Résumé
Oligoasthenozoospermia, teratozoospermia or low sperm motility is the main cause of male infertility. Low sperm motility can be induced by abnormalities of the sperm tail structure and sperm function. The outer dense fiber protein 2 (ODF2) is a protein fiber maintaining cytoskeleton, as a major component of the mammalian sperm tail and centrosome, and its abnormality is closely related to asthenospermia. Recent studies indicate that ODF2 includes many proteins of the same name and homologous splices located in the sperm centrosomes and spindles of cleaved-embryos, necessary for animal ciliogenesis and associated with sperm capacitation. The features of ODF2 indicate that it is not a single-structural protein. This paper reviews the known functions of ODF2, paving a ground for further studies of the relationship between the ODF2 protein and fertilization.
Sujets)
Animaux , Humains , Mâle , Asthénozoospermie , Azoospermie , Centrosome , Chimie , Cytosquelette , Chimie , Protéines du choc thermique , Physiologie , Infertilité masculine , Mobilité des spermatozoïdes , Physiologie , Flagelle du spermatozoïde , Spermatozoïdes , PhysiologieRésumé
Objective@#To investigate the mRNA and protein expressions of outer dense fiber 2 (ODF2) in the sperm of the asthenospermia patient and their differences from those in normal healthy men.@*METHODS@#According to the WHO criteria, we collected semen samples from 45 asthenozoospermia patients and 15 normal healthy volunteers. Using computer-assisted sperm analysis (CASA), we divided the semen samples from the asthenospermia patients into a mild, a moderate and a severe group, and determined the mRNA and protein expressions of ODF2 in different groups by RT-PCR and Western blot.@*RESULTS@#Compared with the normal healthy men, the expression of the ODF2 gene showed no statistically significant difference in the mild asthenospermia group (1.112 0 ± 0.525 5 vs 0.688 0 ± 0.372 0, P >0.05) but remarkably decreased in the moderate (0.483 3 ± 0.186 3, P 0.05), but markedly lower than in the moderate (0.145 4 ± 0.053 6, P <0.05) and severe asthenospermia patients (0.122 7 ± 0.045 7, P <0.01), which was consistent with the results of RT-PCR.@*CONCLUSIONS@#Decreased mRNA and protein expressions of ODF2 in the sperm are positively correlated with declined sperm motility of the asthenospermia patient, which is suggestive of the involvement of the ODF2 gene in the regulation of sperm motility.
Sujets)
Humains , Mâle , Asthénozoospermie , Métabolisme , Études cas-témoins , Régulation négative , Protéines du choc thermique , Génétique , Métabolisme , ARN messager , Métabolisme , Analyse du sperme , Mobilité des spermatozoïdes , Flagelle du spermatozoïde , Spermatozoïdes , MétabolismeRésumé
<p><b>OBJECTIVE</b>To investigate the relationship of the promoter of matrix metalloproteinase-9 (MMP-9) gene polymorphisms with the susceptibility and clinical features of Helicobacter pylori (H. pylori)-related chronic gastritis and duodenal ulcer in children.</p><p><b>METHODS</b>One hundred children with chronic gastritis, 32 children with duodenal ulcer and 102 healthy children were enrolled.The promoter of MMP-9-1562C/T gene polymorphisms were genotyped by polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) and sequencing. MMP-9 mRNA expression in gastric mucosa was confirmed by reverse transcription polymerase chain reaction.</p><p><b>RESULTS</b>The genotype distributions and allele frequencies of MMP-9-1562C/T gene polymorphisms were similar in gastric upper gastrointestinal disease and healthy subjects. The relative risk for H.pylori infection in C/C genetype carriers was 3.1 times as high as that in T allele (C/T+T/T) carriers in children with chronic gastritis. MMP-9-1562 C/T gene polymorphisms did not affect MMP-9 mRNA expression level.</p><p><b>CONCLUSIONS</b>These data suggest that MMP-9-1562 C/T gene polymorphisms are not associated with susceptibility to chronic gastritis and duodenal ulcer in children. The C/C genotype of MMP-9-1562 C/T gene polymorphism might be associated with H.pylori infection.</p>
Sujets)
Adolescent , Enfant , Enfant d'âge préscolaire , Femelle , Humains , Mâle , Maladie chronique , Ulcère duodénal , Génétique , Gastrite , Génétique , Génotype , Infections à Helicobacter , Génétique , Helicobacter pylori , Matrix metalloproteinase 9 , Génétique , Polymorphisme génétiqueRésumé
<p><b>OBJECTIVE</b>To study the expression of CD138 and heparinase in hepatocellular carcinoma (HCC) and its relationship with tumor development, progression, metastasis and recurrence.</p><p><b>METHODS</b>Tissue microarray and immunohistochemical study (EnVision method) for CD138 and heparinase was performed on tissue microarray which consisted of 197 cases of HCC, including adjacent non-neoplastic liver tissues, and 66 cases of HCC metastases.</p><p><b>RESULTS</b>The rates of CD138 expression in HCC and adjacent non-neoplastic liver tissues were 48.7% (96/197) and 65.0% (128/197, P < 0.05) respectively. In early-stage and late-stage tumors, the expression rates were 61.7% (29/47) and 44.7% (67/150, P < 0.05) respectively. The rate in patients with metastasis was 33.3% (22/66), as compared with 53.6% (45/84, P < 0.05) in patients without metastasis. In patients with tumor recurrence occurring within or after 1 post-operative year, the expression rates were 23.3% (7/30) and 61.1% (11/18, P < 0.05) respectively. On the other hand, the rates of expression of heparinase in HCC and adjacent non-neoplastic liver tissues were 35.5% (70/197) and 12.7% (25/197, P < 0.05) respectively. In early-stage and late-stage tumors, the expression rates were 29.8% (14/47) and 37.3% (56/150, P > 0.05) respectively. The rate in patients with metastasis was 48.5% (32/66), as compared with 28.6% (24/84, P < 0.05) in patients without metastasis. In patients with tumor recurrence occurring within or after 1 post-operative year, the expression rates were 50.0% (15/30) and 44.4% (8/18, P > 0.05) respectively. In the 66 cases of metastatic HCC studied, the expression rate of CD138 was lower in the heparinase-positive subgroup (P < 0.05).</p><p><b>CONCLUSIONS</b>Loss of CD138 expression is related to HCC development, progression, metastasis and recurrence. Overexpression of heparinase, when coupled with loss of CD138 expression, may take part in tumor metastasis of HCC.</p>