Table 1.

Fold change in wound closure and mitotic index of fibroblasts in response to various treatments 16 hours after wounding



CONTROL

FBG-ATOW

FBG-PRE
Treatment*
Wound closure
Mitotic index
Wound closure
Mitotic index
Wound closure
Mitotic index
None/nonimmune lgG1  1.0/0.97   1.0   0.81   2.0   1.6   8.0  
FGF-2   1.5   2.2   1.4   2.8   2.0   7.8  
PDGF   1.4   2.25   1.3   3.2   2.0   8.4  
Anti-αvβ3   0.47   0.5   0.68   ND   0.80   0.75  
Anti-FN-III1  0.73   0.75   0.8   ND   0.85   0.64  
FBG-325   NA   NA   0.14   ND   0.25   0.9  
FBG-ΔAαC
 
NA
 
NA
 
0.8
 
ND
 
0.95
 
0.65
 


CONTROL

FBG-ATOW

FBG-PRE
Treatment*
Wound closure
Mitotic index
Wound closure
Mitotic index
Wound closure
Mitotic index
None/nonimmune lgG1  1.0/0.97   1.0   0.81   2.0   1.6   8.0  
FGF-2   1.5   2.2   1.4   2.8   2.0   7.8  
PDGF   1.4   2.25   1.3   3.2   2.0   8.4  
Anti-αvβ3   0.47   0.5   0.68   ND   0.80   0.75  
Anti-FN-III1  0.73   0.75   0.8   ND   0.85   0.64  
FBG-325   NA   NA   0.14   ND   0.25   0.9  
FBG-ΔAαC
 
NA
 
NA
 
0.8
 
ND
 
0.95
 
0.65
 

Wound closure is defined as the number of cells moving into the wound space expressed as the fold change above or below the number of CONTROL cells moving into the wound space at 16 hours. The mitotic index is calculated by dividing the percentage of cells showing 3H-thymidine uptake due to the specific treatment by the percentage of CONTROL cells showing 3H-thymidine uptake.

ND indicates not determined; NA, not applicable.

*

Treatment conditions are described in “Materials and methods” and the figure legends.

Both anti-αvβ3 (LM609) and anti-FN-III1 (9D2) inhibited assembly of plasma FBG into fibroblast matrix fibrils.

Intact plasma FBG and FBG-325 but not FBG-ΔAαC assembled into ECM fibrils.

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