Expression of mRNA for Cell Adhesion Molecules in the Bovine Corpus Luteum During the Estrous Cycle and PGF2.ALPHA.-Induced Luteolysis

Abstract

Abstract. Cell-to-cell interaction via cell contact-dependent pathway is essentially important for maintenance and regulation of corpus luteum (CL) integrity and its physiological actions. The objective of the present study was to evaluate the mRNA expression of the cell adhesion molecules (CAMs) that are constituent factors of gap junctions [connexin (Cx) 43] and adherence junctions (VE-, E-, N-cadherin) in two types of endothelial cells from the mid CL and in CL tissue during the estrous cycle and PGF2α-induced luteolysis in the cow. Specific mRNA expression for Cx43 and N-cadherin was detected in cytokeratin-positive (CK+) and cytokeratin-negative (CK-) luteal endothelial cells (EC) and fully luteinized granulosa cells (LGC). E-cadherin mRNA was expressed in CK+EC andLGC, but not in CK-EC. VE-cadherin mRNA was expressed in both CK+ and CK-EC. During the estrous cycle, Cx43 mRNA expression was significantly lower in the regressing CL. VE-cadherin expression also tended to increase in the mid CL and increased significantly in the regressing CL. Ecadherin mRNA expression was higher in the early and late CL than in the mid-and regressing CL. N-cadherin mRNA expression gradually increased from the early to late CL followed by a decrease in the regressing CL. During PGF2α-induced luteolysis, Cx43 mRNA expression appeared to increase, and VE-cadherin and E-cadherin mRNA significantly increased at 24 h. N-cadherin mRNA expression decreased 2 and 4 h after PGF2α administration. Collectively, expression of the mRNAs for CAMs was different in the two types of luteal endothelial cells and fully luteinized granulosa cells and changed independently in the CL during the estrous cycle and PGF2α-induced luteolysis in the cow. The results suggest that CAMs play physiological roles in cell-to-cell communication to regulate both gap and adherence junctions during CL development and regression in the cow. Key words: Cadherin, Connexin, Corpus luteum, Cow, Luteolysis (J. Reprod. Dev. 53: [1319][1320][1321][1322][1323][1324][1325][1326][1327][1328] 2007) he corpus luteum (CL) is a transient organ that secretes progesterone (P), which is a prerequisite for establishment and maintenance of pregnancy. The CL is formed from the residual cells of a follicle after ovulation, in which cell growth and differentiation occur together with neoangiogenesis, and the CL acquires the capacity to secrete P. If pregnancy does not occur, prostaglandin (PG) F 2α is released from the uterus [1,2], and the CL rapidly looses its P secretory ability (functional luteolysis) [1,2]. Subsequently, its

TGFB1 disrupts the angiogenic potential of microvascular endothelial cells of the corpus luteum

“…The bovine corpus luteum contains multiple endothelial cell populations that differ in their morphology, cytoskeleton proteins and expression of cell adhesion proteins (reviewed in Davis et al, 2003). The CLENDO cells used in the present study, which are cytokeratin negative and VE-cadherin positive, presumptively represent the majority of luteal microvascular endothelial cells (Ricken et al, 1995;Shirasuna et al, 2007;Tscheudschilsuren et al, 2002). It is possible that, as in the examples cited above, subpopulations of luteal endothelial cells respond to TGFB1 in a manner different from that of our CLENDO cells.…”

“…In response to vascular damage, endothelial cells retract, increasing the permeability of the vessel, and as a result the vessel is disrupted (Dejana et al, 2008). Bovine endothelial cells express VE-cadherin (Shirasuna et al, 2007), which forms part of adherens junction complexes with proteins p120, -catenin and plakoglobin. Our results indicate that the exposure of confluent CLENDO cells to TGFB1 resulted in the loss of VE-cadherin from cellular junctions.…”

Patterns of Gene Expression in the Bovine Corpus Luteum Following Repeated Intrauterine Infusions of Low Doses of Prostaglandin F2alpha1

“…Many studies [14][15][16][17][18][19][20] have also investigated luteal regression by using a single injection of a supraphysiological dose of PGF. A single high dose of PGF suppressed steadystate concentrations of mRNA for specific genes that might have been involved in ''luteotropic'' functions, whereas there was an induction of mRNA for genes that might have been involved in functional or structural luteolysis [15,16,[20][21][22][23]. For example, treatment with PGF decreased VEGFA, STAR, PTGFR, and LHCGR mRNA concentrations, but the same PGF treatments increased FAS, FASLG, TNF, IL1B, IFNG, EDN1, MMP1, and PGTS2 mRNA concentrations [15,16,20,[22][23][24].…”

“…A single high dose of PGF suppressed steadystate concentrations of mRNA for specific genes that might have been involved in ''luteotropic'' functions, whereas there was an induction of mRNA for genes that might have been involved in functional or structural luteolysis [15,16,[20][21][22][23]. For example, treatment with PGF decreased VEGFA, STAR, PTGFR, and LHCGR mRNA concentrations, but the same PGF treatments increased FAS, FASLG, TNF, IL1B, IFNG, EDN1, MMP1, and PGTS2 mRNA concentrations [15,16,20,[22][23][24]. Not surprisingly, molecular changes were not always consistent when results of studies of CL during natural luteolysis were compared to those of luteolysis induced by a single large PGF treatment.…”

Effects of Latanoprost and Bimatoprost on the Expression of Molecules Relevant to Ocular Inflow and Outflow Pathways

“…However, a number of previous studies showed that PGAs were not able to decrease aqueous humor formation, and indeed might increase it slightly [ 15 , 48 ]. We hypothesized that PGAs might also regulate other aqueous humor formation related proteins such as cystic fibrosis transmembrane conductance regulator [ 49 , 50 ] or connexin43 [ 51 , 52 ], which could counteract the effect of a reduction in AQP1.…”