53 shRNA (sc-44218, sc-45917), SLC25A28 shRNA (sc-90800, sc-149448), and control shRNA were obtained from Santa Cruz Biotechnology.

Techniques: shRNA, Real-time Polymerase Chain Reaction, Isolation, Western Blot

BRD7-P53-SLC25A28 axis regulated ferroptosis in human HSCs from fibrotic patients with sorafenib monotherapy. (A) The levels of fibrosis markers ACTA2, COL1A1, and fibronectin were examined in sorafenib-treated hepatectomy samples and untreated liver biopsy samples (No treatment, n = 37; sorafenib monotherapy, n = 24; ***P < 0.001). Primary human HSCs were isolated from the collected liver tissue by laser capture microdissection. (B) The levels of BRD7 were examined by Western blot (No treatment, n = 37; sorafenib monotherapy, n = 24). (C) The combination of BRD7 and p53 was determined by immunocoprecipitation (No treatment, n = 37; sorafenib monotherapy, n = 24). (D) The levels of p53 in mitochondria were examined by Western blot (No treatment, n = 37; sorafenib monotherapy, n = 24). (E) The combination of SLC25A28 and p53 was determined by immunocoprecipitation (No treatment, n = 37; sorafenib monotherapy, n = 24). (F) Mitochondrial iron levels were determined by iron assay kit (No treatment, n = 37; sorafenib monotherapy, n = 24; **P < 0.01). (G) The enzymatic activities of mitochondrial complexes were analyzed by commercial kits (No treatment, n = 37; sorafenib monotherapy, n = 24; *P < 0.05, **P < 0.01, ***P < 0.001). (H) The expression of PTGS2 was examined by real-time PCR (No treatment, n = 37; sorafenib monotherapy, n = 24; ***P < 0.001). (I) The levels of lipid ROS, GSH, and MDA were determined by commercial kits (No treatment, n = 37; sorafenib monotherapy, n = 24; **P < 0.01, ***P < 0.001).

Journal: Redox Biology

Article Title: The BRD7-P53-SLC25A28 axis regulates ferroptosis in hepatic stellate cells

doi: 10.1016/j.redox.2020.101619

Figure Lengend Snippet: BRD7-P53-SLC25A28 axis regulated ferroptosis in human HSCs from fibrotic patients with sorafenib monotherapy. (A) The levels of fibrosis markers ACTA2, COL1A1, and fibronectin were examined in sorafenib-treated hepatectomy samples and untreated liver biopsy samples (No treatment, n = 37; sorafenib monotherapy, n = 24; ***P < 0.001). Primary human HSCs were isolated from the collected liver tissue by laser capture microdissection. (B) The levels of BRD7 were examined by Western blot (No treatment, n = 37; sorafenib monotherapy, n = 24). (C) The combination of BRD7 and p53 was determined by immunocoprecipitation (No treatment, n = 37; sorafenib monotherapy, n = 24). (D) The levels of p53 in mitochondria were examined by Western blot (No treatment, n = 37; sorafenib monotherapy, n = 24). (E) The combination of SLC25A28 and p53 was determined by immunocoprecipitation (No treatment, n = 37; sorafenib monotherapy, n = 24). (F) Mitochondrial iron levels were determined by iron assay kit (No treatment, n = 37; sorafenib monotherapy, n = 24; **P < 0.01). (G) The enzymatic activities of mitochondrial complexes were analyzed by commercial kits (No treatment, n = 37; sorafenib monotherapy, n = 24; *P < 0.05, **P < 0.01, ***P < 0.001). (H) The expression of PTGS2 was examined by real-time PCR (No treatment, n = 37; sorafenib monotherapy, n = 24; ***P < 0.001). (I) The levels of lipid ROS, GSH, and MDA were determined by commercial kits (No treatment, n = 37; sorafenib monotherapy, n = 24; **P < 0.01, ***P < 0.001).

Article Snippet: BRD7 shRNA (sc-92998, sc-141741), p53 shRNA (sc-44218, sc-45917), SLC25A28 shRNA (sc-90800, sc-149448), and control shRNA were obtained from Santa Cruz Biotechnology.

Techniques: Isolation, Laser Capture Microdissection, Western Blot, Iron Assay, Expressing, Real-time Polymerase Chain Reaction

The BRD7-P53-SLC25A28 axis may regulate ferroptosis in hepatic stellate cells. X C - inhibition-, GPX4 inhibition-, and GSH depletion-mediated BRD7 upregulation triggers p53 mitochondrial translocation via direct binding with N-terminal transactivation domain, thus aggravating the accumulation of mitochondrial iron, the hyperfunction of electron transfer chain, lipid peroxidation, and eventually leading to iron-dependent ferroptosis.

Journal: Redox Biology

Article Title: The BRD7-P53-SLC25A28 axis regulates ferroptosis in hepatic stellate cells

doi: 10.1016/j.redox.2020.101619

Figure Lengend Snippet: The BRD7-P53-SLC25A28 axis may regulate ferroptosis in hepatic stellate cells. X C - inhibition-, GPX4 inhibition-, and GSH depletion-mediated BRD7 upregulation triggers p53 mitochondrial translocation via direct binding with N-terminal transactivation domain, thus aggravating the accumulation of mitochondrial iron, the hyperfunction of electron transfer chain, lipid peroxidation, and eventually leading to iron-dependent ferroptosis.

Article Snippet: BRD7 shRNA (sc-92998, sc-141741), p53 shRNA (sc-44218, sc-45917), SLC25A28 shRNA (sc-90800, sc-149448), and control shRNA were obtained from Santa Cruz Biotechnology.

Techniques: Inhibition, Translocation Assay, Binding Assay

IRP2-associated mitochondrial iron loading and CS. ( a ) Representative Perls’ stained lung sections (n=3 mice per group) (left) ( n = 2 technical replicates) with quantification (middle) ( n = 10 images per mouse, n = 3 per group) and non-heme iron levels (right, n = 4 mice per group, n = 4 technical replicates) in WT mice exposed to RA or CS (1–6 months). Scale bars, 50 μm. Arrows indicate staining. n.c.; negative control. ( b ) Representative immunoblot (n=3 experiments) (left) with quantification (right) of transferrin and ferritin expression ( n = 5 per group, n = 2 technical replicates), ( c ) total non-heme iron (left, n = 5 mice per group , n = 4 technical replicates) and fold change mitochondrial (RA n = 11; CS 1 month n = 6, 4 months n = 8, 6 months n = 9) and cytosolic non-heme (RA n = 6; CS 1 month n = 11, 4 months n = 3, 6 months n = 5) iron (right) in WT mouse lungs exposed to RA or CS, n = 2 technical replicates. ( d ) Fold change non-heme iron (left, WT and Irp2 −/− ; RA n = 13, CS 1 and 6 months n =5, CS 4 months n =3) and heme-iron (right , WT and Irp2 −/− ; RA n = 10, CS 1–6 months n =5) in mitochondrial fractions from WT mouse lungs exposed to RA or CS, n = 2 technical replicates. ( e ) Mitoferrin 2 (WT and Irp2 −/− ; RA n = 8; CS 1 month n = 3, 4 months n = 6), ( f ) frataxin expression (WT RA n = 5; CS n = 3; Irp2 −/− RA n = 6; CS n = 6) in whole lung of mice exposed to RA or CS. ( g ) Mitochondrial non-heme (left , n = 4 per group), mitochondrial heme iron (right , n = 4 per group), ( h ) 3 hour 99m Tc-SC clearance (left) and IL-6 protein concentrations (right , n = 4 per group) in the lungs of WT and Fxn ki/ko mice exposed to RA or CS (1 month). ( i ) Schematic of mitochondrial iron loading regulated by Irp2. All data are mean ± s.e.m. * P < 0.05. ** P < 0.01, *** P < 0.005 by one-way ANOVA followed by Bonferroni correction. # P < 0.05 by student’s unpaired t -test.

Journal: Nature medicine

Article Title: Mitochondrial iron chelation ameliorates cigarette-smoke induced bronchitis and emphysema in mice

doi: 10.1038/nm.4021

Figure Lengend Snippet: IRP2-associated mitochondrial iron loading and CS. ( a ) Representative Perls’ stained lung sections (n=3 mice per group) (left) ( n = 2 technical replicates) with quantification (middle) ( n = 10 images per mouse, n = 3 per group) and non-heme iron levels (right, n = 4 mice per group, n = 4 technical replicates) in WT mice exposed to RA or CS (1–6 months). Scale bars, 50 μm. Arrows indicate staining. n.c.; negative control. ( b ) Representative immunoblot (n=3 experiments) (left) with quantification (right) of transferrin and ferritin expression ( n = 5 per group, n = 2 technical replicates), ( c ) total non-heme iron (left, n = 5 mice per group , n = 4 technical replicates) and fold change mitochondrial (RA n = 11; CS 1 month n = 6, 4 months n = 8, 6 months n = 9) and cytosolic non-heme (RA n = 6; CS 1 month n = 11, 4 months n = 3, 6 months n = 5) iron (right) in WT mouse lungs exposed to RA or CS, n = 2 technical replicates. ( d ) Fold change non-heme iron (left, WT and Irp2 −/− ; RA n = 13, CS 1 and 6 months n =5, CS 4 months n =3) and heme-iron (right , WT and Irp2 −/− ; RA n = 10, CS 1–6 months n =5) in mitochondrial fractions from WT mouse lungs exposed to RA or CS, n = 2 technical replicates. ( e ) Mitoferrin 2 (WT and Irp2 −/− ; RA n = 8; CS 1 month n = 3, 4 months n = 6), ( f ) frataxin expression (WT RA n = 5; CS n = 3; Irp2 −/− RA n = 6; CS n = 6) in whole lung of mice exposed to RA or CS. ( g ) Mitochondrial non-heme (left , n = 4 per group), mitochondrial heme iron (right , n = 4 per group), ( h ) 3 hour 99m Tc-SC clearance (left) and IL-6 protein concentrations (right , n = 4 per group) in the lungs of WT and Fxn ki/ko mice exposed to RA or CS (1 month). ( i ) Schematic of mitochondrial iron loading regulated by Irp2. All data are mean ± s.e.m. * P < 0.05. ** P < 0.01, *** P < 0.005 by one-way ANOVA followed by Bonferroni correction. # P < 0.05 by student’s unpaired t -test.

Article Snippet: Immunoblot analyses were performed in whole lung homogenates or mitochondrial-enriched fractions isolated from the lungs of mice using standard immunoblotting techniques with the following antibodies: Irp2 (1:1000 7H6: sc-33682, 1:1000 Santa Cruz, NB100-1798, Novus Biologicals and Irp2 antibody from Tracey Rouault at a 1:1000 dilution), Irp1 (1:1000 NBP1-19412, aconitase 1 Antibody, Novus Biologicals), LC3B (1:2000 L7543, Sigma Aldrich), Atg 7 (1:2000 APG7 (H-300): sc-33211, Santa Cruz), transferrin receptor 1 (1:1000 CD71 (H-300): sc-9099, Santa Cruz), actin (1:10,000 A00158, Sigma Aldrich), electron transport chain components including COX MTCO1 (1:500 MitoProfile® Total OXPHOS antibody, ab110413, Abcam), ferritin (1:1000 H-53: sc-25617, Santa Cruz), tom20 (1:2000 FL-145, sc-11415, Santa Cruz), frataxin (1:1000 H-155: sc-25820, Santa Cruz), mitoferrin 2 (1:1000 P-12: sc-138430, Santa Cruz), cleaved- caspase 3 (1:500 Asp175, Cell Signaling technologies), Bcl2 (1:1000 sc-7382, Santa Cruz), FBXL5 (1:1000 N0039, Neoclone Biotechnology) COX4I2 (1:1000 H00084701-M01 Abnova) and HO-1 (1:1000 sc-1797, Santa Cruz).

Techniques: Staining, Negative Control, Western Blot, Expressing