Migration of mouse antibody-secreting hybridoma cells from blood to genital tract and its regulation by sex hormones are associated with the differential expression patterns of adhesion molecules and chemokines in the tract rather than in the antibody-secreting cells.
To understand better the molecular mechanisms of differential migration of antibody-secreting cells (ASCs) into mouse genital tracts, and regulation by sex hormones, surface markers, hormone receptors and adhesion molecules in mouse SG2 and PA4 hybridoma cells, respectively, secreting IgG2b and polymeric IgA antibody were detected by flow cytometry or RT-PCR. Semi-quantitative RT-PCR was also used for measuring mRNA expression of adhesion molecules and chemokines (VCAM-1, ICAM-1, P-selectin, JAM-1 and CXCL12) in genital tracts of various adult mouse groups. The mRNAs of androgen receptor, estrogen receptor beta and CXCR4 were expressed in the ASCs. Sex hormones had no effect on expression of these molecules in ASCs. Except for VCAM-1, mRNA of all examined genes was expressed in normal mouse genital tracts. The mean of relative amounts of ICAM-1 and CXCL12 mRNA in all examined organs of females were higher (2.1- and 1.9-fold) than those in males. After orchiectomy or ovariectomy, the expression of ICAM-1, CXCL12 and P-selectin mRNA in the examined organs increased, except JAM-1 in male and CXCL12 in female. Sex hormone treatment recovered the changes to normal levels of mRNA expression in many examined genital tissues. In combination with our previous work, preferential migration of ASCs into female genital tract and regulation of migration by sex hormones are associated with expression patterns of adhesion molecules and chemokines in genital tract rather than in ASCs.
Yu
Mingcan
M
Laboratory for Molecular and Cell Immunology, Kunming Institute of Zoology, The Chinese Academy of Sciences, Kunming, Yunnan 650223, China.
Cao
Xiaomei
X
Wang
Xiaolei
X
Xu
Jinju
J
Yang
Min
M
Ben
Kunlong
K
D000818:Animals; D000921:Antibody-Producing Cells / Q000502:physiology*; D015815:Cell Adhesion Molecules / Q000276:immunology / Q000378:metabolism* / Q000502:physiology; D002465:Cell Movement; D054377:Chemokine CXCL12; D018925:Chemokines / Q000378:metabolism*; D019743:Chemokines, CXC / Q000378:metabolism; D004958:Estradiol / Q000494:pharmacology / Q000502:physiology; D005260:Female; D015870:Gene Expression; D005836:Genitalia, Female / Q000276:immunology / Q000502:physiology*; D005837:Genitalia, Male / Q000276:immunology / Q000502:physiology*; D012739:Gonadal Steroid Hormones / Q000494:pharmacology*; D006825:Hybridomas / Q000276:immunology / Q000502:physiology; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D008297:Male; D051379:Mice; D011374:Progesterone / Q000494:pharmacology / Q000502:physiology; D013739:Testosterone / Q000494:pharmacology; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
D015815:Cell Adhesion Molecules; D054377:Chemokine CXCL12; D018925:Chemokines; D019743:Chemokines, CXC; C515256:Cxcl12 protein, mouse; D012739:Gonadal Steroid Hormones; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D013739:Testosterone; D011374:Progesterone; D004958:Estradiol