Additional file 1 of Exosomal miR-9-5p derived from iPSC-MSCs ameliorates doxorubicin-induced cardiomyopathy by inhibiting cardiomyocyte senescence
Creators: name: Zheng, Huifeng
name: Liang, Xiaoting
name: Liu, Baojuan
name: Huang, Xinran
name: Shen, Ying
name: Lin, Fang
name: Chen, Jiaqi
name: Gao, Xiaoyan
name: He, Haiwei
name: Li, Weifeng
name: Hu, Bei
name: Li, Xin
name: Zhang, Yuelin
Publisher: name: figshare
Year: 2024
Subjects: subject: Biochemistry
subject: Cell Biology
subject: Genetics
subject: FOS: Biological sciences
subject: Molecular Biology
subject: Physiology
subject: Pharmacology
subject: Environmental Sciences not elsewhere classified
subject: Ecology
subject: Immunology
subject: FOS: Clinical medicine
subject: Developmental Biology
subject: Cancer
subject: Virology

description: Additional file 1: Figure S1. The heart rate of control or mice with DOX that received PBS, BM-MSC-EXO or iPSC-MSC-EXO treatment. Data are expressed as mean±SD. n = 6 mice for each group. ns=not significant. Figure S2. DOX induced NMCM senescence in a time-dependent manner. Representative images of SA-β-gal staining in NMCMs and quantitative of SA-β-gal positive NMCMs under DOX treatment for 0h, 24h, 48h, 72h and 96h. n = 3 biological replicates for each group. Data are expressed as mean±SD, ***p&lt;0.001. ns=not significant. Figure S3. MiR-9-5p mimic treatment inhibited DOX-induced NMCM mitochondrial fragmentation and senescence (A) Representative SA-β-gal staining images in control, DOX, DOX+miR-9-5p mimic-treated NMCMs. (B) Quantitative measurement of SA-β-gal positive NMCMs from the different groups. (C) Representative images showing the fragmented mitochondria in control, DOX, DOX+miR-9-5p mimic-treated NMCMs. (D) Quantitative measurement of fragmented mitochondria in NMCMs from the different groups. n = 3 biological replicates for each group. Data are expressed as mean ± SD. **p &lt; 0.01, ***p &lt; 0.001. Figure S4. Administration of miR-9-5p agomir improved heart function and inhibited mitochondrial fragmentation and cardiomyocyte senescence in hearts of DIC mice. (A) Schematic chart showing the creation of a DIC model and administration of control agomir, or miR-9-5p agomir. (B) Representative echocardiographic images were captured on day 35 after DOX treatment in mice treated with control agomir or miR-9-5p agomir. (C) The LVEF and LVFS were analyzed on Day 0 and 35 in controls or mice with DIC that received control agomir or miR-9-5p agomir treatment. (D) Representative images of Sirius red staining of heart sections from DIC mice that received control agomir or miR-9-5p agomir and control mice. (E) Quantitative analysis of cardiac fibrosis in different experimental groups. (F) Representative images of Troponin and p21 double staining in the heart of DIC mice that received control agomir or miR-9-5p agomir and control mice. (G) Quantitative measurement of Troponin+/p21+ double-positive cells in the heart of DIC mice that received control agomir or miR-9-5p agomir and control mice. (H) Western blotting and quantitative measurement of the protein level of p-Drp1/Drp1, Mfn1 and Mfn2 in the heart of DIC mice that received control agomir or miR-9-5p agomir treatment and control mice. Data are expressed as mean ± SD. n = 6 mice for each group, ***p &lt; 0.001, ns = not significant. Figure S5. Western blotting and quantitative analysis of the expression level of VPO1 and p-ERK in heart tissues from control or mice with DOX that received PBS, BM-MSC-EXO or iPSC-MSC-EXO treatment. Data are expressed as mean±SD. n = 6 mice for each group, ***p&lt;0.001. Figure S6. Original Western blotting images.