| To date, more than 150 kinds of cell surface proteins have been found to be anchored to the plasma membrane by Glycosyl-phosphatidylinositol(GPI). These proteins include complement regulatory proteins, lymphocyte differentiation antigens, tumor markers , etc. They take part in some vital activities, such as cell recognition, cell producing, cell differentiation, programmed cell death and so on. Furthmore, about ten percent CD on plasmalemma of hematopoietic cells have been found to be anchored by GPI, these CD maybe affect the growth, differentiation and maturation of hematopoietic cells. It is known that several GPI anchored CD on human cell membranes, such as CD46, CD55, CD59, are important on the human immunity function. GPI-PLD has been confirmed to be the only enzyme which can specifically hydrolyze GPI, release GPI-anchored proteins and regulate those proteins' expression and biological function. GPI-PLD is present in large amounts in human plasma, about 5?0 ug ?L" . The plasma activity of GPI-PLD is different in patients with different disease. It has been known by molecular biology that liver, pancreatic and bone marrow are the main origins of plasma GPI-PLD. Moreover leucocytes and leukemia cells also express GPI-PLD.We have analyzed the polymorphisms of GPI-PLD gene Exonl and Exon25, the GPI-PLD activities of leucocyte in peripheral blood and their relations of systemic lupus erythematosus(SLE) patients, Leukemia patients and normal individuals of Han nationality in Hunan Chinese. The polymorphisms were analyzed by PCR-SSCP and sequencing. GPI-PLD activity levels were determined by using glycosylphosphatidylinositol (GPI) anchored placental alkaline phosphatase (PLAP) as substrate and triton-Xl 14 partioning.Those results showed as following. There were fourteen variations in the coverage of GPI-PLD gene Exon 1 of systemic lupus erythematosus patients', Leukemia patients' and healthy persons', including seven variations at transcriptional start site upstream and seven variations at Exonl. The codons of variation were 14 TTG?AAG (Leul4Lys), 17 CTC-^GTC (LeulVVal), 20 AGA-+AAA (Arg20Lys), 21 GGT-籊GG (Gly21Gly), 30 GTA->ATA (VaBOIle), which leaded to four missenseinmutations and one synonymous mutation. The variation frequency of combining codon 17 with codon 30 was significantly different between healthy control and leukemia patient. In addition, the frequency of the variation at transcriptional start site upstream -24 C?T was significantly different between healthy control and systemic lupus erythematosus patient. At meanwhile, there was a variation in Exon25, the 60496th bp G?A, among three groups. The total various frequency, which was determined by SSCP, of systemic lupus erythematosus patient was 25.81 percent, leukemia patient was 34.71 percent and healthy person was 31.19 percent. On the basis of the percentage of GPI-anchored PLAP conversion, the leucocyte GPI-PLD activities of total 121 leukemia patients, included 57 acute non-lymphocytic leukemia (ANLL) patients as group A, 40 acute lymphoblastic leukemia (ALL) patients as group B, 19 chronic granulocytic leukemia (CML) patients as group C, 5 chronic lymphocytic leukemia (CLL) patients as group D, were measured. As compared with 109 healthy persons as control group, the leukocyte GPI-PLD activities of group A and D were significantly increased; the activities of group B and C was significantly reduced. At the same time, the changes of GPI-PLD activity in leukemia leukocyte between all paried groups among these four groups were remarkable. The leucocyte GPI-PLD activities of total 62 systemic lupus erythematosus patients were also measured. As compared with 109 healthy persons as control group, the leukocyte GPI-PLD activities of systemic lupus erythematosus patients were significantly raised.We can confirm that the leukocyte GPI-PLD gene in peripheral blood which belongs to leukemia patient, systemic lupus erythematosus patient and healthy person in Han national in Hunan Chinses is polymorphism; the variation frequency o... |
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