The impact of granulocyte colony-stimulating factor (G-CSF) on thin endometrium of an animal model with rats

Işık, Gizem; Öktem, M.; Güler, İsmail; Öktem, Emel Özalp; Özoğul, Candan; Sarıbaş, Sanem; Erdem, Ahmet; Erdem, Mehmet

doi:10.1080/09513590.2020.1786508

Cited by 12 publications

(4 citation statements)

References 20 publications

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“…G-CSF significantly increases EMT in TE rats and may improve endometrial tolerance by stimulating endometrial proliferation and neovascularization ( 79 , 80 ).…”

Section: Te Treatmentsmentioning

confidence: 99%

New advances in the treatment of thin endometrium

Wang,

Tang,

Teng

2024

Front. Endocrinol.

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Thin endometrium (TE) is defined as a mid-luteal endometrial thickness ≤7mm. TE can affect endometrial tolerance, leading to lower embryo implantation rates and clinical pregnancy rates, and is also associated with impaired outcomes from assisted reproductive treatment. Herein, we systematically review TE causes, mechanisms, and treatments. TE pathogenesis has multiple causes, with the endometrium becoming thinner with age under hormonal influence. In addition, uterine cavity factors are important, as the inflammatory environment may affect expressions of certain genes thereby inhibiting endometrial stromal cell proliferation and promoting apoptosis. Long-term oral contraceptive use or the use of ovulation-promoting drugs are also definite factors contributing to endometrial thinning. Other patients have primary factors, for which the clinical etiology remains unknown. The main therapeutic strategies available for TE are pharmacological (including hormonal and vasoactive drugs), regenerative medicine, intrauterine infusion of growth factor-granulocyte colony-stimulating factor, autologous platelet-rich plasma, and complementary alternative therapies (including traditional Chinese herbal medicine and acupuncture). However, the associated mechanisms of action are currently unclear. Clinical scholars have proposed various approaches to improve treatment outcomes in patients with TE, and are exploring the principles of efficacy, offering potentials for novel treatments. It is hoped that this will improve TE tolerance, increase embryo implantation rates, and help more couples with infertility with effective treatments.

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“…G-CSF significantly increases EMT in TE rats and may improve endometrial tolerance by stimulating endometrial proliferation and neovascularization ( 79 , 80 ).…”

Section: Te Treatmentsmentioning

confidence: 99%

New advances in the treatment of thin endometrium

Wang,

Tang,

Teng

2024

Front. Endocrinol.

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“…We established an experimentally induced murine model with thin endometrium via intrauterine administration of 95% ethanol (EtOH), which was adopted and modified from previous reports [27,36,37]. For the validation of successful modeling, 95% EtOH was infused into one side of the mouse uterine horns and saline was infused into the other side of the horns for the control in mice, which were in the estrous cycle.…”

Section: Establishment Of An Etoh-induced Thin Endometrium Murine Modelmentioning

confidence: 99%

Intrauterine botulinum toxin A administration promotes endometrial regeneration mediated by IGFBP3-dependent OPN proteolytic cleavage in thin endometrium

Lee

Ahn

Koo³

et al. 2023

Cell. Mol. Life Sci.

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Adequate endometrial growth is a critical factor for successful embryo implantation and pregnancy maintenance. We previously reported the efficacy of intrauterine administration of botulinum toxin A (BoTA) in improving the endometrial angiogenesis and the rates of embryo implantation. Here, we further evaluated its potent therapeutic effects on the uterine structural and functional repair and elucidated underlying molecular regulatory mechanisms. This study demonstrated that a murine model of thin endometrium was successfully established by displaying dramatically decreased endometrial thickness and the rates of embryo implantation compared to normal endometrium. Interestingly, the expressions of insulin-like growth factor binding protein-3 (IGFBP3) and an active 35 kDa-form of osteopontin (OPN) were significantly reduced in thin endometrium, which were almost fully restored by intrauterine BoTA administration. Neutralization of BoTA-induced IGFBP3 subsequently suppressed proteolytic cleavage of OPN, exhibiting un-recovered endometrial thickness even in the presence of BoTA administration, suggesting that BoTA-induced endometrial regeneration might be mediated by IGFBP3-dependent OPN proteolytic cleavage. Our findings suggest that intrauterine BoTA administration improves the endometrial environment in our murine model with thin endometrium by increasing endometrial receptivity and angiogenesis in a manner dependent on the regulatory effect of IGFBP3 on OPN proteolytic cleavage, proposing BoTA as an efficient therapeutic strategy for the patients with thin endometrium.

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“…, and Ki-67. VEGF (vascular endothelial growth factor) was reported to promote the increase of vascular permeability, degeneration of extracellular matrix, vascular endothelial cell migration, proliferation, and angiogenesis [32]. Matrix metalloproteinase 9 (MMP9) is a matrix metalloproteinase associated with extracellular matrix degradation.…”

Section: Mrna Expression Of Vegf Mmp9mentioning

confidence: 99%

Human Acellular Amniotic Matrix with Previously Seeded Umbilical Cord Mesenchymal Stem Cells Restores Endometrial Function in a Rat Model of Injury

Wang

Shi

Cai

et al. 2021

Mediators of Inflammation

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Background. Abnormal endometrial repair after injury results in the formation of intrauterine adhesions (IUA) and a thin endometrium, which are key causes for implantation failure and infertility. Stem cell transplantation offers a potential alternative for some cases of severe Asherman’s syndrome that cannot be treated with surgery or hormonal therapy. Umbilical cord-derived mesenchymal stem cells (UCMSCs) have been reported to repair the damaged endometrium. However, there is no report on the effects of UCMSCs previously seeded on human acellular amniotic matrix (AAM) on endometrial injury. Methods. Absolute ethanol was injected into rat uteri to damage the endometrium. UCMSCs previously seeded on AAM were surgically transplanted. Using a variety of methods, the treatment response was assessed by endometrial thickness, endometrial biomarker expression, endometrial receptivity, cell proliferation, and inflammatory factors. Results. Endometrial thickness was markedly improved after UCMSC-AAM transplantation. The expression of endometrial biomarkers, namely, vimentin, cytokeratin, and integrin β3, in treated rats increased compared with untreated rats. In the UCMSC-AAM group, the VEGF expression decreased, whereas that of MMP9 increased compared with the injury group. Moreover, in the AAM group, the MMP9 expression increased. The expression of proinflammatory factors (IL-2, TNFα, and IFN-γ) in the UCMSC-AAM group decreased compared with the untreated group, whereas the expression of anti-inflammatory factors (IL-4, IL-10) increased significantly. Conclusions. UCMSC transplantation using AAM as the carrier can be applied to treat endometrial injury in rats. The successful preparation of lyophilized AAM provides the possibility of secondary infectious disease screening and amniotic matrix quality detection, followed by retrospective analysis. The UCMSC-AAM complex may promote the better application of UCMSCs on the treatment of injured endometrium.

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The impact of granulocyte colony-stimulating factor (G-CSF) on thin endometrium of an animal model with rats

Cited by 12 publications

References 20 publications

New advances in the treatment of thin endometrium

New advances in the treatment of thin endometrium

Intrauterine botulinum toxin A administration promotes endometrial regeneration mediated by IGFBP3-dependent OPN proteolytic cleavage in thin endometrium

Human Acellular Amniotic Matrix with Previously Seeded Umbilical Cord Mesenchymal Stem Cells Restores Endometrial Function in a Rat Model of Injury

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