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The canonical smooth muscle cell marker TAGLN is present in endothelial cells and is involved in angiogenesis

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Title: The canonical smooth muscle cell marker TAGLN is present in endothelial cells and is involved in angiogenesis
Authors: Tsuji-Tamura, Kiyomi Browse this author →KAKEN DB
Morino-Koga, Saori Browse this author
Suzuki, Shingo Browse this author →KAKEN DB
Ogawa, Minetaro Browse this author →KAKEN DB
Keywords: TAGLN
Endothelial cells
Cell elongation
Issue Date: 2-Aug-2021
Publisher: The Company of Biologists
Journal Title: Journal of Cell Science
Volume: 134
Issue: 15
Start Page: jcs254920
Publisher DOI: 10.1242/jcs.254920
PMID: 34338296
CiNii Research CRID: 1360013168766241536
Abstract: Elongation of vascular endothelial cells (ECs) is an important process in angiogenesis; however, the molecular mechanisms remain unknown. The actin-crosslinking protein TAGLN (transgelin, also known as SM22 or SM22α) is abundantly expressed in smooth muscle cells (SMCs) and is widely used as a canonical marker for this cell type. In the course of studies using mouse embryonic stem cells (ESCs) carrying an Tagln promoter-driven fluorescence marker, we noticed activation of the Tagln promoter during EC elongation. Tagln promoter activation co-occurred with EC elongation in response to vascular endothelial growth factor A (VEGF-A). Inhibition of phosphoinositide 3-kinase (PI3K)–Akt signaling and mTORC1 also induced EC elongation and Tagln promoter activation. Human umbilical vein endothelial cells (HUVECs) elongated, activated the TAGLN promoter and increased TAGLN transcripts in an angiogenesis model. Genetic disruption of TAGLN augmented angiogenic behaviors of HUVECs, as did the disruption of TAGLN2 and TAGLN3 genes. Tagln expression was found in ECs in mouse embryos. Our results identify TAGLN as a putative regulator of angiogenesis whose expression is activated in elongating ECs. This finding provides insight into the cytoskeletal regulation of EC elongation and an improved understanding of the molecular mechanisms underlying the regulation of angiogenesis.
Type: article
Appears in Collections:歯学院・歯学研究院 (Graduate School of Dental Medicine / Faculty of Dental Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 田村(辻) 潔美

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