Related Experiment Video
Updated: Sep 13, 2025

Isolation of Murine Peritoneal Macrophages to Carry Out Gene Expression Analysis Upon Toll-like Receptors Stimulation
Published on: April 29, 2015
Large Peritoneal Macrophages Promote the Resolution of Inflammation in Injured Endometrium
Jingman Li1, Lijie Yin1, Jiali Wang1
1The State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing, 210093, China.
Macrophages play a significant role in the repair of endometrial injuries. While large peritoneal macrophages (LPMs) have been reported to migrate to injured organs and repair tissues within the peritoneal cavity, their involvement in the repair of injured endometrium remains unclear. In this study, we utilize a mouse model of endometrial injury that does not involve laparotomy, a procedure that typically results in a substantial loss of LPMs. Strikingly, we find that LPMs reach the endometrium within 6 h post-modeling. By depleting or supplementing LPMs, our results reveal that these cells are capable of engulfing dead cells in the endometrium and resolving inflammation. Additionally, we observe that the migration efficiency of LPMs is enhanced with increased levels of 17β-estradiol (E2) in mice. In vitro assays further confirm that E2 accelerates the migration of LPMs towards apoptotic endometrial stromal cells. Overall, our findings demonstrate that LPMs rapidly migrate into injured endometrium in relation to E2 levels and facilitate the process of tissue repair.
Macrophages play a significant role in the repair of endometrial injuries. While large peritoneal macrophages (LPMs) have been reported to migrate to injured organs and repair tissues within the peritoneal cavity, their involvement in the repair of injured endometrium remains unclear. In this study, we utilize a mouse model of endometrial injury that does not involve laparotomy, a procedure that typically results in a substantial loss of LPMs. Strikingly, we find that LPMs reach the endometrium within 6 h post-modeling. By depleting or supplementing LPMs, our results reveal that these cells are capable of engulfing dead cells in the endometrium and resolving inflammation. Additionally, we observe that the migration efficiency of LPMs is enhanced with increased levels of 17β-estradiol (E2) in mice. In vitro assays further confirm that E2 accelerates the migration of LPMs towards apoptotic endometrial stromal cells. Overall, our findings demonstrate that LPMs rapidly migrate into injured endometrium in relation to E2 levels and facilitate the process of tissue repair.
More Related Videos
07:20Intraoperative Detection of Subtle Endometriosis: A Novel Paradigm for Detection and Treatment of Pelvic Pain Associated with the Loss of Peritoneal Integrity
Published on: December 21, 2012
05:40Author Spotlight: Studying Macrophage-Epithelial Cell Interactions in Salivary Gland Regeneration After Injury
Published on: November 17, 2023
Related Concept Videos
Inflammation
Inflammatory Response
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
Immune Surveillance by NK Cells and Phagocytes
Natural Killer Cells: The Fast Responders
NK cells are large granular lymphocytes found in the blood and lymphatic system. These...
Inflammatory Response I: Vascular and Cellular
Phagocytosis of Apoptotic Cells
Normal cells contain receptors that prevent them from being recognized...
Inflammatory Response II: Inflammatory Exudate and Tissue Repair
The typical wound exudate is odorless, transparent, straw-colored, thin, and watery. Exudate, however, can differ depending on the state of wound healing. Likewise, the...