Possible Involvement of CD10 in the Development of Endometriosis Due to Its Inhibitory Effects on CD44-Dependent Cell Adhesion

Iwase, Akira; Kotani, Tomomi; Goto, Maki; Kobayashi, Hiroharu; Takikawa, Sachiko; Nakahara, Tsutomu; Nakamura, Tomoko; Kondo, Mio; Bayasula,; Nagatomo, Yoshinari; Kikkawa, Fumitaka

doi:10.1177/1933719113488449

Cited by 13 publications

(15 citation statements)

References 41 publications

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“…Several research groups evaluated hyaluronic acid (HA) as a potential targeting ligand to the CD44 receptor, which was previously suggested to be overexpressed in endometriosis cells and human endometriotic lesions. [ 75,76 ] It was also revealed that CD44 expression in normal endometrium is detected only in the secretory but not in the proliferative phase, indicating hormonal regulation of this receptor. [ 77 ] Zhao et al.…”

Section: Accumulation Of Nanoparticles In Endometriosis Lesionsmentioning

confidence: 99%

Nanomedicines for Endometriosis: Lessons Learned from Cancer Research

Moses

Demessie

Taratula

et al. 2021

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Endometriosis is an incurable gynecological disease characterized by the abnormal growth of endometrium‐like tissue, characteristic of the uterine lining, outside of the uterine cavity. Millions of people with endometriosis suffer from pelvic pain and infertility. This review aims to discuss whether nanomedicines that are promising therapeutic approaches for various diseases have the potential to create a paradigm shift in endometriosis management. For the first time, the available reports and achievements in the field of endometriosis nanomedicine are critically evaluated, and a summary of how nanoparticle‐based systems can improve endometriosis treatment and diagnosis is provided. Parallels between cancer and endometriosis are also drawn to understand whether some fundamental principles of the well‐established cancer nanomedicine field can be adopted for the development of novel nanoparticle‐based strategies for endometriosis. This review provides the state of the art of endometriosis nanomedicine and perspective for researchers aiming to realize and exploit the full potential of nanoparticles for treatment and imaging of the disorder.

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Section: Accumulation Of Nanoparticles In Endometriosis Lesionsmentioning

confidence: 99%

Nanomedicines for Endometriosis: Lessons Learned from Cancer Research

Moses

Demessie

Taratula

et al. 2021

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“…17 CD44, which was identified as HA receptor, was found to be overexpressed in endometriotic cells. 18 Interestingly, there was no effect on binding characteristics of HA-treated endometrial cell to mesothelial cell, suggesting that endometrial cells might have a potential to bind to HA of surrounding tissue. 2 So, it is a powerful method to shield the positive charge of gene vectors with the targeting ligands (HA) in the guidance of the concept of receptor-mediated endocytosis, which was aimed at directing gene delivery to desired tissues.…”

Section: Introductionmentioning

confidence: 99%

“…The abnormal expression of CD44 in ectopic endometria suggests that CD44 might play a meaningful role in the pathogenesis of endometriosis, as described earlier. 18,25,26 The light micrographs and electron micrograph. Notes: (A) Light micrographs of endometrial lesions.…”

Section: The Endometrial Expression Of Cd44mentioning

confidence: 99%

Hyaluronic acid reagent functional chitosan-PEI conjugate with AQP2-siRNA suppressed endometriotic lesion formation

Zhao¹,

Cheng²,

Yan³

et al. 2016

IJN

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To identify a new drug candidate for treating endometriosis which has fewer side effects, a new polymeric nanoparticle gene delivery system consisting of polyethylenimine-grafted chitosan oligosaccharide (CSO-PEI) with hyaluronic acid (HA) and small interfering RNA (siRNA) was designed. There was no obvious difference in sizes observed between (CSO-PEI/siRNA)HA and CSO-PEI/siRNA, but the fluorescence accumulation in the endometriotic lesion was more significant for (CSO-PEI/siRNA)HA compared with CSO-PEI/siRNA due to the specific binding of HA to CD44. In addition, the (CSO-PEI/siRNA)HA nanoparticle gene therapy significantly decreased the endometriotic lesion sizes with atrophy and degeneration of the ectopic endometrium. The epithelial cells of ectopic endometrium from rat models of endometriosis showed a significantly lower CD44 expression than control after treatment with (CSO-PEI/siRNA)HA. Furthermore, observation under an electron microscope showed no obvious toxic effect on the reproductive organs. Therefore, (CSO-PEI/siRNA)HA gene delivery system can be used as an effective method for the treatment of endometriosis.

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“…It is generally accepted that the establishment and development of Ems require retrograde menstruation or endometrial fragments, which contain aberrantly activated of eutopic EScs. This is followed by the migration, invasion, implantation and proliferation of these EScs on the surface or inner part of pelvic tissues or organs, which occurs simultaneously with a controlled local inflammatory response and angiogenesis (44). Multiple studies have suggested that EScs in patients with Ems possess different properties compared with the EScs of healthy controls (45,46).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑16 inhibits endometrial stromal cell migration and invasion through suppression of the inhibitor of nuclear factor‑κB kinase subunit β/nuclear factor‑κB pathway

Wang

Ren²,

Shao

et al. 2020

Int J Mol Med

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Accumulating evidence has demonstrated that endometrial stromal cells (EScs) are responsible for the pathogenesis of endometriosis (Ems), which is characterized by the presence of functional endometrial-like tissues outside the uterine cavity. Abnormal expression of microRNAs (miRNAs) in EScs may be implicated in the etiology of Ems; however, the exact mechanisms have yet to be fully elucidated. The aim of the present study was to investigate the effects of miRNAs on EScs and the underlying mechanisms. Using a microarray assay, microRNA-16 (miR-16) was found to be significantly downregulated in the ectopic endometrial tissues in patients with Ems, compared with that in eutopic endometrial tissues. Overexpression of miR-16 significantly suppressed the migration and invasion of EScs, whereas miR-16 inhibition exerted the opposite effects. Furthermore, dual luciferase reporter assay demonstrated that miR-16 directly targeted the inhibitor of nuclear factor (NF)-κB kinase subunit β (IKKβ) and suppressed its translation. It was observed that the expression of IKKβ was upregulated and inversely correlated with miR-16 levels in the ectopic endometrial tissues in patients with Ems. Additionally, knockdown of IKKβ by si-IKKβ mimicked the effects of miR-16 overexpression on EScs, while the promoting effects of IKKβ overexpression on the migration and invasion of EScs were attenuated by miR-16 overexpression. Finally, miR-16 inhibited the activation of the NF-κB pathway by targeting IKKβ. collectively, these results demonstrated that miR-16 may suppress Ems by inhibiting the IKKβ/NF-κB pathway, suggesting that miR-16 may be a useful target in the treatment of Ems.

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Possible Involvement of CD10 in the Development of Endometriosis Due to Its Inhibitory Effects on CD44-Dependent Cell Adhesion

Cited by 13 publications

References 41 publications

Nanomedicines for Endometriosis: Lessons Learned from Cancer Research

Nanomedicines for Endometriosis: Lessons Learned from Cancer Research

Hyaluronic acid reagent functional chitosan-PEI conjugate with AQP2-siRNA suppressed endometriotic lesion formation

MicroRNA‑16 inhibits endometrial stromal cell migration and invasion through suppression of the inhibitor of nuclear factor‑κB kinase subunit β/nuclear factor‑κB pathway

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