title: Possible role of hematopoietic CD44/chondroitin sulfate interaction in extravasation of peripheral blood CD16(-) natural killer cells into human endometrium.
abstract: Unique CD16(-) natural killer (NK) cells appear in the human cycling endometrium. Although their origin remains undetermined, one possible explanation is extravasation of circulating peripheral blood CD16(-) NK cells. Hematopoietic CD44 (CD44H) is an adhesion molecule expressed on leukocytes and plays a role in the initial step of leukocyte extravasation (leukocyte tethering/rolling). Recent studies have shown that CD44H binds to chondroitin sulfate (CS). To test the hypothesis that peripheral blood CD16(-) NK cells extravasate using the CD44H/CS interaction, we have compared the binding capacity of CD44H to immobilized CS among peripheral blood lymphocyte subsets, as well as determined the menstrual cycle-dependent expression of CD44H. Additionally, we have investigated the expression of the CS proteoglycan serglycin in human endometrial endothelial cells. CD44H expression on peripheral blood CD16(-) NK cells was higher compared with other lymphocyte subsets throughout the menstrual cycle. Peripheral blood CD16(-) NK cells bound preferentially to immobilized CS-A and CS-C compared with other lymphocyte subsets. The binding was significantly reduced by function-blocking anti-CD44H antibody. Serglycin expression in the human endometrial endothelial cells was greater in the secretory phase than in the proliferative phase. Progesterone (10(-7) M to 10(-8) M) significantly increased serglycin core protein expression in cultured human uterine microvascular endothelial cells, whereas 17beta-estradiol had no effect. These results indicate that the interaction between CD44H on peripheral blood CD16(-) NK cells and CS on endometrial endothelial cells may play a role in extravasation of these NK cells into human endometrium. Serglycin may be a potential CS proteoglycan involved in this phenomenon.
authors.affiliation: Department of Obstetrics and Gynecology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto 602-8566, Japan.
authors.forename: Tadahiro
authors.initials: T
authors.lastname: Yasuo
authors.forename: Kotaro
authors.initials: K
authors.lastname: Kitaya
authors.forename: Takeshi
authors.initials: T
authors.lastname: Yamaguchi
authors.forename: Shinji
authors.initials: S
authors.lastname: Fushiki
authors.forename: Hideo
authors.initials: H
authors.lastname: Honjo
mesh_terms: D000328:Adult; D015703:Antigens, CD; D002809:Chondroitin Sulfates / Q000276:immunology / Q000378:metabolism*; D004717:Endometrium / Q000166:cytology / Q000276:immunology / Q000378:metabolism*; D042783:Endothelial Cells / Q000166:cytology / Q000378:metabolism; D004958:Estradiol / Q000494:pharmacology; D004967:Estrogens / Q000494:pharmacology; D005260:Female; D058851:GPI-Linked Proteins; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D006801:Humans; D018960:Hyaluronan Receptors / Q000276:immunology / Q000378:metabolism*; D007694:Killer Cells, Natural / Q000166:cytology / Q000276:immunology / Q000378:metabolism*; D036904:Leukocyte Rolling / Q000187:drug effects / Q000502:physiology*; D008597:Menstrual Cycle / Q000502:physiology; D008875:Middle Aged; D011374:Progesterone / Q000494:pharmacology; D011372:Progestins / Q000494:pharmacology; D011509:Proteoglycans / Q000096:biosynthesis; D017452:Receptors, IgG; D033921:Vesicular Transport Proteins / Q000096:biosynthesis
chemical_list: D015703:Antigens, CD; C497483:CD44 protein, human; D004967:Estrogens; C428200:FCGR3B protein, human; D058851:GPI-Linked Proteins; D018960:Hyaluronan Receptors; D011372:Progestins; D011509:Proteoglycans; D017452:Receptors, IgG; D033921:Vesicular Transport Proteins; C075430:serglycin; D011374:Progesterone; D004958:Estradiol; D002809:Chondroitin Sulfates