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Estrogen Effects on Abdominal Skeletal Muscle Fibroblasts in Inguinal Hernia Mouse Model

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE226868 | GEO | 2025/03/19

REPOSITORIES: GEO

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Estrogen Effects on Abdominal Skeletal Muscle Fibroblasts in Inguinal Hernia Mouse Model [RNA-Seq]

Project description:Humanized aromatase mice spontaneously develop hernias caused by fibrosis of lower abdominal skeletal muscle. To understand the estrogen action leading to herniation, fibroblasts were isolated and cultured under estrogen-replete and deplete conditions.

2025-03-19 | GSE226867 | GEO

Estrogen Effects on Abdominal Skeletal Muscle Fibroblasts in Inguinal Hernia Mouse Model [ATAC-Seq]

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Estrogen Effects on Abdominal Skeletal Muscle Fibroblasts in Inguinal Hernia Mouse Model [ChIP-seq]

2025-03-19 | GSE226859 | GEO

Estrogen Effects on Abdominal Skeletal Muscle Fibroblasts in Inguinal Hernia Mouse Model

Project description:Estrogen Effects on Abdominal Skeletal Muscle Fibroblasts in Inguinal Hernia Mouse Model

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An estrogen-sensitive fibroblast population drives abdominal muscle fibrosis in an inguinal hernia mouse model.

Project description:Greater than 25% of all men develop an inguinal hernia in their lifetime, and more than 20 million inguinal hernia repair surgeries are performed worldwide each year. The mechanisms causing abdominal muscle weakness, the formation of inguinal hernias, or their recurrence are largely unknown. We previously reported that excessively produced estrogen in the lower abdominal muscles (LAMs) triggers extensive LAM fibrosis, leading to hernia formation in a transgenic male mouse model expressing the human aromatase gene (Aromhum). To understand the cellular basis of estrogen-driven muscle fibrosis, we performed single-cell RNA sequencing on LAM tissue from Aromhum and wild-type littermates. We found a fibroblast-like cell group composed of 6 clusters, 2 of which were validated for their enrichment in Aromhum LAM tissue. One of the potentially novel hernia-associated fibroblast clusters in Aromhum was enriched for the estrogen receptor-α gene (Esr1hi). Esr1hi fibroblasts maximally expressed estrogen target genes and seemed to serve as the progenitors of another cluster expressing ECM-altering enzymes (Mmp3hi) and to upregulate expression of proinflammatory, profibrotic genes. The discovery of these 2 potentially novel and unique hernia-associated fibroblasts may lead to the development of novel treatments that can nonsurgically prevent or reverse inguinal hernias.

| S-EPMC9090253 | biostudies-literature

Estrogen Effects on Abdominal Skeletal Muscle Fibroblasts in Inguinal Hernia Mouse Model [RNA-Seq]

Project description:Estrogen Effects on Abdominal Skeletal Muscle Fibroblasts in Inguinal Hernia Mouse Model [RNA-Seq]

| PRJNA941914 | ENA

Estrogen Effects on Abdominal Skeletal Muscle Fibroblasts in Inguinal Hernia Mouse Model [ATAC-Seq]

Project description:Estrogen Effects on Abdominal Skeletal Muscle Fibroblasts in Inguinal Hernia Mouse Model [ATAC-Seq]

| PRJNA941901 | ENA

Estrogen Effects on Abdominal Skeletal Muscle Fibroblasts in Inguinal Hernia Mouse Model [ChIP-seq]

Project description:Estrogen Effects on Abdominal Skeletal Muscle Fibroblasts in Inguinal Hernia Mouse Model [ChIP-seq]

| PRJNA941902 | ENA

Shift from androgen to estrogen action causes abdominal muscle fibrosis, atrophy, and inguinal hernia in a transgenic male mouse model.

Project description:Inguinal hernia develops primarily in elderly men, and more than one in four men will undergo inguinal hernia repair during their lifetime. However, the underlying mechanisms behind hernia formation remain unknown. It is known that testosterone and estradiol can regulate skeletal muscle mass. We herein demonstrate that the conversion of testosterone to estradiol by the aromatase enzyme in lower abdominal muscle (LAM) tissue causes intense fibrosis, leading to muscle atrophy and inguinal hernia; an aromatase inhibitor entirely prevents this phenotype. LAM tissue is uniquely sensitive to estradiol because it expresses very high levels of estrogen receptor-α. Estradiol acts via estrogen receptor-α in LAM fibroblasts to activate pathways for proliferation and fibrosis that replaces atrophied myocytes, resulting in hernia formation. This is accompanied by decreased serum testosterone and decreased expression of the androgen receptor target genes in LAM tissue. These findings provide a mechanism for LAM tissue fibrosis and atrophy and suggest potential roles of future nonsurgical and preventive approaches in a subset of elderly men with a predisposition for hernia development.

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A Unique Estrogen-Sensitive Cell Population Drives Abdominal Muscle Fibrosis in an Inguinal Hernia Mouse Model

Project description:We performed single cell analysis on lower abdominal muscle tissues in wild-type and a humanized aromatse mice with scrotal hernias

2022-05-11 | GSE174594 | GEO

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