Fig 1: HDAC3 and IL17RA are highly expressed in lung tissues and lung fibroblasts of RA-ILD mice model. (A) Arthritis score and morbidity in mice. (B) HE (×200, above) and Masson (×200, below) staining of inflammation of lung tissues and pulmonary fibrosis of control mice and RA-ILD mice. (C) The hydroxyproline amount in control mice and RA-ILD mice. (D) RT-qPCR examining the expression of HDAC3 and IL17RA in mouse lung tissues and lung fibroblasts (n = 10). (E) Western blot analysis of HDAC3 and IL17RA expression in RA-ILD mice. (F) Analysis of the relationship between HDAC3 and IL17RA in RA-ILD mice. *p < 0.05 compared with control mice. Repeated measure ANOVA was used for comparison between two groups at different time points, and independent sample t-test was used for comparison between two groups. Pearson correlation analysis of HDAC3 and IL17RA in RA-ILD mice.
Fig 2: Experimental design and animal groups. C/EBPβ, CCAAT/enhancer binding protein beta; CRISPR, clustered regularly interspaced short palindromic repeats; DMSO, dimethyl sulfoxide; GFAP, glial fibrillary acidic protein; GMH, germinal matrix hemorrhage; IF, immunofluorescence; IL‐17RA, interleukin‐17 receptor; PCNA, proliferating cell nuclear antigen; Sec, secukinumab; WB, Western blot. *Extra 2 pups were used for IF (IL‐17RA and GFAP) at 72 h after GMH. **Extra 2 pups were used for IF (Ki67, PCNA and GFAP) at the 72 h after GMH
Fig 3: IL‐17A knockout alleviates BLM‐induced lung fibrosis, IL‐17RA upregulation, and mitochondrial abnormalities in AECIIs. (A) Haematoxylin and eosinstaining, Masson's Trichrome staining, and immunohistochemistry staining of fibronectin and α‐SMA of lung sections from WT and IL‐17A−/− mice treated with saline or bleomycin (1.5 U/kg). Scale bars: 100 μm. (B) Representative immunofluorescence images showing IL‐17RA (red) in AECIIs (using anti‐pro‐SPC as a marker, green) of WT and IL‐17A−/− mice treated with saline or bleomycin. Representative cells (asterisks) are shown in detail in the insets. Scale bars: 10 μm. (C) Semiquantitative scoring of pro‐SPC/IL‐17RA double‐positive cells as a percentage of total pro‐SPC‐stained cells. (D) Representative TEM images of AECIIs from wild‐type mice and IL‐17A−/− mice challenged with BLM or saline. Boxed regions are shown enlarged in the lower panels. Black arrows indicate lamellar bodies, the characteristic organelles of AECIIs. Red arrows indicate mitochondria. Scale bars: 1 μm (upper panels), 500 nm (lower panels). (E) Quantitative analysis of the percentage of abnormal mitochondria, defined as damaged and swollen mitochondria with severely disrupted electron‐lucent cristae per cell/group. (F) mtDNA/gDNA in AECIIs isolated from lung samples showed mitochondrial mass after BLM or saline intratracheal injection in wild‐type mice and IL‐17A−/− mice. (G) Western blot and quantitative analysis of markers of mitochondrial dynamics (DRP1, OPA1, and MFN1) in AECIIs isolated from lung samples derived from each group of mice indicated. Immunoblot gels were cropped and uncropped images of the immunoblot gels are in Figure S2A. Data are expressed as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001
Fig 4: Effect of bilateral PVN microinjection of IL-17RA siRNA on mRNA expression of c-Fos (a marker of neuronal activity, A) in the PVN and on levels of plasma norepinephrine (NE, a marker of sympathetic nerve activity, B) in SHAM and HF rats 4 weeks after CL. Values are mean ± SEM (n = 8 for each group); *p < 0.05.
Fig 5: The process of interstitial pulmonary fibrosis in RA mice was promoted by HDAC3 through miR-19a-3p targeting IL17RA. (A) RT-qPCR results of IL17RA expression after silencing HDAC3 or miR-19-3p. (B) RT-qPCR results of the expression of COL1A1, COL3A1, and FN after silencing HDAC3 or miR-19-3p. (C) HDAC3 mRNA expression in lung tissues of mice in each group. (D) Examination of arthritis scores and morbidity in different mice. (E) HE (×200, above) and Masson (×200, below) staining examining the degree of damage in lung tissues of mice in each group. (F) Examination of the change of hydroxyproline amount in the lung tissues of mice in each group. (G) Examination of the expression of miR-19a-3p in lung tissues of mice in each group. (H) Examination of the expression of IL17RA in lung tissues of mice in each group. *p < 0.05 compared with control. Multiple comparisons at different time points were analyzed by repeated measures ANOVA, and comparisons among groups were applied using one-way ANOVA.
Supplier Page from Abcam for Anti-IL-17RA Receptor antibody - N-terminal