Degradation of bovine nasal cartilage by a neutral protease from human leukocyte granules

1977 ◽  
pp. 361-370 ◽  
Author(s):  
D. Kruze ◽  
P. Salgam ◽  
K. Fehr ◽  
A. Böni
1987 ◽  
Author(s):  
S D Berkowitz ◽  
H Nozaki ◽  
K Titani ◽  
T Murachi ◽  
T S Zimmerman

Recent evidence suggests that proteolysis plays an important role in some forms of inherited and acquired von Willebrand disease (vWD). Using monoclonal epitope mapping, we have examined the proteolysis of the von Willebrand factor (vWF) subunit with platelet calcium activated neutral protease (CANP) and human leukocyte elastase and found that they are not responsible for the proteolytic cleavage sejen in normal individuals and IIA vWD. Previously we have shown that in vivo proteolysis of vWF is a normal event with a small but consistent proportion of plasma vWF being composed of 189, 176, and 140 kD fragments cleaved from the 225 kD subunit. In IIA vWD the proportion of cleaved vWF is increased. Because calcium activated neutral protease (CANP, calpain) and one or more enzymes released from polymorphonuclear leukocytes are known to proteolyze vWF in vitro with resultant loss of large multimers similar to that seen in IIA vWD, they have been suggested as being responsible for the proteolysis in vivo. We have now digested highly purified vWF with porcine CANP I and II and performed monoclonal epitope mapping on the resulting fragments. We found no difference in the size, location, and quantity of the fragments produced by calpain I versus calpain II. New fragments were detected of approximately 200, 170, 150, and 125 kD. There was no evidence for generation of the native fragments. Mapping of the 170 and 150 kD calpain-cleaved fragments revealed them to be from different parts of the molecule than the native 176 and 140 kD fragments. Digestion of vWF with human leukocyte elastase produced new fragments at 210/205, 190, 165, 145/140, and 130/125 kD. No generation of native fragments was detected. Monoclonal epitope mapping of the 190 and 145/140 kD elastase-cleaved bands proved that they come from opposite ends of the vWF molecule than the native 189 and 140 kD fragments, respectively. Therefore, CANP and human leukocyte elastase do not produce the proteolyzed fragments present in normal and IIA vWD and probably do not cause the loss of large multimers seen in that disorder.


2016 ◽  
Vol 22 ◽  
pp. 6
Author(s):  
Leena Kinnunen ◽  
Valma Harjutsalo ◽  
Heljä-Marja Surcel ◽  
Christel Lamberg-Allardt ◽  
Jaakko Tuomilehto ◽  
...  

2020 ◽  
Vol 5 ◽  

Human leukocyte antigen (HLA) loci are highly polymorphic and determine differential features of the immune response in subjects from different regions. HLA genes have been proposed to determine genetic susceptibility to several diseases, particularly to viral infections. Moreover, it has been suggested that each ethnic group could have a different specificity of T-lymphocyte reactivity to the same viral infections. In this review, we analyzed the distribution of HLA types in countries of the Asian, European and North African region. Also, we studied the relation between these HLA polymorphisms and susceptibility to infection by the coronavirus. Our findings indicated that homozygosity would increase susceptibility to viral infections and, in some cases, to coronavirus infection. HLA types showing higher susceptibility were reported in Asian population, including China, Singapore, and Taiwan. In contrast, lower susceptibility HLA variants were detected among African populations, some Asian populations, and Mediterranean populations. The presented evidence along with the spread pattern of COVID-19 infection suggests that HLA genetic variants might be related to its infection susceptibility and severity. The investigation of HLA genetic variants distribution would be a useful tool to predict different populations’ susceptibility to viral infections.


2008 ◽  
Vol 11 (1) ◽  
pp. E42-E45 ◽  
Author(s):  
Cheng-Hon Yap ◽  
Peter D. Skillington ◽  
George Matalanis ◽  
Bruce B. Davis ◽  
Brian D. Tait ◽  
...  

2000 ◽  
Vol 71 (2) ◽  
pp. 218 ◽  
Author(s):  
Brian J. F. Wong ◽  
Thomas E. Milner ◽  
Hong K. Kim ◽  
Ken Chao ◽  
Chung-Ho Sun ◽  
...  

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