Journal: Zoological Research

Article Title: Red light promotes dermis-epidermis remodeling via TGFβ and AKT-mediated collagen dynamics in naturally aging mice

doi: 10.24272/j.issn.2095-8137.2024.405

Figure Lengend Snippet: Red light inhibits type I collagen degradation via AKT/NRF2/HO-1 signaling pathway activation A, B: qPCR analysis of NRF2 (A) and HO-1 (B) mRNA expression in mouse skin tissue following red light treatment. n =4. C: Representative western blot assays of p-AKT, HO-1, NRF2, and type I collagen expression in aged mice treated with red light, API-2, or both. D: Western blot analysis of nuclear-cytoplasmic separation in skin tissue. Cytosolic and nuclear extracts were immunoblotted for NRF2, while GAPDH and histone H3 proteins were probed to confirm thorough separation of the cytosolic and nuclear fractions. E: Representative western blot analysis of type I collagen expression in skin tissue after red light treatment with or without HO-1i. F: Representative immunofluorescence images of type I collagen in skin sections from aged mice after 28 days of red light treatment with or without HO-1i. Scale bar: 50 μm. G: Heatmaps showing relative expression levels of DEGs involved in various MMPs. n =3. H: qPCR analysis of MMP3, MMP9, MMP12, and MMP13 mRNA expression in mouse skin tissue following red light treatment, with and without HO-1i. *** : P <0.001; **** : P <0.0001 compared to control group, and #### : P <0.0001 compared to indicated groups, one-way ANOVA for multiple groups. Data are mean±SEM.

Article Snippet: To inhibit AKT, mice received intraperitoneal (i.p.) injections of API-2 (HY-15457, MCE, USA) at a dose of 2 mg/kg every 48 h. To inhibit TGFβ, mice received i.p. injections of SB431542 (HY-10431, MCE, USA), a TGFβR1 inhibitor, at a dose of 10 mg/kg every 48 h. To inhibit cAMP, mice received i.p. injections of SQ22536 (HY-100396, MCE, USA), an adenylate cyclase (AC) inhibitor, at a dose of 10 mg/kg every 48 h. To inhibit HO-1, mice received i.p. injections of HO-1i (HY-111798A, MCE, USA) at a dose of 1.357 mg/kg every 48 h. To inhibit intracellular free Ca 2+ , mice received i.p. injections of diltiazem (HY-B0632, MCE, USA) at a dose of 20 mg/kg every 48 h. To inhibit reactive oxygen species (ROS), mice received daily topical application of 100 mg/mL ascorbic acid (HY-B0166, MCE, USA), applied to the skin 30 min after red light exposure.

Techniques: Activation Assay, Expressing, Western Blot, Immunofluorescence, Control

Journal: PLOS One

Article Title: Autophagy regulates MK-2206-induced LDL receptor expression and cholesterol efflux pathways

doi: 10.1371/journal.pone.0338076

Figure Lengend Snippet: The autophagy-inducing effects of MK-2206 (MK) and triciribine (TCN), along with their impact on LDLR and ABCA1 expression, were evaluated in HepG2 cells. HepG2 cells were cultured for 14-16 h in the absence (DMSO) or the presence of A) MK-2206 (5 µM) or B) triciribine (0.5 µM) alone, or C-D) pretreated with SBI-0206965 (SBI; 6.4 µM) for 30 minutes prior to administration. Protein levels of ABCA1, LDLR, LC3BI and LC3BII were analyzed by immunoblotting, showing one representative western blot. Quantified values were normalized to β-actin and expressed relative to levels observed in untreated cells (n = 4). Quantitative PCR was used to assess gene expression of ABCA1 , LDLR , LC3B , ULK1 and p62 , with values normalized to GAPDH and expressed relative to levels observed in untreated cells (n = 3). Error bars represent SD. * P < 0.05, ** P < 0.01, and *** P < 0.001 compared with untreated cells.

Article Snippet: MK-2206–2HCl (MK-2206; S1078) and triciribine (TCN; S1117) from Selleck Chemicals (Houston, TZ), and Rapamycin (R8781) and SBI-0206965 (SBI; SML1540) from Sigma-Aldrich were utilized as indicated in the figure legends.

Techniques: Expressing, Cell Culture, Western Blot, Real-time Polymerase Chain Reaction, Gene Expression