Journal article
Changes in PKC isoforms in human alveolar macrophages compared with blood monocytes
American journal of physiology. Lung cellular and molecular physiology, Vol.275(2), pp.L389-L397
08/01/1998
DOI: 10.1152/ajplung.1998.275.2.L389
PMID: 9700101
Abstract
Alveolar macrophages play an important role in host defense and in other types of inflammatory processes in the lung. These cells exhibit many alterations in function compared with their precursor cells, blood monocytes. To evaluate a potential mechanism for these differences in function, we evaluated expression of protein kinase C (PKC) isoforms. We found an increase in Ca2+-dependent PKC isoforms in monocytes compared with alveolar macrophages. We also found differential expression of the Ca2+-independent isoforms in alveolar macrophages compared with monocytes. One consequence of the activation of PKC can be increased expression of mitogen-activated protein (MAP) kinase pathways. Therefore, we also evaluated activation of the MAP kinase extracellular signal-regulated kinase (ERK) 2 by the phorbol ester phorbol 12-myristate 13-acetate (PMA). PMA activated ERK2 kinase in both alveolar macrophages and monocytes; however, monocytes consistently showed a significantly greater activation of ERK2 kinase by PMA compared with alveolar macrophages. Another known consequence of the activation of PKC and subsequent activation of ERK kinase is activation of the transcription factor activator protein-1 (AP-1). We evaluated the activation of AP-1 by PMA in both monocytes and macrophages. We found very little detectable activation of AP-1, as assessed in a gel shift assay, in alveolar macrophages, whereas monocytes showed a substantial activation of AP-1 by PMA. These studies show that the differential expression of PKC isoforms in alveolar macrophages and blood monocytes is associated with important functional alterations in the cells.
Details
- Title: Subtitle
- Changes in PKC isoforms in human alveolar macrophages compared with blood monocytes
- Creators
- Martha M Monick - Department of Medicine, University of Iowa College of Medicine and Veterans Affairs Medical Center, Iowa City, Iowa 52242A. Brent Carter - Department of Medicine, University of Iowa College of Medicine and Veterans Affairs Medical Center, Iowa City, Iowa 52242Gunnar Gudmundsson - Department of Medicine, University of Iowa College of Medicine and Veterans Affairs Medical Center, Iowa City, Iowa 52242Lois J Geist - Department of Medicine, University of Iowa College of Medicine and Veterans Affairs Medical Center, Iowa City, Iowa 52242Gary W Hunninghake - Department of Medicine, University of Iowa College of Medicine and Veterans Affairs Medical Center, Iowa City, Iowa 52242
- Resource Type
- Journal article
- Publication Details
- American journal of physiology. Lung cellular and molecular physiology, Vol.275(2), pp.L389-L397
- DOI
- 10.1152/ajplung.1998.275.2.L389
- PMID
- 9700101
- ISSN
- 1040-0605
- eISSN
- 1522-1504
- Language
- English
- Date published
- 08/01/1998
- Academic Unit
- Pulmonary, Critical Care, and Occupational Medicine; Radiation Oncology; Provost Office Administration; Internal Medicine
- Record Identifier
- 9984213447402771
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