Journal: Molecular Medicine Reports

Article Title: Integrative bioinformatics and experimental analysis reveals FRA1 as a key mediator of tubulointerstitial inflammation in lupus nephritis

doi: 10.3892/mmr.2026.13813

Figure Lengend Snippet: FRA1 expression in MRL/lpr mouse kidneys. Representative H&E staining of kidney sections from 20-week-old (A) MRL/lpr mice and (B) MRL/MPJ controls, showing tubulointerstitial inflammation and damage in MRL/lpr mice. MRL/lpr mice exhibit diffuse and extensive tubulointerstitial inflammation and structural damage. (C-H) FRA1 expression in mouse kidney sections. (C, E and G) Three independent mice from the MRL/lpr group, all demonstrating elevated FRA1 levels in the tubular epithelium. (D, F and H) Three independent mice from the control group, displaying baseline FRA1 immunoreactivity. (I) Quantification of FRA1-positive area from IHC images. (J) Western blot analysis of FRA1 protein levels from MRL/lpr and control mice. (K) Densitometric quantification of FRA1 bands normalized to β-actin. Scale bar, 50 µm; Data are plotted as the mean ± SEM; n=3 per group; group comparisons were performed using two-sided Welch's t-tests; ***P<0.001.

Article Snippet: The primary antibodies used in the present study included: β-actin (1:5,000; cat. no. bs-0061R; BIOSS), FRA1 (1:1,000; cat. no. A5372; ABclonal Biotech Co., Ltd.), IL-1β (1:1,000; cat. no. HA601002 ; clone no. A7F9; HUABIO), IL-8 (1:1,000; cat. no. ab289967; clone no. EPR26511-74; Abcam), RANTES (1:1,000; cat. no. 36467; CST Biological Reagents Co., Ltd.), IL-6 (1:2,000; cat. no. DF6087; Affinity Biosciences, Ltd.), MCP-1 (1:2,000; cat. no. A7277; ABclonal Biotech Co., Ltd.), TNF-α (1:2,000; cat. no. 17590-1-AP; Proteintech Group, Inc.), and TGF-β (1:2,000; cat. no. 81746-2-RR; clone no. 230544B7; Proteintech Group, Inc.).

Techniques: Expressing, Staining, Control, Western Blot

Journal: Molecular Medicine Reports

Article Title: Integrative bioinformatics and experimental analysis reveals FRA1 as a key mediator of tubulointerstitial inflammation in lupus nephritis

doi: 10.3892/mmr.2026.13813

Figure Lengend Snippet: Effect of FRA1 on inflammatory cytokine expression in HK-2 cells. (A) Representative western blots of FRA1 and inflammatory cytokines (IL-1β, IL-6, and IL-8) in HK-2 cells 144 h after transduction with FRA1-OE, FRA1-shRNA or their corresponding controls. (B) Representative western blots of MCP-1, RANTES, TGF-β and TNF-α in HK-2 cells following the same transduction conditions. Densitometric semi-quantification of protein bands normalized to β-actin for: (C) FRA1, (D) IL-1β, (E) IL-6, (F) IL-8, (G) MCP-1, (H) RANTES, (I) TGF-β and (J) TNF-α. Data are presented as the mean ± SEM; n=3 per group; comparisons among subgroups were assessed using the two-sided Kruskal-Wallis test; *P<0.05, **P<0.01 and ***P<0.001. OE, over expression; ns, not significant; sh, short hairpin.

Article Snippet: The primary antibodies used in the present study included: β-actin (1:5,000; cat. no. bs-0061R; BIOSS), FRA1 (1:1,000; cat. no. A5372; ABclonal Biotech Co., Ltd.), IL-1β (1:1,000; cat. no. HA601002 ; clone no. A7F9; HUABIO), IL-8 (1:1,000; cat. no. ab289967; clone no. EPR26511-74; Abcam), RANTES (1:1,000; cat. no. 36467; CST Biological Reagents Co., Ltd.), IL-6 (1:2,000; cat. no. DF6087; Affinity Biosciences, Ltd.), MCP-1 (1:2,000; cat. no. A7277; ABclonal Biotech Co., Ltd.), TNF-α (1:2,000; cat. no. 17590-1-AP; Proteintech Group, Inc.), and TGF-β (1:2,000; cat. no. 81746-2-RR; clone no. 230544B7; Proteintech Group, Inc.).

Techniques: Expressing, Western Blot, Transduction, shRNA, Over Expression

Journal: bioRxiv

Article Title: Antidepressants interact with sex steroid receptors and their intracellular signaling components

doi: 10.64898/2026.03.17.712321

Figure Lengend Snippet: Antidepressants selectively activate MAPK signaling and induce ERα-dependent gene expression in MCF-7 cells. (A) Quantification of MAPK phosphorylation (pMAPK/MAPK) by Western blot densitometry following treatment with vehicle, imipramine, S-ketamine, or estradiol (E2), in the presence or absence of the ERα degrader/antagonist fulvestrant and/or tunicamycin. Antidepressant treatment significantly increased MAPK phosphorylation, indicating enhanced MAPK pathway activation. (B) Total MAPK levels normalized to β-actin were unchanged across treatment conditions. Representative immunoblots for MAPK and pMAPK are shown above. (C) Quantification of Akt phosphorylation (pAkt/Akt) revealed no significant changes following antidepressant or E2 treatment, but there was a trend for a reduction by imipramine. (D) Total Akt levels normalized to β-actin were unaltered. Representative immunoblots for Akt and pAkt are shown above. One imipramine-treated sample was excluded from analysis due to an outlier pMAPK/MAPK ratio exceeding 1. Data from technical and biological replicates were pooled. (E–F) mRNA expression of the extranuclear-initiated ERα target gene LRRC54 (E) and the classical nuclear ERα target gene PgR (F) , quantified by qPCR following treatment with E2, imipramine, or S-ketamine. Antidepressants significantly increased LRRC54 and PgR expression, comparable to E2 and relative to vehicle control. Pretreatment with fulvestrant attenuated these effects, indicating ERα dependency. Data are presented as mean ± SEM from three independent biological replicates (n = 3). Statistical significance is indicated as *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, and ns as not significant.

Article Snippet: Membranes were then stripped for 10 minutes and reprobed with antibodies against ERα (mouse anti-ERα (1D5)) and β-actin (mouse or rabbit Licor 926–42212/Licor 926-42210).

Techniques: Gene Expression, Phospho-proteomics, Western Blot, Activation Assay, Expressing, Control