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Estradiol enhances neutrophil infiltration into traumatically‐injured skeletal muscle
Author(s) -
Le Gengyun,
Jergenson Matthew,
Lowe Dawn,
Warren Gordon
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.lb704
Subject(s) - infiltration (hvac) , myeloperoxidase , medicine , endocrinology , neutrophile , inflammation , andrology , chemistry , physics , thermodynamics
Purpose To probe how estradiol modulates neutrophil infiltration and function following traumatic muscle injury. Methods Adult, female C57BL/6 mice were ovariectomized and randomly assigned to no treatment or implantation of a 17‐b estradiol slow‐release pellet. Four weeks later, freeze injury was induced to tibialis anterior (TA) muscles and mice were allowed to recover for 1, 2, 3, or 4 days before sacrifice, blood collection, and TA muscle excision. Myeloperoxidase (MPO) activity, an indicator of neutrophil function, was examined in the muscles. H&E staining of TA cross‐sections were used to address neutrophil localization and FACS analysis was performed to quantify neutrophil infiltration. Neutrophils in the blood were counted by automated hematological analysis. Results MPO activity was 25‐125% greater in the injured muscles of estradiol‐treated mice (P<0.0001). Infiltration of neutrophils appeared in the first 24 hours and peaked at 3‐days post‐injury in muscles of mice with and without estradiol. FACS analysis revealed that compared to injured muscles from untreated mice, infiltrated neutrophils were 6‐61% greater in injured muscles from estradiol‐treated mice, with the peak difference at day 4 (24±6 vs 15±3 % of hematopoietic cells). The concentration of neutrophils in blood of estradiol‐treated mice was 40‐60% lower than that in untreated mice at 1, 2, and 3‐days post‐injury (P<0.001). Conclusion Estradiol increases neutrophil infiltration into muscle following traumatic injury. Supported by NIH grant R01‐AG031743.