PPFIA1 drives active α5β1 integrin recycling and controls fibronectin fibrillogenesis and vascular morphogenesis

Mana, Giulia; Clapero, Fabiana; Panieri, Emiliano; Panero, Valentina; Böttcher, Ralph T.; Tseng, Hui Yuan; Saltarin, Federico; Astanina, Elena; Wolanska, Katarzyna; Morgan, Mark R.; Humphries, Martin J.; Santoro, Massimo; Serini, Guido; Valdembri, Donatella

doi:10.1038/ncomms13546

Cited by 74 publications

(130 citation statements)

References 63 publications

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“…Furthermore, it was recently reported that kank proteins (in cooperation with liprin‐β) control FA dynamics by acting as talin activators that decrease the grip between the integrin–talin complex and actomyosin (Sun et al., ). The notion that liprin‐α1 is relevant for FA‐proximal insulin granule localisation (Gan et al., ) is corroborated by the targeting of TGN‐derived secretory vesicles and the polarised secretion of fibronectin from the TGN of vascular endothelial cells (Stehbens et al., ; Mana et al., ). Unfortunately, not much is known about the specific role of liprin's in β‐cells; however, studies in neuronal and non‐neuronal cells demonstrated that these proteins have several functions related to cell adhesion and spreading, signal transduction and organisation of the cytoskeleton (Asperti et al., ; de Curtis, ).…”

Section: Ecm and Isletsmentioning

confidence: 96%

Role and impact of the extracellular matrix on integrin‐mediated pancreatic β‐cell functions

Arous

Wehrle-Haller

2017

Biology of the Cell

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Understanding the organisation and role of the extracellular matrix (ECM) in islets of Langerhans is critical for maintaining pancreatic β-cells, and to recognise and revert the physiopathology of diabetes. Indeed, integrin-mediated adhesion signalling in response to the pancreatic ECM plays crucial roles in β-cell survival and insulin secretion, two major functions, which are affected in diabetes. Here, we would like to present an update on the major components of the pancreatic ECM, their role during integrin-mediated cell-matrix adhesions and how they are affected during diabetes. To treat diabetes, a promising approach consists in replacing β-cells by transplantation. However, efficiency is low, because β-cells suffer of anoikis, due to enzymatic digestion of the pancreatic ECM, which affects the survival of insulin-secreting β-cells. The strategy of adding ECM components during transplantation, to reproduce the pancreatic microenvironment, is a challenging task, as many of the regulatory mechanisms that control ECM deposition and turnover are not sufficiently understood. A better comprehension of the impact of the ECM on the adhesion and integrin-dependent signalling in β-cells is primordial to improve the healthy state of islets to prevent the onset of diabetes as well as for enhancing the efficiency of the islet transplantation therapy.

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Section: Ecm and Isletsmentioning

confidence: 96%

Role and impact of the extracellular matrix on integrin‐mediated pancreatic β‐cell functions

Arous

Wehrle-Haller

2017

Biology of the Cell

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“…To maintain homeostasis, components of the ECM are continuously turned over and remodeled through several mechanisms, including MMP/matrix metalloproteinase-dependent cleavage, integrin-mediated endocytosis, and lysosomal degradation [39,43,47,134]. Interestingly, RAB11B-mediated integrin ITGA5-ITGB1 internalization and recycling not only degrades FN1, but can also promote fibrillogenesis by facilitating FN1 secretion and vascular morphogenesis [135]. Thus, FN1 matrix assembly is a cell-dependent process that is regulated by secretory and integrin recycling pathways, as well as by integrin surface expression.…”

Section: Reciprocal Regulation Between Autophagy and The Ecmmentioning

confidence: 99%

Mechanisms and context underlying the role of autophagy in cancer metastasis

et al. 2018

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Macroautophagy/autophagy is a fundamental cellular degradation mechanism that maintains cell homeostasis, regulates cell signaling, and promotes cell survival. Its role in promoting tumor cell survival in stress conditions is well characterized, and makes autophagy an attractive target for cancer therapy. Emerging research indicates that autophagy also influences cancer metastasis, which is the primary cause of cancer-associated mortality. However, data demonstrate that the regulatory role of autophagy in metastasis is multifaceted, and includes both metastasis-suppressing and -promoting functions. The metastasis-suppressing functions of autophagy, in particular, have important implications for autophagy-based treatments, as inhibition of autophagy may increase the risk of metastasis. In this review, we discuss the mechanisms and context underlying the role of autophagy in metastasis, which include autophagy-mediated regulation of focal adhesion dynamics, integrin signaling and trafficking, Rho GTPase-mediated cytoskeleton remodeling, anoikis resistance, extracellular matrix remodeling, epithelial-to-mesenchymal transition signaling, and tumor-stromal cell interactions. Through this, we aim to clarify the context-dependent nature of autophagy-mediated metastasis and provide direction for further research investigating the role of autophagy in cancer metastasis.

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“…Endocytic recycling also plays a key role in endothelial cell function (particularly through the recycling of integrin cargoes), and VEGFR2 trafficking is important in regulating angiogenic signalling . During angiogenesis, sprouting endothelial cells are classified as either migratory tip cells or proliferative stalk cells, which respond differently to VEGF (vascular endothelial growth factor).…”

Section: Rtk Trafficking and Signalling In Cell Migrationmentioning

confidence: 99%

Vesicle trafficking pathways that direct cell migration in 3D matrices and in vivo

Wilson

Allen

Caswell

2018

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Cell migration is a vital process in development and disease, and while the mechanisms that control motility are relatively well understood on two‐dimensional surfaces, the control of cell migration in three dimensions (3D) and in vivo has only recently begun to be understood. Vesicle trafficking pathways have emerged as a key regulatory element in migration and invasion, with the endocytosis and recycling of cell surface cargos, including growth factor and chemokine receptors, adhesion receptors and membrane‐associated proteases, being of major importance. We highlight recent advances in our understanding of how endocytic trafficking controls the availability and local activity of these cargoes to influence the movement of cells in 3D matrix and in developing organisms. In particular, we discuss how endocytic trafficking of different receptor classes spatially restricts signals and activity, usually to the leading edge of invasive cells.

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PPFIA1 drives active α5β1 integrin recycling and controls fibronectin fibrillogenesis and vascular morphogenesis

Cited by 74 publications

References 63 publications

Role and impact of the extracellular matrix on integrin‐mediated pancreatic β‐cell functions

Role and impact of the extracellular matrix on integrin‐mediated pancreatic β‐cell functions

Mechanisms and context underlying the role of autophagy in cancer metastasis

Vesicle trafficking pathways that direct cell migration in 3D matrices and in vivo

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