Journal: Biochemistry and Biophysics Reports

Article Title: LncRNA RMST knockout inhibits fibrosis by down-regulating Smad3 during mouse skin wound healing

doi: 10.1016/j.bbrep.2025.102386

Figure Lengend Snippet: RMST-KO reduces fibrosis in mouse skin wound healing. (A) Differences of RMST expression between unwounded skin and the 21 dps group. (B) Agarose gel electrophoresis confirmed the successful knockout of RMST. (C) QPCR assay showing the expression of RMST 21 dps. (D) H&E and Masson staining of the wounds 21 dps as indicated. (E–F) RMST-KO reduced the (E) thickness and (F) area of neogenic fibrous tissue at 21 dps. (G–H) QPCR showing the COL1A1 and α-SMA levels were significantly decreased in the RMST-KO group compared to the WT group 21 dps. (I) Representative blot of COL1A1 and α-SMA 21 dps. (J–K) Statistical analysis of the immunoblot bands indicated that RMST-KO significantly suppressed the expression of COL1A1 and α-SMA 21 dps. Data were shown as mean ± SD, n = 6, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: Il-1β (16806-1-AP) , 1:2000 , Proteintech.

Techniques: Expressing, Agarose Gel Electrophoresis, Knock-Out, Staining, Western Blot

Journal: Biochemistry and Biophysics Reports

Article Title: LncRNA RMST knockout inhibits fibrosis by down-regulating Smad3 during mouse skin wound healing

doi: 10.1016/j.bbrep.2025.102386

Figure Lengend Snippet: RMST-KO reduced the inflammation during mouse skin wound healing. (A–B) QPCR assay showed the mRNA expression of TNF-α and IL-1β were significantly decreased in the RMST-KO group 21 dps. (C) Representative blot of TNF-α, IL-1β 21 dps. (D–E) Statistical analysis of the immunoblot bands indicated that RMST-KO significantly suppressed TNF-α, IL-1β expression 21 dps. Data were shown as mean ± SD, n = 6, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: Il-1β (16806-1-AP) , 1:2000 , Proteintech.

Techniques: Expressing, Western Blot

Journal: Biochemistry and Biophysics Reports

Article Title: LncRNA RMST knockout inhibits fibrosis by down-regulating Smad3 during mouse skin wound healing

doi: 10.1016/j.bbrep.2025.102386

Figure Lengend Snippet: Smad3 was a downstream molecule of lncRNA RMST. (A) The heatmap shows the upregulated long non-coding RNAs in the GSE28914 dataset. (B) The catRAPID omics v2.1 software was used to predict the proteins interacting with RMST. (C) A Venn diagram displays the intersection of the two groups of data. (D) GO and KEGG pathway analysis was performed for these 273 intersections.

Article Snippet: Il-1β (16806-1-AP) , 1:2000 , Proteintech.

Techniques: Software

Journal: Biochemistry and Biophysics Reports

Article Title: LncRNA RMST knockout inhibits fibrosis by down-regulating Smad3 during mouse skin wound healing

doi: 10.1016/j.bbrep.2025.102386

Figure Lengend Snippet: Smad3-OE reversed the fibrosis suppression resulting from RMST-KO. (A) QPCR confirmed the upregulating effect of Smad3-OE lentivirus. (B) Representative blot of Smad3 under the effect of Smad3-OE and/or RMST-KO. (C) Statistical analysis of the immunoblot bands. (D) H&E and Masson staining of the wounds as indicated. (E–F) Statistical analysis of the (E) thickness and (F) area of neogenic fibrous tissue 21 dps. (G–I) qPCR detection of fibrosis markers and proteins in classical fibrosis pathways, including COL1, α-SMA, and TGF-β1. (J–M). Representative blot of COL1, α-SMA, and TGF-β1. (N–O) qPCR detection of inflammatory cytokines TNF-α and IL-1β. (P–R) Representative blot of TNF-α and IL-1β. Data were shown as mean ± SD, n = 6, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: Il-1β (16806-1-AP) , 1:2000 , Proteintech.

Techniques: Western Blot, Staining

Journal: Redox Biology

Article Title: Ultrasmall Cu 2−x Se nanoparticles alleviate vascular calcification through inhibiting oxidative stress and NF-κB/NLRP3-mediated inflammation

doi: 10.1016/j.redox.2025.103961

Figure Lengend Snippet: CSP NPs inhibit NF-κB/NLRP3 signaling pathway during vascular calcification. Rat vascular smooth muscle cells (VSMCs) were treated with growth medium (GM), calcifying medium (CM), or CM with CSP NPs (2, 5, and 10 μg/mL) for 7 days (n = 4). (A) Representative western blots of p-p65 and p65. (B) Quantification of p-p65 protein expression by densitometry. Rat VSMCs were treated with GM, CM, or CM with CSP NPs (10 μg/mL) for 7 days (n = 4). (C) Representative immunostaining images of p65. Nuclear localization of p65 was determined by confocal microscopy. Scale bar = 25 μm. Rat VSMCs were treated with GM, CM, or CM with CSP NPs (2, 5, and 10 μg/mL) for 7 days (n = 4). (D) Representative western blots of NLRP3, Cleaved-Caspase1, IL-1β, and IL-6. (E) Quantification of NLRP3, Cleaved-Caspase1, IL-1β, and IL-6 protein expression by densitometry. VitD 3 -overloaded mice were treated with CSP NPs (1 mg/kg) for 8 days (n = 6). (F) Representative western blots of p-p65, p65, and NLRP3. (G) Quantification of p-p65 and NLRP3 protein expression by densitometry. Rats subjected to 5/6 nephrectomy were treated with CSP NPs (0.7 mg/kg) for 4 weeks (n = 6). (H) Representative western blots of p-p65, p65, and NLRP3. (I) Quantification of p-p65 and NLRP3 protein expression by densitometry. ∗ P< 0.05, ∗∗ P< 0.01.

Article Snippet: IL-1β (WL00891) and IL-6 (WL02841) primary antibodies were purchased from Wanleibio (China). β-actin (HRP-66009) primary antibody was purchased from Proteintech (USA).

Techniques: Western Blot, Expressing, Immunostaining, Confocal Microscopy