Fig 1: Correlations between GDF-15 and other indicators. GDF-15 was negatively correlated with (a) IGF-1 (r = −0.303, P=0.006). GDF-15 was positively correlated with (b) WHR (r = 0.26, P=0.018), (c) TG (r = 0.323, P=0.007), (d) TC (r = 0.196, P=0.099), (e) hs-CRP (r = 0.248, P=0.046), and (f) FRS (r = 0.428, P < 0.001) (∗P < 0.05; ∗∗P < 0.001).
Fig 2: The serum levels of GDF-15. (a) Serum GDF-15 levels of AGHD increased; (b) serum GDF-15 levels increased significantly in the subgroup with IGF-1 < 140 ng/mL of AGHD patients (∗∗P < 0.01).
Fig 3: Validation of DEGs in circulation and placental tissues: (a–c) PCR and ELISA were used to detect Top 5 downregulated genes (TRIM34, DEFA3, DEFA1B, DEFA1, QPCT) and Top 5 upregulated genes (CHPT1, SMOX, FAM83A, GDF15, NAPG) in cord serum (a), maternal serum (b), and placental tissue (c). (d) The protein levels of Top 5 downregulated genes (TRIM34, DEFA3, DEFA1B, DEFA1, QPCT) and Top 5 upregulated genes (CHPT1, SMOX, FAM83A, GDF15, NAPG) were detected by western blot in placental tissues. ∗P < 0.05 vs. control. N = 5 samples/group for the validation of DEGs.
Fig 4: GDF15 attenuates NaI-induced inflammation. (A) Cell viability in different concentrations of NaI in Nthy-ori 3-1 cells (n = 7). (B) The treatment protocol in the NaI-induced Nthy-ori 3-1 cells. (C) The mRNA level of GDF15 in cell supernatants after NaI treatment (n = 4). (D) GDF15 level in cell supernatants after NaI treatment (n = 6). (E) Representative gel images of GDF15 after NaI treatment (n = 4, left panel) and statistical analysis of protein band gray values (right panel). (F) The mRNA level of NLRP3, ASC, NLRP1, NLRC4, TNF-α, IL-1β and IL-6 after NaI treatment (n = 4). (G) Cell viability in different concentrations of rhGDF15 in Nthy-ori 3-1 cells (n = 5). (H) The mRNA level of NLRP3, ASC, NLRP1, NLRC4, TNF-α, IL-1β and IL-6 after rhGDF15 and NaI treatment (n = 4). *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
Fig 5: Thyroid-derived GDF15 expression is elevated in HT mouse model. (A) Schematic overview of NaI-induced HC mouse model. (B) Serum TgAb levels were measured in mice 12–16 weeks after NaI treatment (n = 6). (C–E) Body weight (C), liver weight (D), liver/body weight ratio (E) were determined in mice 12–16 weeks after NaI treatment (n = 6). (F–I) Serum ALT (F), AST (G), TG (H) and TC (I) levels were measured in mice 16 weeks after NaI treatment (n = 6). (J) Representative images of HE (upper panel) and F4/80 IHC staining (lower panel) of thyroid tissues from 16 weeks NaI treatment. Scale bar: 50 μm. (K) Statistical data of the positive area of F4/80 in the thyroid (n = 6). Scale bar: 50 μm. (L) Representative images of HE (upper panel) and Oil Red O staining (lower panel) of liver tissues from 16 weeks NaI treatment. Scale bar: 50 μm. (M) Quantification of lipid droplet area using Oil Red O staining (n = 6). (N) Hepatic TG content in 16 weeks NaI treated mice (n = 6). (O) Changes in mRNA levels of Gdf15 in heart, liver, kidney, colon, spleen, sWAT and thyroid (n = 3–6). sWAT, subcutaneous white adipose tissue; GDF15, growth differentiation factor 15. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
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