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Intermittent Hypoxia Induces Fra‐1 in Rat Carotid Body Cells Expressing Leptin
Author(s) -
Messenger Scott,
Moreau Jason M.,
Ciriello John
Publication year - 2012
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.26.1_supplement.897.5
Subject(s) - glomus cell , carotid body , leptin , medicine , endocrinology , hypoxia (environmental) , chemistry , intermittent hypoxia , paracrine signalling , immunohistochemistry , autocrine signalling , biology , receptor , carotid arteries , obstructive sleep apnea , obesity , organic chemistry , oxygen
Carotid body glomus cells have recently been found to express leptin. In this study, we investigated whether intermittent hypoxia (IH) induced immediate early gene Fra‐1 expression in carotid body cells expressing leptin. Adult male Sprague‐Dawley rats were subjected to eucapnic and isobaric IH (120s normoxia, 80s hypoxia; 6.5% O 2 ) or normoxia for 8 h. A blood sample was immediately taken after IH for determination of plasma leptin levels and then the rats were transcardially perfused with Zamboni's fixative. The carotid bodies and the carotid arteries at their bifurcation were excised, paraffin embedded and sectioned at 6 μm for immunohistochemistry. Circulating leptin levels were increased in response to IH. Additionally, glomus cells containing leptin immunoreactivity were found to co‐express Fra‐1 in response to IH. Additionally, these glomus cells that expressed leptin, also expressed the Ob‐Rb, and an increase in pSTAT3 to IH. Taken together, these data suggest that the activation of carotid body glomus cells during IH may contribute to the elevated circulatory leptin levels and that leptin released by the glomus cells may also act in an autocrine/paracrine manner to alter the activity of carotid body glomus cells during IH. Supported by the Heart and stroke Foundation of Ontario.