Gonadal and nongonadal FSHR and LHR dysfunction during lipopolysaccharide induced failure of blastocyst implantation in mouse

Abstract

Purpose: The purpose of the present study was to investigate the impact of lipopolysaccharide (LPS) on follicle-stimulating hormone (FSH), luteinizing hormone (LH) and their receptors during preimplantation days of pregnancy.

Method: The PBS or lipopolysaccharide (LPS) was injected intraperitoneally in the pregnant females on day 0.5 of pregnancy and serum, embryos, ovaries and uterine horns were collected on days 1.5, 2.5, 3.5, 4.0, 4.125, 4.33 and 4.42 of pregnancy.

Result(s): In the LPS-treated pregnant females, the secretion of FSH and LH is disturbed with respect to normal pregnancy. Furthermore, the expression of FSHR mRNA in embryos and ovaries, LHR mRNA in embryos and uterus get modulated in response to LPS during preimplantation days of pregnancy.

Conclusion(s): The disturbance in the serum level of FSH and LH in response to LPS leads implantation failure in mouse which suggests that these gonadotropins plays an integral role in the process of the successful implantation. This study also suggests a possible nongonadal role of FSHR and LHR in LPS-induced implantation failure in the mouse.

Fig. 1

Level of FSH in serum during different preimplantation days of pregnancy in control and LPS-treated animals (n = 8 in each group). *P < 0.05, **P < 0.01 versus counterparts (based on Duncan’s multiple-range test). Values are expressed as the mean ± SEM

Fig. 2

Level of LH in serum during different preimplantation days of pregnancy in control and LPS-treated animals (n = 8 in each group). *P < 0.05, **P < 0.01 versus counterparts (based on Duncan’s multiple-range test). Values are expressed as the mean ± SEM

Fig. 3

Expression of FSHR and LHR transcripts in the mouse embryos collected from PBS (control) or LPS-treated animals. The FSHR, LHR and β-actin transcripts were detected by RT-PCR followed by nested PCR. FSHR (a) control (b) LPS-treated, LHR (c) control (d) LPS-treated, β-actin (e) control (f) LPS-treated, depicted is a representative figure from among three repeat experiments. Ratios of the relative signal intensities of (g) FSHR/β-actin and (h) LHR/β-actin are depicted (n = 15 in each group). *P < 0.05 versus counterparts (based on Duncan’s multiple-range test). Values are expressed as the mean ± SEM

Fig. 4

Expression of FSHR transcripts in the mouse uterus collected from PBS (control) or LPS-treated animals. The FSHR and β-actin transcripts were detected by RT-PCR. FSHR (a) control and LPS-treated, β-actin (b) control and LPS-treated, depicted is a representative figure from among three repeat experiments. (n = 12 in each group)

Fig. 5

Expression of FSHR transcripts in the mouse ovaries collected from PBS (control) or LPS-treated animals. The FSHR and β-actin transcripts were detected by RT-PCR. FSHR (a) control (b) LPS-treated, β-actin (c) control (d) LPS-treated, depicted is a representative figure from among three repeat experiments. Ratios of the relative signal intensities of (e) FSHR/β-actin is depicted (n = 12 in each group). *P < 0.05 versus counterparts (based on Duncan’s multiple-range test). Values are expressed as the mean ± SEM

Fig. 6

Expression of LHR transcripts in the mouse uterus collected from PBS (control) or LPS-treated animals. The LHR and β-actin transcripts were detected by RT-PCR. LHR (a) control (b) LPS-treated, β-actin (c) control (d) LPS-treated, depicted is a representative figure from among three repeat experiments. Ratios of the relative signal intensities of (e) LHR/β-actin is depicted (n = 12 in each group). *P < 0.05 versus counterparts (based on Duncan’s multiple-range test). Values are expressed as the mean ± SEM