Embryo implantation is one of the earliest and critical events of the mammalian reproduction.1 A clinical association between implantation failure and thyroid dysfunction has been extensively reported, although the molecular mechanism governing this correlation has not been elucidated yet. TH machinery is expressed in the feto-maternal unit at the time of implantation, suggesting a locaI action of TH. We have investigated the role of TH in mouse hatching and outgrowth, since dysregulation of these events induces implantation failure, leading to infertility.2 Mouse blastocysts were cultured on a feeder-layer of primary endometrial cells or on plastic, with or without TH supplementation, and hatching and outgrowth evaluated. TH stimulation was also studied on endometrial cell cultures without blastocysts. By qRT-PCR, the expression of two proteases involved in blastocyst hatching in mice (Ispl and Isp2 3,4) and MMPS was studied. TH supplementation significantly increased the number of hatching blastocysts cultured on the endometrial cells, while had limited effect on blastocysts cultured on plastic. Ispl and Isp2 were significantly up-regulated in both blastocysts and endometrial cells, independently analyzed after an overnight coculture with TH; a less pronounced effect was observed in both blastocysts and endometrial cells cultured alone. TH also induced a significant upregulation of several MMPs in endometrial cells, independently from the presence of the blastocysts, although the coculture induced a much higher increase. TH also significantly increased the expansion of trophectodermal cells in both culture conditions, however expansion was more pronounced in the presence of the endometrial feeder layer. TH plays a key role in the bidirectional crosstalk between the competent blastocyst and the receptive endometrium at the time of implantation. TH supplementation may improve implantation success. 1. Zhang S et al. Mol Aspects Med 2013,34;939 2. Petersen CG et al. Reprod Biomed Online 2005, 10;24 3. O'Sullivan CM et al. Mol Reprod Devel 2002, 62; 328 4. Sharma et al. BMC Dev Biol 2006, 6;61
Thyroid hormone-regulated molecular mechanisms driving mouse blastocyst implantation / Campagnolo, Luisa; Piccirilli, Diletta; Massimiani, Micol; Baldini, Enke; Ulisse, Salvatore; Moretti, Costanzo. - In: EUROPEAN JOURNAL OF HISTOCHEMISTRY. - ISSN 1121-760X. - STAMPA. - 61 (Suppl. 1):(2017), pp. 6-7. (Intervento presentato al convegno 63rd Congress of the Italian Embryologival Group tenutosi a Rome nel 12-15 June 2017).
Thyroid hormone-regulated molecular mechanisms driving mouse blastocyst implantation
BALDINI, ENKE;ULISSE, SALVATORE;
2017
Abstract
Embryo implantation is one of the earliest and critical events of the mammalian reproduction.1 A clinical association between implantation failure and thyroid dysfunction has been extensively reported, although the molecular mechanism governing this correlation has not been elucidated yet. TH machinery is expressed in the feto-maternal unit at the time of implantation, suggesting a locaI action of TH. We have investigated the role of TH in mouse hatching and outgrowth, since dysregulation of these events induces implantation failure, leading to infertility.2 Mouse blastocysts were cultured on a feeder-layer of primary endometrial cells or on plastic, with or without TH supplementation, and hatching and outgrowth evaluated. TH stimulation was also studied on endometrial cell cultures without blastocysts. By qRT-PCR, the expression of two proteases involved in blastocyst hatching in mice (Ispl and Isp2 3,4) and MMPS was studied. TH supplementation significantly increased the number of hatching blastocysts cultured on the endometrial cells, while had limited effect on blastocysts cultured on plastic. Ispl and Isp2 were significantly up-regulated in both blastocysts and endometrial cells, independently analyzed after an overnight coculture with TH; a less pronounced effect was observed in both blastocysts and endometrial cells cultured alone. TH also induced a significant upregulation of several MMPs in endometrial cells, independently from the presence of the blastocysts, although the coculture induced a much higher increase. TH also significantly increased the expansion of trophectodermal cells in both culture conditions, however expansion was more pronounced in the presence of the endometrial feeder layer. TH plays a key role in the bidirectional crosstalk between the competent blastocyst and the receptive endometrium at the time of implantation. TH supplementation may improve implantation success. 1. Zhang S et al. Mol Aspects Med 2013,34;939 2. Petersen CG et al. Reprod Biomed Online 2005, 10;24 3. O'Sullivan CM et al. Mol Reprod Devel 2002, 62; 328 4. Sharma et al. BMC Dev Biol 2006, 6;61I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.