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Capillary Ca 2+ increase induces venular P‐selectin expression in lung
Author(s) -
Parthasarathi Kaushik,
Bhattacharya Jahar
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.a752-d
Subject(s) - gap junction , connexin , chemistry , lung , venule , biophysics , endothelium , microbiology and biotechnology , anatomy , medicine , biology , endocrinology , biochemistry , intracellular
The function of endothelial (EC) gap junctions in the lung microvascular bed remains unclear. To determine this role, we blood‐perfused isolated rat lungs at constant pulmonary artery, left atrial and airway pressures of 10, 3 and 5 cm H2O, respectively. We imaged EC of lung microvessels in situ , to quantify fluorescence of fluo 4 and FITC‐tagged IgG to determine respectively, cytosolic Ca 2+ (Ca 2+ cyt ) and cell‐surface P‐selectin expression. We loaded EC of peri‐alveolar capillaries with the Ca 2+ cage, NP‐EGTA and uncaged Ca 2+ using UV illumination. Uncaging increased Ca 2+ cyt from 74±11 to 129±17 gray levels in the target capillary. Concomitantly, P‐selectin expression increased by 48±3 gray levels (n=3, P<0.05) in a venule located 100 μm from the target site. We pretreated capillaries with a mixture of the peptides, gap26 and gap27 that inhibits communication through connexin 43 containing gap junctions. Gap26/27, but not scrambled peptides, completely inhibited uncaging‐induced P‐selectin expression (n=3, P<.05). We interpret, EC gap junctions communicated Ca 2+ increases in capillaries to induce P‐selectin expression in venules. EC gap junctions may underlie spread of proinflammatory responses in the lung microvascular bed (supported by HL75503, HL57556).