Ca2+ signalling in endothelial progenitor cells: A novel means to improve cell-based therapy and impair tumour vascularisation

Francesco Moccia, Francesco Lodola, Silvia Dragoni, Elisa Bonetti, Cinzia Bottino, Germano Guerra, Umberto Laforenza, Vittorio Rosti, Franco Tanzi

Research output: Contribution to journalArticle

Abstract

Endothelial progenitor cells (EPCs) have recently been employed in cell-based therapy (CBT) to promote regeneration of ischemic organs, such as heart and limbs. Furthermore, EPCs may sustain tumour vascularisation and provide an additional target for anticancer therapies. CBT is limited by the paucity of cells harvested from peripheral blood and suffers from several pitfalls, including the low rate of engrafted EPCs, whereas classic antiangiogenic treatments manifest a number of side effects and may induce resistance into the patients. CBT will benefit of a better understanding of the signal transduction pathway(s) which drive(s) EPC proliferation, trafficking, and incorporation into injured tissues. At the same time, this information might outline alternative molecular targets to impair tumor neovascularisation and improve the therapeutic outcome of antiangiogenic strategies. An increase in intracellular Ca2+ concentration is the key signal in the regulation of cellular replication, migration, and differentiation. In particular, Ca2+ signalling may regulate cellcycle progression, due to the Ca2+-sensitivity of a number of cycline-dependent kinases, and gene expression, owing to the Ca2+-dependence of several transcription factors. Recent work has outlined the role of the so-called store-operated Ca2+ entry in driving EPC proliferation and migration. Unravelling the mechanisms guiding EPC engraftment into neovessels might supply the biological bases required to improve CBT and anticancer treatments. For example, genetic manipulation of the Ca2+ signalling machinery could provide a novel approach to increase the extent of limb regeneration or preventing tumour vascularisation by EPCs.

Original languageEnglish
Pages (from-to)87-105
Number of pages19
JournalCurrent Vascular Pharmacology
Volume12
Issue number1
Publication statusPublished - 2014

Fingerprint

Cell- and Tissue-Based Therapy
Neoplasms
Regeneration
Extremities
Cell Proliferation
Therapeutics
Endothelial Progenitor Cells
Cell Movement
Signal Transduction
Transcription Factors
Phosphotransferases
Gene Expression

Keywords

  • Cell therapy
  • Endothelial progenitor cells
  • Orail Stim1
  • Tumor vascularization

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Pharmacology

Cite this

Moccia, F., Lodola, F., Dragoni, S., Bonetti, E., Bottino, C., Guerra, G., ... Tanzi, F. (2014). Ca2+ signalling in endothelial progenitor cells: A novel means to improve cell-based therapy and impair tumour vascularisation. Current Vascular Pharmacology, 12(1), 87-105.

Ca2+ signalling in endothelial progenitor cells : A novel means to improve cell-based therapy and impair tumour vascularisation. / Moccia, Francesco; Lodola, Francesco; Dragoni, Silvia; Bonetti, Elisa; Bottino, Cinzia; Guerra, Germano; Laforenza, Umberto; Rosti, Vittorio; Tanzi, Franco.

In: Current Vascular Pharmacology, Vol. 12, No. 1, 2014, p. 87-105.

Research output: Contribution to journalArticle

Moccia, F, Lodola, F, Dragoni, S, Bonetti, E, Bottino, C, Guerra, G, Laforenza, U, Rosti, V & Tanzi, F 2014, 'Ca2+ signalling in endothelial progenitor cells: A novel means to improve cell-based therapy and impair tumour vascularisation', Current Vascular Pharmacology, vol. 12, no. 1, pp. 87-105.
Moccia, Francesco ; Lodola, Francesco ; Dragoni, Silvia ; Bonetti, Elisa ; Bottino, Cinzia ; Guerra, Germano ; Laforenza, Umberto ; Rosti, Vittorio ; Tanzi, Franco. / Ca2+ signalling in endothelial progenitor cells : A novel means to improve cell-based therapy and impair tumour vascularisation. In: Current Vascular Pharmacology. 2014 ; Vol. 12, No. 1. pp. 87-105.
@article{1cc7ac6134d742998a7fa037e63e7a04,
title = "Ca2+ signalling in endothelial progenitor cells: A novel means to improve cell-based therapy and impair tumour vascularisation",
abstract = "Endothelial progenitor cells (EPCs) have recently been employed in cell-based therapy (CBT) to promote regeneration of ischemic organs, such as heart and limbs. Furthermore, EPCs may sustain tumour vascularisation and provide an additional target for anticancer therapies. CBT is limited by the paucity of cells harvested from peripheral blood and suffers from several pitfalls, including the low rate of engrafted EPCs, whereas classic antiangiogenic treatments manifest a number of side effects and may induce resistance into the patients. CBT will benefit of a better understanding of the signal transduction pathway(s) which drive(s) EPC proliferation, trafficking, and incorporation into injured tissues. At the same time, this information might outline alternative molecular targets to impair tumor neovascularisation and improve the therapeutic outcome of antiangiogenic strategies. An increase in intracellular Ca2+ concentration is the key signal in the regulation of cellular replication, migration, and differentiation. In particular, Ca2+ signalling may regulate cellcycle progression, due to the Ca2+-sensitivity of a number of cycline-dependent kinases, and gene expression, owing to the Ca2+-dependence of several transcription factors. Recent work has outlined the role of the so-called store-operated Ca2+ entry in driving EPC proliferation and migration. Unravelling the mechanisms guiding EPC engraftment into neovessels might supply the biological bases required to improve CBT and anticancer treatments. For example, genetic manipulation of the Ca2+ signalling machinery could provide a novel approach to increase the extent of limb regeneration or preventing tumour vascularisation by EPCs.",
keywords = "Cell therapy, Endothelial progenitor cells, Orail Stim1, Tumor vascularization",
author = "Francesco Moccia and Francesco Lodola and Silvia Dragoni and Elisa Bonetti and Cinzia Bottino and Germano Guerra and Umberto Laforenza and Vittorio Rosti and Franco Tanzi",
year = "2014",
language = "English",
volume = "12",
pages = "87--105",
journal = "Current Vascular Pharmacology",
issn = "1570-1611",
publisher = "Bentham Science Publishers B.V.",
number = "1",

}

TY - JOUR

T1 - Ca2+ signalling in endothelial progenitor cells

T2 - A novel means to improve cell-based therapy and impair tumour vascularisation

AU - Moccia, Francesco

AU - Lodola, Francesco

AU - Dragoni, Silvia

AU - Bonetti, Elisa

AU - Bottino, Cinzia

AU - Guerra, Germano

AU - Laforenza, Umberto

AU - Rosti, Vittorio

AU - Tanzi, Franco

PY - 2014

Y1 - 2014

N2 - Endothelial progenitor cells (EPCs) have recently been employed in cell-based therapy (CBT) to promote regeneration of ischemic organs, such as heart and limbs. Furthermore, EPCs may sustain tumour vascularisation and provide an additional target for anticancer therapies. CBT is limited by the paucity of cells harvested from peripheral blood and suffers from several pitfalls, including the low rate of engrafted EPCs, whereas classic antiangiogenic treatments manifest a number of side effects and may induce resistance into the patients. CBT will benefit of a better understanding of the signal transduction pathway(s) which drive(s) EPC proliferation, trafficking, and incorporation into injured tissues. At the same time, this information might outline alternative molecular targets to impair tumor neovascularisation and improve the therapeutic outcome of antiangiogenic strategies. An increase in intracellular Ca2+ concentration is the key signal in the regulation of cellular replication, migration, and differentiation. In particular, Ca2+ signalling may regulate cellcycle progression, due to the Ca2+-sensitivity of a number of cycline-dependent kinases, and gene expression, owing to the Ca2+-dependence of several transcription factors. Recent work has outlined the role of the so-called store-operated Ca2+ entry in driving EPC proliferation and migration. Unravelling the mechanisms guiding EPC engraftment into neovessels might supply the biological bases required to improve CBT and anticancer treatments. For example, genetic manipulation of the Ca2+ signalling machinery could provide a novel approach to increase the extent of limb regeneration or preventing tumour vascularisation by EPCs.

AB - Endothelial progenitor cells (EPCs) have recently been employed in cell-based therapy (CBT) to promote regeneration of ischemic organs, such as heart and limbs. Furthermore, EPCs may sustain tumour vascularisation and provide an additional target for anticancer therapies. CBT is limited by the paucity of cells harvested from peripheral blood and suffers from several pitfalls, including the low rate of engrafted EPCs, whereas classic antiangiogenic treatments manifest a number of side effects and may induce resistance into the patients. CBT will benefit of a better understanding of the signal transduction pathway(s) which drive(s) EPC proliferation, trafficking, and incorporation into injured tissues. At the same time, this information might outline alternative molecular targets to impair tumor neovascularisation and improve the therapeutic outcome of antiangiogenic strategies. An increase in intracellular Ca2+ concentration is the key signal in the regulation of cellular replication, migration, and differentiation. In particular, Ca2+ signalling may regulate cellcycle progression, due to the Ca2+-sensitivity of a number of cycline-dependent kinases, and gene expression, owing to the Ca2+-dependence of several transcription factors. Recent work has outlined the role of the so-called store-operated Ca2+ entry in driving EPC proliferation and migration. Unravelling the mechanisms guiding EPC engraftment into neovessels might supply the biological bases required to improve CBT and anticancer treatments. For example, genetic manipulation of the Ca2+ signalling machinery could provide a novel approach to increase the extent of limb regeneration or preventing tumour vascularisation by EPCs.

KW - Cell therapy

KW - Endothelial progenitor cells

KW - Orail Stim1

KW - Tumor vascularization

UR - http://www.scopus.com/inward/record.url?scp=84897453981&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84897453981&partnerID=8YFLogxK

M3 - Article

C2 - 22724469

AN - SCOPUS:84897453981

VL - 12

SP - 87

EP - 105

JO - Current Vascular Pharmacology

JF - Current Vascular Pharmacology

SN - 1570-1611

IS - 1

ER -