Fig 1: Pigr deficiency in the hematopoietic compartment decreases AAA development. A Experimental design and (B) incidence of AAA in Ldlr−/− Pigr+/+ (n = 14) and Ldlr−/− Pigr−/− (n = 14) chimeras at 28 days after subcutaneous AngII infusion via osmotic pumps. C Representative H&E staining and quantification of the maximal abdominal aortic diameter. D Representative photographs and quantification of CD68 immunostaining. Data represent means ± SEM. *p < 0.05, Mann–Whitney U test. Scale bars, 100 µm
Fig 2: PIGR is expressed and released by human macrophages. A Relative PIGR mRNA expression of THP-1 monocytes vs. PMA-stimulated THP-1 macrophages (100 nM) at 24 and 48 h upon stimulation. PCR values normalized by GAPDH mRNA endogenous control are expressed as fold increases over basal condition at 24 or 48 h. B Quantification by ELISA of PIGR concentration (ng/mL) in the tissue-conditioned media of THP-1 monocytes and THP-1 macrophages at 24 and 48 h upon PMA stimulation. C Relative PIGR mRNA expression of non-polarized THP-1 macrophages (PMA 100 nM for 72 h, M0), polarized M1 macrophages (20 ng/mL IFN-γ + 100 ng/mL LPS, 24 h) and polarized M2 macrophages (20 ng/mL IL-4 + 20 ng/mL IL-13, 24 h). PCR values normalized by GAPDH mRNA endogenous control are expressed as fold increases over basal condition at 24 or 48 h. D Quantification by ELISA of PIGR concentration (ng/mL) in the tissue-conditioned media of non-polarized THP-1 macrophages (PMA 100 nM for 72 h, M0), polarized M1 macrophages (20 ng/mL IFN-γ + 100 ng/mL LPS, 48 h) and polarized M2 macrophages (20 ng/mL IL-4 + 20 ng/mL IL-13, 48 h). Data represent means ± SEM. Student's t-test. *p < 0.05, **p < 0.01, ****p < 0.0001. A.U., arbitrary units
Fig 3: Polymeric immunoglobulin receptor levels are increased in human AAA wall. A Western blot and densitometric analysis of PIGR after correction for GAPDH (loading control) in medial and adventitial layers of human AAA and healthy aortas (healthy media n = 14; AAA media n = 11; healthy adventitia n = 11; AAA adventitia n = 12). B Quantification by ELISA of PIGR concentration (ng/mL) in the tissue-conditioned media of AAA and healthy aortas (healthy media n = 9; AAA media n = 9; healthy adventitia n = 9; AAA adventitia n = 9). C Representative immunohistochemistry and quantification of PIGR in serial aortic cross-sections from AAA and healthy aortas (n = 4 for both). Scale bars, 100 µm. D Representative double immunofluorescence staining of PIGR (red) and CD68 (green) in AAA wall. DAPI nuclear staining (blue) is shown. Scale bars, 50 μm. Data represent means ± SEM. Mann–Whitney U test for healthy media vs. AAA media and healthy adventitia vs. AAA adventitia in (A) and (B). **p < 0.01, ***p < 0.001. A.U., arbitrary units
Fig 4: Representative photographs (A) and quantification of lesion area (μm2), (B), maximum atherosclerotic lesion area (μm2) as a function of distance (μm) (C), and area under the curve (AUC) values, representing total plaque volume (μm3) (D), in the aortic root from Ldlr−/− Pigr−/− (n=22) and Ldlr−/− Pigr+/+ (n=21) mice. Data represent means ± SEM. Mann-Whitney U test. *p<0,05, **p<0,01. Scale bars, 100 µm.
Fig 5: Pigr deficiency decreases intralesional lipids and macrophage infiltration in Ldlr knockout mice. Representative photographs and quantification of ORO (A), CD68 (B), α-SMA (C) and collagen (D) in the aortic root from Ldlr−/− Pigr−/− (n=22) and Ldlr−/− Pigr+/+ (n=21) mice. Data represent means ± SEM. Mann-Whitney U test. *p<0,05, ***p<0,001. Scale bars, 100 µm.
Supplier Page from Abcam for Human Polymeric immunoglobulin receptor ELISA Kit (PIGR)