Dynamic actin remodeling in response to lysophosphatidic acid

Mir, Saima S.; Bhat, Hina F.; Bhat, Zuhaib F.

doi:10.1080/07391102.2019.1696230

Cited by 2 publications

(1 citation statement)

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“…This is reminiscent of our previous findings that the LPAR-Rho-ROCK-LIM kinase pathway and actin polymerization are necessary for large lysosome formation in VE cells ( Koike et al, 2009 ). Given that LPA signaling remodels actin dynamics ( Mir et al, 2020 ) and that the actin cytoskeleton is involved in membrane trafficking ( Lanzetti, 2007 ), the defects in intracellular membrane trafficking in Enpp2 −/− VE cells are likely related to and caused by dysregulation of the Rho-ROCK-LIM kinase pathway. Association between LPA and membrane trafficking was reported in other cell systems: LPA enhanced internalization of LPA 1 and transferrin receptors via a clathrin- and cholesterol-dependent manner ( Urs et al, 2005 ); LPA stimulated micropinocytosis via Rho GTPases and subsequent actin modification in Entamoeba histolytica , an anaerobic parasitic amoebozoan ( Apte et al, 2022 ).…”

Section: Discussionmentioning

confidence: 99%

The autotaxin-LPA axis promotes membrane trafficking and secretion in yolk sac visceral endoderm cells

Koike,

Keino-Masu,

Tanimoto

et al. 2023

Biology Open

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Autotaxin, encoded by the Enpp2 gene, is an exoenzyme that produces lysophosphatidic acid, thereby regulating many biologic functions. We previously reported that Enpp2 mRNA was abundantly expressed in yolk sac visceral endoderm (VE) cells and that Enpp2−/− mice were lethal at embryonic day 9.5 owing to angiogenic defects in the yolk sac. Enpp2−/− mice showed lysosome fragmentation in VE cells and embryonic abnormalities including allantois malformation, neural tube defects, no axial turning, and head cavity formation. However, whether the defects in endocytic vesicle formation affect membrane trafficking in VE cells remained to be directly examined. In this study, we found that pinocytosis, transcytosis, and secretion of angiogenic factors such as vascular endothelial growth factor and transforming growth factor β1 were impaired in Enpp2−/− VE cells. Moreover, pharmacologic inhibition of membrane trafficking phenocopied the defects of Enpp2−/− mice. These findings demonstrate that Enpp2 spromotes endocytosis and secretion of angiogenic factors in VE cells, thereby regulating angiogenesis/vasculogenesis and embryonic development.

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