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Last update 08 May 2025

MFGE8

Last update 08 May 2025

Basic Info

Synonyms

BA46, Breast epithelial antigen BA46, EDIL1

+ [14]

Introduction

Plays an important role in the maintenance of intestinal epithelial homeostasis and the promotion of mucosal healing. Promotes VEGF-dependent neovascularization (By similarity). Contributes to phagocytic removal of apoptotic cells in many tissues. Specific ligand for the alpha-v/beta-3 and alpha-v/beta-5 receptors. Also binds to phosphatidylserine-enriched cell surfaces in a receptor-independent manner. Zona pellucida-binding protein which may play a role in gamete interaction. Main constituent of aortic medial amyloid.

Drugs associated with MFGE8

Mfge8(Empire)

Target

MFGE8

Mechanism

MFGE8 modulators

Active Org.

Empire Biotechnologies, Inc.

Originator Org.

Empire Biotechnologies, Inc.

Active Indication

Enterocolitis, Necrotizing

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

RM026

Target

MFGE8

Mechanism

MFGE8 inhibitors

Active Org.

Zhejiang University

Originator Org.

Zhejiang University

Active Indication

Breast Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

rhMFG-E8

Target

MFGE8

Mechanism

MFGE8 modulators

Active Org.

TheraSource LLC

Originator Org.

TheraSource LLC

Active Indication

Radiation Injuries

Inactive Indication

Acute Kidney Injury [+2]

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MFGE8

100 Translational Medicine associated with MFGE8

0 Patents (Medical) associated with MFGE8

1,211

Literatures (Medical) associated with MFGE8

01 Jun 2025·Life Sciences

BTN3A2 interacted with MFGE8 to alleviate preeclampsia by promoting ferroptosis and inhibiting angiogenesis

Article

Author: Wang, Qi ; Li, Ping ; Hu, Caihong ; Yong, Wenjing ; Yuan, Xi

AIMSPreeclampsia (PE) is a major cause of maternal and perinatal morbidity and mortality and is characterized by placental ischemia. Angiogenic disorders and ferroptosis are key mechanisms in PE; however, their relationship remains unclear. The butyrophilin 3A (BTN3A) family member BTN3A2 is involved in the progression of many cancers; however, its role in PE angiogenesis and ferroptosis is unclear. In this study, we investigated the role of BTN3A2 in PE angiogenesis and ferroptosis.MATERIALS AND METHODSPlacental tissues were collected from healthy individuals and PE patients to explore the correlation between ferroptosis and angiogenesis. Human umbilical vein endothelial cells (HUVECs) were subjected to hypoxia, ferrostatin-1, Erastin, and gene manipulations (oe-BTN3A2, si-BTN3A2, and si-milk factor-globule-EFG factor 8 (MFGE8)) to elucidate the underlying mechanisms. Finally, a rat model of PE was established by intraperitoneal injection of Nomega-nitro-L-arginine methyl ester to verify the effects of BTN3A2 on angiogenesis.KEY FINDINGSPlacental ferroptosis was negatively correlated with angiogenesis in PE. Clone number, migration, and tube number decreased in HUVECs after hypoxic exposure, and these effects were reversed by ferrostatin-1. BTN3A2 was increased in PE placentae and inhibited the viability of hypoxic HUVECs by inducing ferroptosis. Mechanistically, BTN3A2 interacted with MFGE8, and BTN3A2 promoted hypoxia-induced ferroptosis in HUVECs by downregulating MFGE8. Additionally, BTN3A2 knockdown promoted placental angiogenesis and improved the prognosis in PE rats.SIGNIFICANCEBTN3A2 interacted with MFGE8 to alleviate PE by promoting ferroptosis and inhibiting angiogenesis. Therefore, it may serve as a potential therapeutic target for the diagnosis and treatment of PE.

01 Jun 2025·Journal of Controlled Release

A fusion protein that targets antigen-loaded extracellular vesicles to B cells enhances antigen-specific T cell expansion

Article

Author: Steiner, Loïc ; Gucluler Akpinar, Gozde ; Vader, Pieter ; Wiklander, Oscar P B ; Eldh, Maria ; Mamand, Doste ; Kooijmans, Sander ; Käll, Alexander ; El-Andaloussi, Samir ; Weissinger, Hannah ; Offens, Annemarijn ; Gabrielsson, Susanne ; Teeuwen, Loes ; Karlsson, Mikael C I

Extracellular vesicles (EVs) have the potential to modulate immune responses via their cargo molecules and are being explored as vehicles in cancer immunotherapy. Dendritic cell-derived EVs can induce antigen-specific immune responses leading to reduced tumor burden. This response was shown to depend partially on B cells. EVs can be targeted to certain cells or tissues, and EVs from Epstein-Barr Virus (EBV) infected cells were shown to carry the EBV glycoprotein GP350 on their surface and target human CD21 (hCD21) on B cells. We therefore investigated whether targeting EVs to B cells via this mechanism could improve antigen-specific immune responses. A soluble fusion protein containing the phosphatidylserine-binding domain (C1C2) of lactadherin and hCD21-binding domain (D123) of GP350 was used to decorate and target EVs to B cells. D123-decorated EVs increased in vitro B cell targeting 5-fold compared to EVs decorated with a non-targeting control protein or undecorated EVs. Furthermore, in vivo, D123-decoration did not alter the biodistribution of EVs across organs but specifically targeted them to B cells in the spleen, blood and lymph nodes of hCD21-transgenic mice. Immunization with hCD21-targeted, OVA-loaded EVs resulted in a higher percentage of antigen-specific CD8⁺ T cells compared to untargeted EVs. Our data show that D123-decorated EVs efficiently target B cells and improve antigen-specific T cell responses in vivo, which could be explored in future therapeutic applications.

01 May 2025·Journal of Ethnopharmacology

Xin-shu-bao tablets ameliorates ventricular remodeling against HFrEF via PPARγ/MFGE8 pathway based on MALDI-MSI and lipidomics

Article

Author: Zhang, Ying ; Xiao, Honghe ; Yang, Hongjun ; Li, Zhenkun ; Yang, Jicheng ; Zhang, Fengrong ; Li, Xianyu

ETHNOPHARMACOLOGICAL RELEVANCEXin-shu-bao tablets (XSB), a traditional Chinese medicine widely prescribed in China, have received approval for its role in enhancing cardiac function in coronary heart disease patients. Lipid metabolism plays a critical role in the onset and progression of ventricular remodeling in heart failure with reduced ejection fraction (HFrEF). However, the pharmacological mechanisms through which XSB influences lipid metabolism in the context of ventricular remodeling with HFrEF have yet to be elucidated.AIM OF THE STUDYThe aim of the present study was to explore the potential of XSB as an inhibitor of ventricular remodeling in patients with HFrEF and to uncover the mechanisms by which XSB exerts myocardial protection via lipid metabolism.MATERIALS AND METHODSTo investigate the cardioprotective effects of XSB on HFrEF following myocardial infarction (MI), a murine model of MI generated by ligating the left anterior descending artery. The myocardial protective effects of XSB were evaluated through histological analysis of cardiac tissue and quantification of serum biomarkers associated with myocardial injury. Cardiac fibrosis was assessed using Masson's trichrome staining and Western blot analysis. Apoptosis, efferocytosis, and inflammation were measured through TUNEL staining, WB, and q-PCR in myocardial tissues. Differentially expressed metabolites in the myocardium were identified using MALDI-MSI and lipidomics analysis. Additionally, the involvement of the PPARγ/MFGE8 pathway in the cardioprotective effects of XSB was explored using Western blot validation in heart tissues. These approaches collectively aimed to elucidate the underlying mechanisms by which XSB exerts its cardioprotective effects, particularly through lipid metabolism.RESULTSOur findings demonstrated that treatment with XSB significantly attenuated structural and functional cardiac impairments, as indicated by improvements in cardiac function and reductions in apoptosis, efferocytosis, inflammation, and cardiac fibrosis in myocardial tissues. Specifically, XSB markedly decreased the levels of pro-inflammatory cytokines, such as IL-6, IL-10, and TNF-α. Additionally, XSB downregulated the expression of apoptosis-related proteins BAX and Caspase-3, while increasing the expression of the anti-apoptotic protein Bcl-2. Metabolomic analyses using MALDI-MSI and lipidomics revealed that XSB suppressed the elevated levels of glycerol phospholipids, such as PC(16:1e_22:5), PI(18:0_20:4), PI(18:2_20:4), PC(16:0e_22:4), LPS(18:0), PI(16:0_18:2), PC(19:0_22:6), and PS(18:1_22:6) in myocardial tissues. Furthermore, XSB modulated the expression of key proteins associated with lipid metabolism, including upregulation of PPARγ and SLC27A1, and downregulation of MFGE8, MERTK, and GSN. These results suggest that XSB exerts its cardioprotective effects through modulation of lipid metabolism and related signaling pathways.CONCLUSIONSXSB demonstrate cardioprotective effects by improving cardiac function and modulating ventricular remodeling processes in mice with HFrEF. These processes involve attenuation of inflammation, apoptosis, efferocytosis, and cardiac fibrosis. The cardioprotective mechanisms of XSB are mediated through the regulation of lipid metabolism via the PPARγ/MFGE8 signaling pathway.

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MFGE8

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