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研究生:HO NGUYEN TUONG
研究生(外文):HO NGUYEN TUONG
論文名稱:ROLE OF OSTEOPONTIN IN HUMAN REPRODUCTION AND THE IMPACT OF GONADOTROPIN-RELEASING HORMONE AGONIST ON ENDOMETRIOSIS-RELATED INFERTILITY
論文名稱(外文):ROLE OF OSTEOPONTIN IN HUMAN REPRODUCTION AND THE IMPACT OF GONADOTROPIN-RELEASING HORMONE AGONIST ON ENDOMETRIOSIS-RELATED INFERTILITY
指導教授:高淑慧高淑慧引用關係曾啟瑞曾啟瑞引用關係
指導教授(外文):KAO, SHU-HUEITZENG, CHII-RUEY
口試委員:高淑慧曾啟瑞謝榮鴻張壯榮周雅菁
口試委員(外文):KAO, SHU-HUEITZENG, CHII-RUEYHSIEH, RONG-HONGCHANG, CHUANG-RUNGCHOU, YA-CHING
口試日期:2023-06-16
學位類別:博士
校院名稱:臺北醫學大學
系所名稱:國際醫學研究博士學位學程
學門:醫藥衛生學門
學類:醫學學類
論文種類:學術論文
論文出版年:2023
畢業學年度:111
語文別:英文
論文頁數:154
中文關鍵詞:OsteopontinGonadotropin-releasing hormone agonistEndometriosisImplantation
外文關鍵詞:OsteopontinGonadotropin-releasing hormone agonistEndometriosisImplantation
DOI:https://doi.org/10.3390/ijms232315328
ORCID或ResearchGate:https://orcid.org/0000-0002-6561-1596
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Osteopontin (OPN), an extracellular phosphorylated glycoprotein, was initially identified in the extracellular protein layer of bone tissue. Due to the capability of stimulating the expression of adhesion molecules and contributing to inflammation activity, OPN has been proposed to contribute to the process of implanting embryos. Our study demonstrates that OPN supplementation at an appropriate level can enhance mouse embryo development and implantation ability, via interacting with αvβ3 integrin and RGS2 pathway. In validation on in vitro trophoblast-like cells, OPN overexpression promoted migration and increased cell spheroid size via proliferation. Mouse embryos supplemented with OPN enhanced the potency for implantation in mice, which was then validated on spheroid adhesion assay with JAR cells. These findings suggest that OPN has the potential as a supplement in in vitro embryo culture to improve embryo implantation in embryology laboratory settings.
Additionally, an excessive expression of OPN and its isoforms was detected in the ectopic endometriosis tissue. The involvement of OPN and its isoforms in the pathogenesis of endometriosis was mediated through the PI3K and NF-ĸB signaling pathways. Notably, while OPNb was primarily implicated in enhanced cell proliferation, the selective overexpression of OPNc was strongly linked with a marked enhancement in migratory ability. Intriguingly, a decrease in both serum and tissue levels of OPN was observed following treatment with gonadotropin-releasing hormone agonist (GnRHa). OPN has manifested multifaceted roles across diverse biological contexts, exerting significant effects on both embryo implantation and the pathogenesis of endometriosis in women. Meanwhile, OPN has the potential of a target for endometriosis management, as well as a useful marker for monitoring treatment response in patients suffering from endometriotic diseases.
Based on the observation that OPN can be partially inhibited by GnRHa, we were further to verify whether GnRHa could mitigate the deleterious effects of endometriosis on female reproductive function. A retrospective study was conducted on infertile patients with ovarian endometriosis who were recommended for frozen embryo transfer (FET). The study revealed that patients who received GnRHa pretreatment exhibited improved pregnancy rates and embryo implantation outcomes.
Despite the favorable results, there is no consensus on the effectiveness of GnRHa pretreatment in the frozen-thawed embryo transfer (FET) cycles. Our objective was to investigate the impact of GnRHa on FET cycles, focusing on its effect on women with endometriosis in particular, as well as infertile women in general, through a systematic review and meta-analysis. The meta-analysis demonstrated that GnRHa pretreatment improved pregnancy outcomes of FET cycles in the patients undergoing FET, including embryo implantation and live birth rates, particularly when a long-term pituitary suppression strategy and depot GnRHa protocol were used.
In summary, this work has shed light on the multifaceted role of OPN in reproductive biology, including its involvement in embryonic implantation and endometriosis, as well as the potential benefits of using GnRHa in frozen-thawed embryo transfer (FET) cycles. The findings provide new insights into the underlying mechanisms of reproductive disorders and offer promising strategies for managing infertility in women with endometriosis and adenomyosis.

Osteopontin (OPN), an extracellular phosphorylated glycoprotein, was initially identified in the extracellular protein layer of bone tissue. Due to the capability of stimulating the expression of adhesion molecules and contributing to inflammation activity, OPN has been proposed to contribute to the process of implanting embryos. Our study demonstrates that OPN supplementation at an appropriate level can enhance mouse embryo development and implantation ability, via interacting with αvβ3 integrin and RGS2 pathway. In validation on in vitro trophoblast-like cells, OPN overexpression promoted migration and increased cell spheroid size via proliferation. Mouse embryos supplemented with OPN enhanced the potency for implantation in mice, which was then validated on spheroid adhesion assay with JAR cells. These findings suggest that OPN has the potential as a supplement in in vitro embryo culture to improve embryo implantation in embryology laboratory settings.
Additionally, an excessive expression of OPN and its isoforms was detected in the ectopic endometriosis tissue. The involvement of OPN and its isoforms in the pathogenesis of endometriosis was mediated through the PI3K and NF-ĸB signaling pathways. Notably, while OPNb was primarily implicated in enhanced cell proliferation, the selective overexpression of OPNc was strongly linked with a marked enhancement in migratory ability. Intriguingly, a decrease in both serum and tissue levels of OPN was observed following treatment with gonadotropin-releasing hormone agonist (GnRHa). OPN has manifested multifaceted roles across diverse biological contexts, exerting significant effects on both embryo implantation and the pathogenesis of endometriosis in women. Meanwhile, OPN has the potential of a target for endometriosis management, as well as a useful marker for monitoring treatment response in patients suffering from endometriotic diseases.
Based on the observation that OPN can be partially inhibited by GnRHa, we were further to verify whether GnRHa could mitigate the deleterious effects of endometriosis on female reproductive function. A retrospective study was conducted on infertile patients with ovarian endometriosis who were recommended for frozen embryo transfer (FET). The study revealed that patients who received GnRHa pretreatment exhibited improved pregnancy rates and embryo implantation outcomes.
Despite the favorable results, there is no consensus on the effectiveness of GnRHa pretreatment in the frozen-thawed embryo transfer (FET) cycles. Our objective was to investigate the impact of GnRHa on FET cycles, focusing on its effect on women with endometriosis in particular, as well as infertile women in general, through a systematic review and meta-analysis. The meta-analysis demonstrated that GnRHa pretreatment improved pregnancy outcomes of FET cycles in the patients undergoing FET, including embryo implantation and live birth rates, particularly when a long-term pituitary suppression strategy and depot GnRHa protocol were used.
In summary, this work has shed light on the multifaceted role of OPN in reproductive biology, including its involvement in embryonic implantation and endometriosis, as well as the potential benefits of using GnRHa in frozen-thawed embryo transfer (FET) cycles. The findings provide new insights into the underlying mechanisms of reproductive disorders and offer promising strategies for managing infertility in women with endometriosis and adenomyosis.

TABLE OF CONTENTS
DECLARATION i
ABSTRACT ii
ACKNOWLEDGEMENT iv
ABBREVIATIONS v
TABLE OF CONTENTS viii
LIST OF FIGURES xiii
LIST OF TABLES xv
CHAPTER 1: THE ROLE OF OSTEOPONTIN IN IN VITRO EMBRYONIC DEVELOPMENT AND IMPLANTATION POTENTIAL 1
1.1. Introduction 2
1.2.1. Osteopontin and its roles in reproduction 2
1.2.2. Embryo implantation physiology 4
1.2.3. Current understanding of the effect of osteopontin on embryo implantation process 5
1.2. Materials and methods 7
1.2.1. Chemicals 7
1.2.2. Mouse superovulation stimulation and embryo collection 7
1.2.3. Analysis of the effects of OPN on embryo hatching and implantation capability during in vitro culture 8
1.2.4. Culturing condition and transfection protocol for human syncytiotrophoblast-like JAR cell line 9
1.2.5. Analysis of the gene expression involved in the regulation of embryo implantation by OPN 10
1.2.6. The effect of OPN on migration ability of embryonic trophoblast cells: scratch wound assay 12
1.2.7. Spheroid formation and adhesion assay 12
1.2.8. Data analysis 13
1.3. Results 13
1.3.1. OPN improved hatching and implantation rate in mouse embryos 13
1.3.2. OPN regulated mouse embryo development and implantation via αvβ3 intergrin and RGS2 pathway 14
1.3.3. The effect of OPN on the migration ability of embryonic trophoblast JAR cells 16
1.3.4. OPN promoted the adhension ability of JAR spheroid in a three dimension co-culturing model 16
1.3.5. Validation of genes related to embrionic development and implantation in OPN overexpressed JAR cells 17
1.4. Discussion 18
1.5. Conclusion 22
1.6. Tables and figures 22
CHAPTER 2: OSTEOPONTIN AND ITS SPLICING ISOFORMS CONTRIBUTE TO ENDOMETRIOSIS PATHOGENESIS 35
2.1. Introduction 36
2.2. Materials and methods 38
2.2.1. Chemicals 38
2.2.2.. Sample collection 38
2.2.3. ELISA to measure OPN levels in body fluids 39
2.2.4. Endometrial epithelial cell culture 39
2.2.4. Overexpression of OPN isoforms by plasmid transfection in endometrial epithelial HEC1A cells 40
2.2.5. Scratch wound assay 40
2.2.6. Protocol for protein extraction and quantification 40
2.2.7. RNA extraction and RT‒PCR for gene expressions 41
2.2.8. siRNA transfection 42
2.2.9. Laser confocal microscopy 43
2.2.10. Cell proliferation assay 43
2.2.11. Statistical analysis 43
2.3. Results 44
2.3.1. Expressions of OPN isoforms, CD44 variants, and EMT markers differed in different types of endometriotic lesions 44
2.3.2. OPN variants mediated epithelial-mesenchymal transaction via inducing actin skeleton remodeling 46
2.3.3. OPN splice variants increased cell proliferation and migration via interacting with αvβ3 integrin and CD44 receptors in HEC1A endometriotic cells 47
2.3.4. OPN splice variants regulated the migration of HEC1A epithelial cells through the signaling pathways of PI-3k and NF-ĸB 47
2.4. Discussion 48
2.5. Conclusion 53
2.6. Tables and figures 53
CHAPTER 3: GONADOTROPIN RELEASING HORMONE AGONIST ADMINISTRATION PRIOR TO FROZEN-THAWED EMBRYO TRANSFER IMPROVES PREGNANCY OUTCOMES IN WOMEN WITH OVARIAN ENDOMETRIOSIS: EVIDENCE FROM A SINGLE-CENTER STUDY 64
3.1. Introduction 65
3.2.1. The influence of endometriosis on female fertility 65
3.2.2. Effect of pituitary down-regulation with gonadotropin-releasing hormone agonist (GnRHa) on endometriosis-related infertility 65
3.2. Methedology 66
3.2.1. Study design 66
3.2.2. Endometrial prepration protocol prior to FET 67
3.2.3. Embryo culture and grading 67
3.2.4. Outcome definitions 68
3.2.5. Statistical analysis 68
3.3. Results 68
3.3.1. Baseline characteristics of the studied populations 68
3.3.2. Pregnancy and neonatal outcomes of FET with and without GnRHa pretreatment 69
3.4. Discussion 69
3.5. Conclusion 72
1.6. Tables and figures 73
CHAPTER 4: THE EFFECTIVENESS OF GONADOTROPIN-RELEASING HORMONE AGONIST PRIOR TO FROZEN-THAWED EMBRYO TRANSFER: A SYSTEMATIC REVIEW AND META-ANALYSIS 76
4.1. Introduction 77
4.2. Materials and Methods 78
4.2.1. Search strategy and study selection 78
4.2.2. Population, intervention, comparison, outcomes, and study design (PICOS) 79
4.2.3. Systematic review protocol and registration 79
4.2.4. Data extraction 79
4.2.5. Data analysis 80
4.3. Results 80
4.3.1. Literature search and study selection 80
4.3.2. Study and participant characteristics 81
4.3.3. Main findings 81
4.4. Discussion 85
4.5. Conclusion 90
4.6. Tables and figures 90
CHAPTER 5: REFERENCES 121
Appendix I: Supplementary tables and figures 143
Appendix II: Publications and conference papers 152
LIST OF FIGURES
Figure 1.1: Flowchart of experimental design 23
Figure 1.2: Plasmid DNA vector pcDNA3.1 for transfection of OPN 24
Figure 1.3: Observations were made using a 200x microscope on embryos at various stages 25
Figure 1.4: Effects of OPN supplementation on the developmental ability and implantation
ability of mouse embryos 26
Figure 1.5: The interaction between OPN and αvβ3 integrin in regulating mouse embryonic development and implantation potential 27
Figure 1.6: Expression of Rgs2 in mouse embryos treated with recombinant OPN and αvβ3 integrin inhibitor 29
Figure 1.7: The effect of OPN on the migration of JAR cells 30
Figure 1.8: The effects of OPN on JAR spheroid size 32
Figure 1.9: OPN increased spheroid attachment to endometrial epithelial RL95-2 monolayer 33
Figure 1.10: Expression levels of genes related to embryonic development and implantation
Potential 34
Figure 2.1: Expression of OPN and OPN isoforms in endometriotic lesions 54
Figure 2.2: Differential expression of OPN ligand-receptor CD44s and its variant CD44v in endometriotic samples 55
Figure 2.3: EMT markers and cell adhesion molecules (CAM) in myoma, adenomyosis and ectopic endometriosis lesions 56
Figure 2.4: Real-time PCR was employed to determine the effectiveness of OPN isoform transfection and CD44 knockdown in HEC1A cells overexpressed OPN 57
Figure 2.5: Impact of OPN on actin filament remodeling of HEC1A cells and the expression of OPN ligand receptors or EMT markers 59
Figure 2.6: Changes in HEC1A cell migration mediated by OPN isoforms 60
Figure 2.7: The effect of OPN on cell proliferation in OPN-overexpressed HEC1A cells 61
Figure 2.8: The effect of OPN variants on HEC1A cell migration via the PI3K or NF-κB signaling pathway 62
Figure 2.9: Schematic illustration of the role of OPN isoforms in endometriosis pathogenesis 63
Figure 3.1: Multivariate logistic regression analysis for clinical pregnancy outcome and covariates 75
Figure 4.1: PRISMA flowchart 111
Figure 4.2: Summary of study quality assessment using the Effective Public Health Practice Project (EPHPP) quality assessment tool 112
Figure 4.3: Forest plots of meta-analysis for pregnancy outcomes following HRT-FET cycles with and without GnRHa pretreatment 113
Figure 4.4: Forest plots of meta-analysis for pregnancy outcomes following HRT-FET cycles with and without GnRHa pretreatment in PCOS patients 117
Figure 4.5: Forest plots of meta-analysis for pregnancy outcomes following HRT-FET cycles with and without GnRHa pretreatment in ovulatory women with reported regular cycles 118
Figure 4.6: Forest plots of meta-analysis for pregnancy outcomes following HRT-FET cycles with and without GnRHa pretreatment in women with adenomyosis. 119
Figure 4.7: Forest plots of meta-analysis for pregnancy outcomes following HRT-FET cycles with and without GnRHa pretreatment in women with endometriosis 120
LIST OF TABLES
Table 3.1: Baseline characteristics of the study population 73
Table 3.2: Outcomes of FET cycles with and without depot GnRHa pretreatment 74
Table 4.1. Detailed search strategy for electronic database searches 91
Table 4.2: Characteristics of the studies in the systematic review and meta-analysis 92
Table 4.3: Inclusion and exclusion criteria of the studies in the systematic review and meta-analysis 97
Table 4.4: Subgroup analyses of interested FET outcomes in women with and without GnRHa pretreatment 105
Table 4.5. Sensitive analysis for outcomes with publication biases in the general infertile population 109


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