Abstract
Soluble receptors are produced by proteolytic cleavage of membrane-bound receptors to release soluble forms, or by alternative mRNA splicing resulting in dedicated transcript encoding soluble receptors. It has been reported that M-CSF receptor could be cleaved from the cell surface by a protease induced by activation of protein kinase C. We have developed an enzyme-linked immunosorbent assay (ELISA) to quantify the concentration of soluble M-CSFR (Rao Q. et al. Exp Hematol 27:105, 1999). Now via M-CSFR specific ELISA, the soluble M-CSFR level in serum and urea from normal donors and patients with hematological diseases is reported. The average level of soluble M-CSFR in normal human individuals (n=102) was 0.457±0.303ng/ml. There was no statistical difference in soluble M-CSFR levels between males and females groups or between the different age groups. The average levels of soluble M-CSFR in the serum from ALL and AML patients were 0.184±0.368 ng/ml (n=36) and 0.124ng/ml±0.223ng/ml (n=60), which were much lower than normal human (p= 0.0002 and p<0.0001, respectively). For the patients with benign hematological disease, the serum levels of M-CSFR in IDA (n= 25) and ITP patients (n=34) were slightly higher than normal individuals (0.662±0.468ng/ml and 0.828±0.960ng/ml respectively), but no statistical difference (p=0.05 and p=0.06) was found. Using our ELISA, the soluble M-CSFR in the urea of normal human (n=109) and hematological patients was also investigated. The results showed that the urea M-CSFR level of patients with malignant hematological disease (n=35) was significantly lower than that of normal donor (0.291±0.502ng/ml versus 0.894±0.715ng/ml, p=0.0007). In contrast, the urea M-CSFR level of patients with benign hematological disease (n=33) was higher than that of normal adult (6.98±13.14ng/ml versus 0.894±0.715ng/ml, p=0.01). Result of the urea M-CSFR levels is consistent with that of serum. It has been reported that detectable levels of some soluble receptors can be measured in normal individuals and in some diseases. Our results showed that soluble M-CSFR exited in normal human serum and urea. The function of soluble M-CSFR and whether the abnormalities of soluble M-CSFR level in serum and urea may contribute to leukemia or other hematological diseases should further be verified.
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