Fig 1: Homeobox a5 (Hoxa5) promotes white adipose tissue (WAT) browning and inhibits WAT inflammation in mice. All mice were injected with lipopolysaccharide and cold exposure. (A) Hoxa5 mRNA level of inguinal white adipose tissue (iWAT) in mice (n = 8). (B) Gene mRNA expression of TNFα, IL6, Toll-like receptor (TLR) 4, and NLRP3 in iWAT (n = 8). (C) Relative mRNA level of BMP4, UCP1, and PGC1α in mice iWAT in different groups (n = 8). (D) Correlation analysis of TLR4 and tenascin C (TNC) mRNA level in mice iWAT (n = 10). (E) Adipocyte size was monitored in frozen-section iWAT samples by hematoxylin-eosin staining (n = 8). (F) Images of immunohistochemical staining of iWAT in different groups. (G) Serum levels of TNFα and IL6 in different groups (n = 6). (H–J) Images of iWAT stained by immunofluorescent staining in different groups (n = 4). (K) Quantitate of immunofluorescent staining in Figures 3H–G. Values are represented as means ± SD vs. control group, *p < 0.05.
Fig 2: Homeobox a5 (Hoxa5) reverses the inhibition of adipocytes browning in lipopolysaccharide (LPS)-treated adipocytes. (A–C) mRNA expressions of Hoxa5, tenascin C (TNC), IL1β, IL6, MCP1, TNFα and UCP1, PGC1α, and Cidea in mice adipocytes in the pc-control group, pc-Hoxa5 group, and sh-Hoxa5 group with or without LPS treatment (n = 4). (D) Fluorescence staining of ROS in different groups with LPS treatment (n = 4). (E–I) Immunofluorescent staining of adipocytes in different groups with LPS treatment (n = 4). (J) Immunoblots images of UCP1, PGC1α, and BMP4 in different groups with LPS treatment (n = 4). (K) Immunoblots images of IL1β, IL6, TNFα, and NLRP3 in different groups with LPS treatment (n = 4). Values are represented as means ± SD vs. control group, *p < 0.05.
Fig 3: Homeobox a5 (Hoxa5) promotes white adipose tissue browning through reducing tenascin C (TNC)/toll-like receptor (TLR) 4/nuclear factor kappa B (NF-κB) inflammatory signaling in mice. Hoxa5 promotes adipose tissue browning by activating BMP4/Smad1 signal and alleviating inflammation via inhibiting TNC/TLR4/NF-κB pathway.
Fig 4: Homeobox a5 (Hoxa5) promotes adipocytes browning by activating the BMP4/Smad1 signal pathway. (A) The network of the target genes of Hoxa5 by bioinformatics analysis. (B,C) mRNA expressions of Hoxa5, BMP4, UCP1, PGC1α, PRDM16, Cidea, Dio2, TNFα, and Toll-like receptor (TLR) 4 in mice adipocytes in the pc-control group, pc-Hoxa5 group, and sh-Hoxa5 group with or without β3-adrenoceptor agonists CL314,243 (n = 4). (D) Relative mRNA level of Hoxa5, BMP4, UCP1, PGC1α, TNFα, and TLR4 in mice adipocytes in control group, pc-Hoxa5 group, and sh-Hoxa5 group with or without Smad1 inhibitor LDN193,189 (n = 4). (E) Representative immunoblots and densitometric quantification for BMP4, p-Smad1, UCP1, PRDM16, and PGC1α in mice adipocytes in pc-control group, pc-Hoxa5 group, and sh-Hoxa5 group with or without DN193,189 (n = 4). Values are represented as means ± SD vs. control group, *p < 0.05.
Fig 5: BMP4 IHC staining of cornea from 2–3-month-old WT and AP-2β NCC KO mice. WT mice ((A,C) n = 5) display nuclear epithelial expression of BMP4 across the central corneal epithelium (A), with the most consistent expression observed for the basal layer. In the peripheral (C) corneal epithelium, we continue to see this pattern of nuclear staining. However, BMP4 expression is absent from the limbal (arrowheads) and conjunctival epithelial regions. BMP4 expression is not conserved in the mutant (B,D) n = 5) with staining being absent from the central (B) and peripheral regions (D). CE, corneal epithelium; CEn, corneal endothelium; CS, corneal stroma; IR, iris; LE, lens epithelium. Scale bars represent 150 μm.
Supplier Page from Abcam for Anti-BMP4 antibody