Cytokine-dependent gp130 receptor subunit regulates rat modified axial-pattern epigastric flap.
We investigated axial-pattern flap survival by modulating the cytokine receptor component, gp130, to elucidate the mechanism of the cytokine receptor modulation subsequently leading to the initiation of local angiogenesis and blood-flow augmentation. Fifty-two male Wistar rats were divided into four groups. The flap size was 8 x 8 cm, with the medial middle branch of the superficial epigastric artery as the only nutrient supply vessel. Group 1 received only a control vehicle, group 2 received leukemia inhibitory factor(LIF), cDNA treated, group 3 received combined treatment of LIF and anti-gp130 antibody, and group 4 was the anti-gp130-treated group. All groups received 0.1 mL phosphate-buffered saline (PBS) via 30-gauge needle injected into the proximal site of the femoral artery after distal sites of the bifurcated femoral artery to epigastric artery and vein were clamped. All clamps were removed after 10 min of incubation of the injected agents. During the first 3 postoperative days, the flap survival was significantly more improved in the anti-gp130-treated and combined-treated groups than in the control (88 +/- 1.5% and 77 +/- 5.3 vs. 45 +/- 7.8, respectively, p <.01). Laser blood flowmetry on day 3 showed a significant increase of blood flow in three different flap sites in anti-gp130-treated and combined-treated groups than in the other groups (p <.001). Microangiography showed remarkable differences between all four groups. The anti-gp130-treated flap showed augmented vessel formation at the base of the pedicle, which elongated the vessel interconnection up to the distal area. Strong gp130 transcripts and vascular endothelial growth factor (VEGF) expression were observed in all groups, as determined using reverse-transcription polymerase chain reaction (RT-PCR). The intensity of VEGF expression was the strongest in the anti-gp130-treated group. Attenuation of the gp130 receptor subunit can improve axial-pattern flap survival along with angiogenesis.
Department of Plastic and Reconstructive Surgery, Nagasaki University School of Medicine, Nagasaki, Japan. akitas@hf.rim.or.jp
Sadanori
S
Akita
Mohammad Abdur
MA
Rashid
Hiroshi
H
Ishihara
Takehiro
T
Daian
Seiji
S
Dazai
Tohru
T
Fujii
D000818:Animals; D001483:Base Sequence; D016207:Cytokines / Q000502:physiology*; D017931:DNA Primers; D016228:Endothelial Growth Factors / Q000235:genetics; D006131:Growth Inhibitors / Q000032:analysis / Q000235:genetics; D007150:Immunohistochemistry; D036341:Intercellular Signaling Peptides and Proteins / Q000235:genetics; D015850:Interleukin-6; D017078:Laser-Doppler Flowmetry; D053605:Leukemia Inhibitory Factor; D008222:Lymphokines / Q000032:analysis / Q000235:genetics; D008297:Male; D023421:Models, Animal; D016133:Polymerase Chain Reaction; D021122:Protein Subunits; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D018121:Receptors, Cytokine / Q000737:chemistry / Q000235:genetics*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013270:Stomach / Q000601:surgery*; D013524:Surgical Flaps; D014158:Transcription, Genetic; D016896:Treatment Outcome; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors
D016207:Cytokines; D017931:DNA Primers; D016228:Endothelial Growth Factors; D006131:Growth Inhibitors; D036341:Intercellular Signaling Peptides and Proteins; D015850:Interleukin-6; D053605:Leukemia Inhibitory Factor; D008222:Lymphokines; D021122:Protein Subunits; D012333:RNA, Messenger; D018121:Receptors, Cytokine; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; C456339:cytokine receptor, GLM-R