The possible role of hematopoietic cell kinase in the pathophysiology of COPD.
BACKGROUND
Hematopoietic cell kinase (Hck) is a myeloid cell-specific tyrosine kinase, which is known to induce neutrophil infiltration to the lungs. Although the overexpression of Hck causes emphysema-like histologic changes in mice, its expression and activity in patients with COPD are unclear.


METHODS
The aim of this study was to clarify the expression and activity of Hck in neutrophils from COPD patients, and to investigate the association between the degree of Hck expression and the lung function parameters in COPD patients. Peripheral blood neutrophils were isolated from 22 patients with COPD and 9 healthy subjects (HSs). The protein levels of Hck and phosphorylated Hck were assessed, and the correlation with various background characteristics was evaluated.


RESULTS
The Hck protein level was significantly higher in neutrophils from COPD patients compared with HSs (COPD patients, 1.094; HSs, 0.801; p < 0.05). A significant positive correlation was observed between the protein level of Hck and the surface expression of the integrin molecule CD-11b (r = 0.540; p < 0.01) or CXC chemokine receptor-1 (r = 0.432; p < 0.05). In contrast, there was no difference in the phosphorylation of the Hck protein between COPD patients and HSs.


CONCLUSIONS
The Hck protein level in peripheral blood neutrophils was increased in COPD patients, suggesting that Hck might have an important role in the neutrophil function and play a key role in the pathophysiology of COPD.
Yanagisawa
Satoru
S
Third Department of Internal Medicine, School of Medicine, Wakayama Medical University, Wakayama, Japan.
Sugiura
Hisatoshi
H
Third Department of Internal Medicine, School of Medicine, Wakayama Medical University, Wakayama, Japan.
Yokoyama
Tomonori
T
Third Department of Internal Medicine, School of Medicine, Wakayama Medical University, Wakayama, Japan.
Yamagata
Toshiyuki
T
Third Department of Internal Medicine, School of Medicine, Wakayama Medical University, Wakayama, Japan.
Ichikawa
Tomohiro
T
Third Department of Internal Medicine, School of Medicine, Wakayama Medical University, Wakayama, Japan.
Akamatsu
Keiichirou
K
Third Department of Internal Medicine, School of Medicine, Wakayama Medical University, Wakayama, Japan.
Koarai
Akira
A
Third Department of Internal Medicine, School of Medicine, Wakayama Medical University, Wakayama, Japan.
Hirano
Tsunahiko
T
Third Department of Internal Medicine, School of Medicine, Wakayama Medical University, Wakayama, Japan.
Nakanishi
Masanori
M
Third Department of Internal Medicine, School of Medicine, Wakayama Medical University, Wakayama, Japan.
Matsunaga
Kazuto
K
Third Department of Internal Medicine, School of Medicine, Wakayama Medical University, Wakayama, Japan.
Minakata
Yoshiaki
Y
Third Department of Internal Medicine, School of Medicine, Wakayama Medical University, Wakayama, Japan.
Ichinose
Masakazu
M
Third Department of Internal Medicine, School of Medicine, Wakayama Medical University, Wakayama, Japan. Electronic address: masakazu@wakayama-med.ac.jp.
D000368:Aged; D015703:Antigens, CD / Q000097:blood; D016022:Case-Control Studies; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000502:physiology; D051572:Proto-Oncogene Proteins c-hck / Q000097:blood*; D029424:Pulmonary Disease, Chronic Obstructive / Q000097:blood / Q000201:enzymology* / Q000503:physiopathology*; D054387:Receptors, CXCR / Q000097:blood; D013147:Spirometry; D014797:Vital Capacity
D015703:Antigens, CD; D054387:Receptors, CXCR; D051572:Proto-Oncogene Proteins c-hck