AMH protects the ovary from doxorubicin by regulating cell fate and the response to DNA damage

N Ngoc Minh Phuong Nguyen (Pediatric Surgical Research Laboratories, Massachusetts General Hospital) E Eun Mi Chang (Pediatric Surgical Research Laboratories, Massachusetts General Hospital) M Maëva Chauvin N Natalie Sicher (Pediatric Surgical Research Laboratories, Massachusetts General Hospital) A Aki Kashiwagi (Pediatric Surgical Research Laboratories, Massachusetts General Hospital) N Nicholas Nagykery (Pediatric Surgical Research Laboratories, Massachusetts General Hospital) C Christina Chow (Pediatric Surgical Research Laboratories, Massachusetts General Hospital) P Phoebe May (Pediatric Surgical Research Laboratories, Massachusetts General Hospital) A Alana Mermin-Bunnell (Pediatric Surgical Research Laboratories, Massachusetts General Hospital) J Josephine Cleverdon (Pediatric Surgical Research Laboratories, Massachusetts General Hospital) T Thy Duong (Pediatric Surgical Research Laboratories, Massachusetts General Hospital) M Motohiro Kano (Pediatric Surgical Research Laboratories, Massachusetts General Hospital) P Philippe Godin (Pediatric Surgical Research Laboratories, Massachusetts General Hospital) M Marie-Charlotte Meinsohn (Pediatric Surgical Research Laboratories, Massachusetts General Hospital) D Dadi Gao (Department of Neurology, Massachusetts General Hospital and Harvard Medical School) P Patricia K. Donahoe (Pediatric Surgical Research Laboratories, Massachusetts General Hospital) D David Pépin

Abstract

Anti-Müllerian hormone (AMH) protects the ovarian reserve from chemotherapy, and this effect is most pronounced with Doxorubicin (DOX). However, DOX toxicity and AMH rescue mechanisms in the ovary have remained unclear. Herein, we characterize the consequences of these treatments in ovarian cell types using scRNAseq. DOX-induced DNA damage activates Tp53 class mediators across ovarian cell types. In the mesenchyme, cotreatment with AMH halts theca progenitor differentiation and reduces apoptotic gene expression. In preantral granulosa cells, DOX upregulates the cell cycle inhibitor Cdkn1a and dysregulates Wnt signaling, which are ameliorated by AMH cotreatment. Finally, AMH induces Id3 , a gene involved in DNA repair, which is necessary to prevent the accumulation of DNA lesions marked by γ-H2AX. Altogether these mechanisms of AMH protection contribute to sustained fertility in mice, offering promising broad avenues for fertility preservation in cancer patients undergoing chemotherapy.

Article Details

Volume / Issue Vol. 122, Issue 5
Published February 04, 2025
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (17)

N

Ngoc Minh Phuong Nguyen

Pediatric Surgical Research Laboratories, Massachusetts General Hospital

E

Eun Mi Chang

Pediatric Surgical Research Laboratories, Massachusetts General Hospital

M

Maëva Chauvin

N

Natalie Sicher

Pediatric Surgical Research Laboratories, Massachusetts General Hospital

A

Aki Kashiwagi

Pediatric Surgical Research Laboratories, Massachusetts General Hospital

N

Nicholas Nagykery

Pediatric Surgical Research Laboratories, Massachusetts General Hospital

C

Christina Chow

Pediatric Surgical Research Laboratories, Massachusetts General Hospital

P

Phoebe May

Pediatric Surgical Research Laboratories, Massachusetts General Hospital

A

Alana Mermin-Bunnell

Pediatric Surgical Research Laboratories, Massachusetts General Hospital

J

Josephine Cleverdon

Pediatric Surgical Research Laboratories, Massachusetts General Hospital

T

Thy Duong

Pediatric Surgical Research Laboratories, Massachusetts General Hospital

M

Motohiro Kano

Pediatric Surgical Research Laboratories, Massachusetts General Hospital

P

Philippe Godin

Pediatric Surgical Research Laboratories, Massachusetts General Hospital

M

Marie-Charlotte Meinsohn

Pediatric Surgical Research Laboratories, Massachusetts General Hospital

D

Dadi Gao

Department of Neurology, Massachusetts General Hospital and Harvard Medical School

P

Patricia K. Donahoe

Pediatric Surgical Research Laboratories, Massachusetts General Hospital

D

David Pépin