Fig 1: Aging caused dilation of cardiac lymphatics and impaired integrity of lymphatic vessels. (A) Confocal imaging and quantification of vessel diameter of LYVE‐1+ lymphatic vessels in hearts from young 2‐month‐old and aged 20‐month‐old mice. (B) Representative whole mount staining of CD31 + LYVE‐1+ initial lymphatics in the hearts from young and aged mice with quantification of lymphatic diameter. (C) Representative whole mount staining of CD31 + LYVE1‐ collecting lymphatics from young and aged mice with quantification of lymphatic diameter. (D) Confocal imaging of VE cadherin‐positive initial lymphatics and (E) RNA quantification of VE‐cadherin in hearts from young and aged mice. (F) Confocal imaging and quantification of lymphatic vessel density in the epicardium of young and aged mice. Magnified insets show LYVE1+/VEGFR‐3+ lymphatic endothelial cells (yellow upon merge). (n = 3 for all groups) *p < 0.05; **p < 0.01.
Fig 2: Exercise training induced cardiac lymphangiogenesis in young mice after 8 weeks of voluntary wheel running. (A) LYVE‐1 immunohistochemical staining of the lymphatic network in hearts from sedentary (Sed) control and exercise‐trained (ExTr) mice. (B) Confocal imaging for LYVE‐1 and VEGFR‐3 in heart tissues from sedentary control and exercised mice with quantification of cardiac lymphatic density (n = 5 per group). (C) Representative whole mount staining of LYVE‐1+ epicardial lymphatics from sedentary control and exercised mice with quantification of lymphatic diameter and branching points (white arrows) (n = 5 per group). (D) mRNA levels of CD31 and lymphatic markers LYVE‐1, PDPN, and VEGFR‐3 in sedentary control and exercised mice. *p < 0.05; **p < 0.01; ns: Not significant.
Fig 3: Exercise remodeled the perilymphatic microenvironment in aged hearts. (A) Confocal imaging and quantification of CD3+ T cells in peri‐lymphatic regions in the hearts of aged sedentary (aSed) and aged exercise‐trained (aExTr) mice (n = 5 per group). (B) Confocal imaging and quantification of CD68+/CD206+ macrophages in peri‐lymphatic regions in the hearts of aged sedentary and aged exercised mice (n = 5 per group). (C) Confocal imaging of collagen1, alpha‐actinin‐2, and LYVE‐1 with quantification of perilymphatic collagen (n = 3 per group). (D) Representative images and quantification of perilipin1+ cardiac fat in aged sedentary and aged exercised mice (n = 4 per group). (E) Confocal imaging of WGA‐stained cardiomyocytes and quantification of their size after exercise training in regions either adjacent to or remote from lymphatic vessels (n = 3–4 per group). *p < 0.05; ***p < 0.001; ns: Not significant.
Fig 4: Eight weeks of exercise training enhanced lymphangiogenesis and lymphatic remodeling in the hearts of 20‐month‐old mice. (A) Confocal imaging and quantification of lymphatic vessels costained with LYVE‐1 and the proliferative marker Ki67 in the hearts of aged sedentary (aSed) control and aged exercise‐trained (aExTr) mice (n = 3 per group). (B) Whole mount staining for LYVE‐1+ epicardial lymphatics from aged sedentary and aged exercised mice with quantification of diameter and branching points (white arrows) (n = 5 per group). (C) Flow plots and quantification of lymphatic endothelial cells (CD45‐/CD31+/LYVE‐1+/VEGFR‐3+) in hearts from aged sedentary and aged exercised mice (n = 3 per group). (D) mRNA levels of lymphangiogenic markers in aged hearts following exercise training (n = 4 per group). (E) Whole mount staining of peripheral lymphatics under the ear skin in aged sedentary and aged exercised mice with quantification of diameter and branch points (n = 4 per group). *p < 0.05; **p < 0.01.
Supplier Page from Novus Biologicals, a Bio-Techne Brand for LYVE-1 Antibody [DyLight 680]
Available conjugates: DyLight 680