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Inappropriate Production of Galectin‐1 Affects Vascular Homeostasis during Pulmonary Hypertension
Author(s) -
Majka Susan M,
Case David,
Ivestor Charles,
Imamura Masa,
Roedersheimer Mark,
Patterson Abby,
Carr Michelle,
Saavedra Milene,
Crossno Joseph,
Poirer Francoise,
West James
Publication year - 2006
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.20.4.a639-a
Subject(s) - pulmonary hypertension , hypoxia (environmental) , galectin 3 , medicine , ventricle , lung , pathology , vascular disease , knockout mouse , endocrinology , cardiology , receptor , chemistry , organic chemistry , oxygen
Pulmonary vascular disease, which may be primary or secondary to underlying lung disease, leads to significant morbidity and mortality in affected patients. Contributing factors to pulmonary vascular hypertension include the presence of hypoxia and physiologic responses by affected tissues leading to abnormal differentiation, repair and matrix deposition. Sequelae of pulmonary vascular hypertension involve vascular smooth muscle cell and ECM dependent defects. The hypothesis of this study was that inappropriate expression of galectin‐1, an ECM protein, causes abnormal vascular responses in pulmonary hypertension. Using a murine model of hypobaric hypoxic pulmonary hypertension we examined the changes in galectin‐1 expression, cardiac function as well as pulmonary alveolar and vessel counts. Western analysis identified higher galectin‐1 protein expression in lung tissue following hypoxic exposure when compared to normoxic controls. Cardiac hemodynamics showed no significant changes for galectin‐1 knockout mice in reponse to hypoxia relative to normoxic controls, which corresponded to right ventricle over left ventricle plus septum ratios. Alveolar and vessel quantification indicated that galectin‐1 knockout mice had higher pulmonary microvessel density compared to control mice following hypoxic exposure. These experiments suggest that galectin‐1 knockout mice are less susceptible than control mice to hypobaric hypoxia induced pulmonary vascular hypertension.