자료유형  

 학위논문

Control Number  

0016934735

International Standard Book Number  

9798380151757

Dewey Decimal Classification Number  

610

Main Entry-Personal Name  

Ochoa Bernal, Maria Ariadna.

Publication, Distribution, etc. (Imprint  

[S.l.] : Michigan State University., 2023

Publication, Distribution, etc. (Imprint  

Ann Arbor : ProQuest Dissertations & Theses, 2023

Physical Description  

1 online resource(198 p.)

General Note  

Source: Dissertations Abstracts International, Volume: 85-02, Section: B.

General Note  

Advisor: Fazleabas, Asgi.

Dissertation Note  

Thesis (Ph.D.)--Michigan State University, 2023.

Restrictions on Access Note  

This item must not be sold to any third party vendors.

Summary, Etc.  

요약Endometriosis is one of the most common causes of chronic pelvic pain and infertility that affects 10% of women of reproductive age. A delay of up to 9 years is estimated between the onset of symptoms and the diagnosis of endometriosis. Endometriosis is currently defined as the presence of endometrial epithelial and stromal cells at ectopic sites, however, advances in the research of endometriosis has some authors believing that endometriosis should be re-defined as "a fibrotic condition in which endometrial stroma and epithelium can be identified." There are several theories on the etiology of the disease, but the origin of endometriosis remains unclear. MicroRNAs (miRNAs) are naturally occurring posttranscriptional regulatory molecules that potentially play a role in endometriotic lesion development. The presence of endometriotic lesions can alter miRNAs expression in both the eutopic endometrium and ectopic lesions. There is evidence that suggests that miRNAs, including miR-21, participate in the fibrotic process in different organs including the heart, kidney, liver and lungs. This dissertation has aimed to understand the role of miR-21, which is upregulated in endometriosis, and the mechanisms that can contribute to the development of fibrosis and lesion development in endometriosis. The studies have been focused on the mechanisms by which IL-6 regulates miR-21 and how this miRNA contributes to TGF-β signaling pathway by blocking Smad7, promoting fibrosis and lesion development. These studies collectively showed that inflammation and fibrosis are present at a very early stage of endometriosis. The inflammatory environment in the peritoneal cavity of women with endometriosis, which includes the cytokine IL-6, can regulate the expression of miR-21 in vitro and in vivo. The upregulation of miR-21 was correlated with the development of fibrosis during lesion progression of endometriosis, but other components may be also implicated during this process may contribute to the development of fibrosis. These studies also revealed that B cells could play an important role, however their function remains unknown and should be further investigated in the future. Future work should aim to understand the mechanisms that drive miR-21 to regulate fibrosis in endometriosis and the potential therapeutic mechanisms to treat the disease. In addition to this, further studies should also be focused on the role of B cells that would help to explain their function during the development of endometriosis and could potentially serve as suitable candidates for new therapeutic strategies. This could open up different and less invasive approaches for the treatment of women with endometriosis.

Subject Added Entry-Topical Term  

Medicine.

Subject Added Entry-Topical Term  

Physiology.

Subject Added Entry-Topical Term  

Public health.

Subject Added Entry-Topical Term  

Cellular biology.

Index Term-Uncontrolled  

Endometriosis

Index Term-Uncontrolled  

IL-6

Index Term-Uncontrolled  

Inflammation

Index Term-Uncontrolled  

MicroRNAs

Index Term-Uncontrolled  

Fibrosis

Added Entry-Corporate Name  

Michigan State University Animal Science- Doctor of Philosophy

Host Item Entry  

Dissertations Abstracts International. 85-02B.

Host Item Entry  

Dissertation Abstract International

Electronic Location and Access  

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Control Number  

joongbu:640431