Endothelial angiogenic activity and adipose angiogenesis is controlled by extracellular matrix protein TGFBI

Seul Gi Lee; Jin Soo Kim; Ha Jeong Kim; David D. Schlaepfer; In San Kim; Ju Ock Nam

doi:10.1038/s41598-021-88959-1

Endothelial angiogenic activity and adipose angiogenesis is controlled by extracellular matrix protein TGFBI

Seul Gi Lee, Jin Soo Kim, Ha Jeong Kim, David D. Schlaepfer, In San Kim, Ju Ock Nam

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20 Citations (Scopus)

Abstract

Several studies have suggested that extracellular matrix (ECM) remodeling and the microenvironment are tightly associated with adipogenesis and adipose angiogenesis. In the present study, we demonstrated that transforming growth factor-beta induced (TGFBI) suppresses angiogenesis stimulated by adipocyte-conditioned medium (Ad-CM), both in vitro and in vivo. TGFBI knockout (KO) mice exhibited increased numbers of blood vessels in adipose tissue, and blood vessels from these mice showed enhanced infiltration into Matrigel containing Ad-CM. The treatment of Ad-CM-stimulated SVEC-10 endothelial cells with TGFBI protein reduced migration and tube-forming activity. TGFBI protein suppressed the activation of the Src and extracellular signaling-related kinase signaling pathways of these SVEC-10 endothelial cells. Our findings indicated that TGFBI inhibited adipose angiogenesis by suppressing the activation of Src and ERK signaling pathways, possibly because of the stimulation of the angiogenic activity of endothelial cells.

Original language	English
Article number	9644
Journal	Scientific reports
Volume	11
Issue number	1
DOIs	https://doi.org/10.1038/s41598-021-88959-1
Publication status	Published - 2021 Dec

Bibliographical note

Funding Information:
JON was supported by the National Research Foundation of Korea (NRF) funded by the Korean government (NRF-2017R1A2B4011003 and NRF-2019R1A2C1090619). SGL was supported by the National Research Foundation of Korea (NRF) funded by the Korean government (NRF-2019R1A6A3A13094827).

Publisher Copyright:
© 2021, The Author(s).

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title = "Endothelial angiogenic activity and adipose angiogenesis is controlled by extracellular matrix protein TGFBI",

abstract = "Several studies have suggested that extracellular matrix (ECM) remodeling and the microenvironment are tightly associated with adipogenesis and adipose angiogenesis. In the present study, we demonstrated that transforming growth factor-beta induced (TGFBI) suppresses angiogenesis stimulated by adipocyte-conditioned medium (Ad-CM), both in vitro and in vivo. TGFBI knockout (KO) mice exhibited increased numbers of blood vessels in adipose tissue, and blood vessels from these mice showed enhanced infiltration into Matrigel containing Ad-CM. The treatment of Ad-CM-stimulated SVEC-10 endothelial cells with TGFBI protein reduced migration and tube-forming activity. TGFBI protein suppressed the activation of the Src and extracellular signaling-related kinase signaling pathways of these SVEC-10 endothelial cells. Our findings indicated that TGFBI inhibited adipose angiogenesis by suppressing the activation of Src and ERK signaling pathways, possibly because of the stimulation of the angiogenic activity of endothelial cells.",

author = "Lee, {Seul Gi} and Kim, {Jin Soo} and Kim, {Ha Jeong} and Schlaepfer, {David D.} and Kim, {In San} and Nam, {Ju Ock}",

note = "Funding Information: JON was supported by the National Research Foundation of Korea (NRF) funded by the Korean government (NRF-2017R1A2B4011003 and NRF-2019R1A2C1090619). SGL was supported by the National Research Foundation of Korea (NRF) funded by the Korean government (NRF-2019R1A6A3A13094827). Publisher Copyright: {\textcopyright} 2021, The Author(s).",

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doi = "10.1038/s41598-021-88959-1",

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AU - Lee, Seul Gi

AU - Kim, Jin Soo

AU - Kim, Ha Jeong

AU - Schlaepfer, David D.

AU - Kim, In San

AU - Nam, Ju Ock

N1 - Funding Information: JON was supported by the National Research Foundation of Korea (NRF) funded by the Korean government (NRF-2017R1A2B4011003 and NRF-2019R1A2C1090619). SGL was supported by the National Research Foundation of Korea (NRF) funded by the Korean government (NRF-2019R1A6A3A13094827). Publisher Copyright: © 2021, The Author(s).

PY - 2021/12

Y1 - 2021/12

N2 - Several studies have suggested that extracellular matrix (ECM) remodeling and the microenvironment are tightly associated with adipogenesis and adipose angiogenesis. In the present study, we demonstrated that transforming growth factor-beta induced (TGFBI) suppresses angiogenesis stimulated by adipocyte-conditioned medium (Ad-CM), both in vitro and in vivo. TGFBI knockout (KO) mice exhibited increased numbers of blood vessels in adipose tissue, and blood vessels from these mice showed enhanced infiltration into Matrigel containing Ad-CM. The treatment of Ad-CM-stimulated SVEC-10 endothelial cells with TGFBI protein reduced migration and tube-forming activity. TGFBI protein suppressed the activation of the Src and extracellular signaling-related kinase signaling pathways of these SVEC-10 endothelial cells. Our findings indicated that TGFBI inhibited adipose angiogenesis by suppressing the activation of Src and ERK signaling pathways, possibly because of the stimulation of the angiogenic activity of endothelial cells.

AB - Several studies have suggested that extracellular matrix (ECM) remodeling and the microenvironment are tightly associated with adipogenesis and adipose angiogenesis. In the present study, we demonstrated that transforming growth factor-beta induced (TGFBI) suppresses angiogenesis stimulated by adipocyte-conditioned medium (Ad-CM), both in vitro and in vivo. TGFBI knockout (KO) mice exhibited increased numbers of blood vessels in adipose tissue, and blood vessels from these mice showed enhanced infiltration into Matrigel containing Ad-CM. The treatment of Ad-CM-stimulated SVEC-10 endothelial cells with TGFBI protein reduced migration and tube-forming activity. TGFBI protein suppressed the activation of the Src and extracellular signaling-related kinase signaling pathways of these SVEC-10 endothelial cells. Our findings indicated that TGFBI inhibited adipose angiogenesis by suppressing the activation of Src and ERK signaling pathways, possibly because of the stimulation of the angiogenic activity of endothelial cells.

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Endothelial angiogenic activity and adipose angiogenesis is controlled by extracellular matrix protein TGFBI

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