AGGF1

Last update 23 Jan 2025

Basic Info

Synonyms

AGGF1, Angiogenic factor VG5Q, Angiogenic factor with G patch and FHA domains 1

+ [9]

Introduction

Promotes angiogenesis and the proliferation of endothelial cells. Able to bind to endothelial cells and promote cell proliferation, suggesting that it may act in an autocrine fashion.

100 Clinical Results associated with AGGF1

100 Translational Medicine associated with AGGF1

0 Patents (Medical) associated with AGGF1

Literatures (Medical) associated with AGGF1

01 Aug 2024·The Journal of Dermatology

Serum levels of AGGF1: Potential association with cutaneous and cardiopulmonary involvements in systemic sclerosis

Article

Author: Sumida, Hayakazu ; Sato, Shinichi ; Takahashi, Takuya ; Segawa, Yuichiro ; Terui, Hitoshi ; Takahashi, Takehiro ; Ikawa, Tetsuya ; Yoshizaki, Ayumi ; Takahashi, Toshiya ; Asano, Yoshihide

AbstractSystemic sclerosis (SSc) is an autoimmune disease characterized by vasculopathy, aberrant immune activation, and extensive tissue fibrosis of the skin and internal organs. Because of the complicated nature of its pathogenesis, the underlying mechanisms of SSc remain incompletely understood. Angiogenic factor with a G‐patch domain and a Forkhead‐associated domain 1 (AGGF1) is a critical factor in angiogenesis expressed on vascular endothelial cells, associated with inflammatory and fibrotic responses. To elucidate the possible implication of AGGF1 in SSc pathogenesis, we investigated the association between serum AGGF1 levels and clinical manifestations in SSc patients. We conducted a cross‐sectional analysis of AGGF1 levels in sera from 60 SSc patients and 19 healthy controls with enzyme‐linked immunosorbent assay. Serum AGGF1 levels in SSc patients were significantly higher than those in healthy individuals. In particular, diffuse cutaneous SSc patients with shorter disease duration had higher levels compared to those with longer disease duration and limited cutaneous SSc patients. Patients with higher serum AGGF1 levels had a higher incidence of digital ulcers, higher modified Rodnan Skin Scores (mRSS), elevated serum Krebs von den Lungen‐6 (KL‐6) levels, C‐reactive protein levels, and right ventricular systolic pressures (RVSP) on the echocardiogram, whereas they had reduced percentage of vital capacity (%VC) and percentage of diffusing capacity of the lungs for carbon monoxide (%DLCO) in pulmonary functional tests. In line, serum AGGF1 levels were significantly correlated with mRSS, serum KL‐6 and surfactant protein D levels, RVSP, and %DLCO. These results uncovered notable correlations between serum AGGF1 levels and key cutaneous and vascular involvements in SSc, suggesting potential roles of AGGF1 in SSc pathogenesis.

01 Jun 2024·Biochemical and Biophysical Research Communications

Diosgenin improves post-myocardial infarction cardiac function via HAND2-induced angiogenesis

Article

Author: Liu, Longfei ; Lu, Qiulun ; Liu, Xuehua ; Peng, Yuzhu ; Shen, Dehong

While diosgenin has been demonstrated effective in various cardiovascular diseases, its specific impact on treating heart attacks remains unclear. Our research revealed that diosgenin significantly improved cardiac function in a myocardial infarction (MI) mouse model, reducing cardiac fibrosis and cell apoptosis while promoting angiogenesis. Mechanistically, diosgenin upregulated the Hand2 expression, promoting the proliferation and migration of endothelial cells under hypoxic conditions. Acting as a transcription factor, HAND2 activated the angiogenesis-related gene Aggf1. Conversely, silencing Hand2 inhibited the diosgenin-induced migration of hypoxic endothelial cells and angiogenesis. In summary, these findings provide new insights into the protective role of diosgenin in MI, validating its effect on angiogenic activity and providing a theoretical basis for clinical treatment strategies.

01 Dec 2023·Arteriosclerosis, Thrombosis, and Vascular Biology

Aggf1 Specifies Hemangioblasts at the Top of Regulatory Hierarchy via Npas4l and mTOR-S6K-Emp2-ERK Signaling

Article

Author: Yang, Zhongcheng ; Zhang, Yidan ; Ke, Tie ; Guo, Di ; Zhao, Jinyan ; Zhang, Rui ; Li, Jia ; Wang, Qing K. ; Xu, Chengqi

BACKGROUND:Hemangioblasts are mesoderm-derived multipotent stem cells for differentiation of all hematopoietic and endothelial cells in the circulation system. However, the underlying molecular mechanism is poorly understood.METHODS: CRISPR (clustered regularly interspaced short palindromic repeats)/Cas9 (type II CRISPR RNA-guided endonuclease) editing was used to develop aggf1−/− and emp2−/− knockout zebra fish. Whole-mount in situ hybridization and transgenic Tg( gata1 -EGFP [enhanced green fluorescent protein]), Tg( mpx -EGFP), Tg( rag2 -DsRed [discosoma sp. red fluorescent protein]), Tg( cd41 -EGFP), Tg( kdrl -EGFP), and Tg( aggf1−/− ; kdrl -EGFP) zebra fish were used to examine specification of hemangioblasts and hematopoietic stem and progenitor cells (HSPCs), hematopoiesis, and vascular development. Quantitative real-time polymerase chain reaction and Western blot analyses were used for expression analysis of genes and proteins. RESULTS: Knockout of aggf1 impaired specification of hemangioblasts and HSPCs, hematopoiesis, and vascular development in zebra fish. Expression of npas4l / cloche —the presumed earliest marker for hemangioblast specification—was significantly reduced in aggf1−/− embryos and increased by overexpression of aggf1 in embryos. Overexpression of npas4l rescued the impaired specification of hemangioblasts and HSPCs and development of hematopoiesis and intersegmental vessels in aggf1−/− embryos, placing aggf1 upstream of npas4l in hemangioblast specification. To identify the underlying molecular mechanism, we identified emp2 as a key aggf1 downstream gene. Similar to aggf1 , emp2 knockout impaired the specification of hemangioblasts and HSPCs, hematopoiesis, and angiogenesis by increasing the phosphorylation of ERK1/2 (extracellular signal-regulated protein kinase 1/2). Mechanistic studies showed that aggf1 knockdown and knockout significantly decreased the phosphorylated levels of mTOR (mammalian target of rapamycin) and p70 S6K (ribosomal protein S6 kinase), resulting in reduced protein synthesis of Emp2 (epithelial membrane protein 2), whereas mTOR activator MHY1485 (4,6-dimorpholino-N-(4-nitrophenyl)-1,3,5-triazin-2-amine) rescued the impaired specification of hemangioblasts and HSPCs and development of hematopoiesis and intersegmental vessels and reduced Emp2 expression induced by aggf1 knockdown. CONCLUSIONS: These results indicate that aggf1 acts at the top of npas4l and becomes the earliest marker during specification of hemangioblasts. Our data identify a novel signaling axis of Aggf1 (angiogenic factor with G-patch and FHA domain 1)-mTOR-S6K-ERK1/2 for specification of hemangioblasts and HSPCs, primitive and definitive hematopoiesis, and vascular development. Our findings provide important insights into specification of hemangioblasts and HSPCs essential for the development of the circulation system.

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AGGF1

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