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Developmental expression and transcriptional regulation of claudin‐6 in the murine lung
Author(s) -
Jimenez Felix R,
Lewis Josh B,
Wood Tyler T,
Reynolds Paul R
Publication year - 2013
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.27.1_supplement.256.4
Subject(s) - claudin , tight junction , paracellular transport , microbiology and biotechnology , transcriptional regulation , biology , sox2 , transcription factor , transfection , occludin , extracellular , cell culture , gene , genetics , permeability (electromagnetism) , membrane
Claudins contribute to tight junctions that prevent paracellular transport of extracellular fluid and diverse substances. Claudin‐6 was evaluated by qPCR and immunohistochemistry and its expression was confirmed to peak at E12.5 and diminish as development progressed. Co‐immunofluorescence revealed that Claudin‐6 co‐localized with Sox2 and Sox9, both factors that influence cell differentiation in the proximal and distal lung, respectively. Claudin‐6 was also detected in cells that express TTF‐1, a critical regulator of pulmonary branching morphogenesis. In order to assess transcriptional control of Claudin‐6, its promoter was ligated into a luciferase reporter vector and co‐transfected with TTF‐1 and other important transcriptional regulators. Factor‐specific effects were confirmed using site‐directed mutagenesis of putative response elements located in the Claudin‐6 promoter. This work revealed for the first time that Claudin‐6 might be an important tight junctional component during lung organogenesis. Furthermore, these and other data may reveal important Claudin‐6‐ mediated aspects of lung cell metastasis, remodeling, and disease states coincident with abnormal membrane permeability. This work was supported by a grant from the Flight Attendant's Medical Research Institute (FAMRI, PRR) and a BYU Mentoring Environment Grant (PRR).