Expression of neural and neurotrophic markers in nucleus pulposus cells isolated from degenerated intervertebral disc

Stefania E. Navone, Giovanni Marfia, Laura Canzi, Emilio Ciusani, Alessandra Canazza, Sergio Visintini, Rolando Campanella, Eugenio A. Parati

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Intervertebral disc (IVD) degeneration is a common disorder of the lower spine. Since it is caused by loss of cellularity, there is interest in the comprehension of the cellular phenotypes. This study aimed to verify if stem cells isolated from nucleus pulposus of intervertebral discs (NPs-IVD), which may express neurogenic properties, may be implicated in IVD disease. NPs-IVD isolated from 14 human pathological discs were cultured under mesenchymal and neural differentiation. An induction of the neural markers GFAP, NF, MAP2, O4, and a decrement of the expression of the immature neural markers β-tubulin III, Nestin, NG2, occurred within the neural differentiation. The expression of TrkA and p75NGFR, the receptors of NGF, was not correlated with neural induction; in contrast, TrkB, the BDNF receptor, increased and was co-expressed with acid sensing ion channel 3 (ASIC3). In the same condition, neuroinflammatory markers were over-expressed. We confirm our hypothesis that stem cells within IVD degeneration acquire neurogenic phenotype, causing the induction of markers related to inflammatory condition. These cells could promote the enrolment of neurotrophines in adaptation to the acidic microenvironment in degenerative conditions. These data could improve our knowledge about IVD cellularity and eventually lead to the development of pharmacological therapies.

Original languageEnglish
Pages (from-to)1470-1477
Number of pages8
JournalJournal of Orthopaedic Research
Volume30
Issue number9
DOIs
Publication statusPublished - Sep 2012

Fingerprint

Intervertebral Disc
trkB Receptor
Intervertebral Disc Degeneration
Stem Cells
Acid Sensing Ion Channels
trkA Receptor
Phenotype
Nestin
Nerve Growth Factor
Tubulin
Cell Nucleus
Spine
Pharmacology
Nucleus Pulposus
Therapeutics

Keywords

  • intervertebral disc
  • mesenchymal stem cells
  • neural differentiation
  • neuroinflammation
  • nucleus pulposus cells

ASJC Scopus subject areas

  • Orthopedics and Sports Medicine

Cite this

Expression of neural and neurotrophic markers in nucleus pulposus cells isolated from degenerated intervertebral disc. / Navone, Stefania E.; Marfia, Giovanni; Canzi, Laura; Ciusani, Emilio; Canazza, Alessandra; Visintini, Sergio; Campanella, Rolando; Parati, Eugenio A.

In: Journal of Orthopaedic Research, Vol. 30, No. 9, 09.2012, p. 1470-1477.

Research output: Contribution to journalArticle

@article{62f7811b10424b9783ca1fef883c89e3,
title = "Expression of neural and neurotrophic markers in nucleus pulposus cells isolated from degenerated intervertebral disc",
abstract = "Intervertebral disc (IVD) degeneration is a common disorder of the lower spine. Since it is caused by loss of cellularity, there is interest in the comprehension of the cellular phenotypes. This study aimed to verify if stem cells isolated from nucleus pulposus of intervertebral discs (NPs-IVD), which may express neurogenic properties, may be implicated in IVD disease. NPs-IVD isolated from 14 human pathological discs were cultured under mesenchymal and neural differentiation. An induction of the neural markers GFAP, NF, MAP2, O4, and a decrement of the expression of the immature neural markers β-tubulin III, Nestin, NG2, occurred within the neural differentiation. The expression of TrkA and p75NGFR, the receptors of NGF, was not correlated with neural induction; in contrast, TrkB, the BDNF receptor, increased and was co-expressed with acid sensing ion channel 3 (ASIC3). In the same condition, neuroinflammatory markers were over-expressed. We confirm our hypothesis that stem cells within IVD degeneration acquire neurogenic phenotype, causing the induction of markers related to inflammatory condition. These cells could promote the enrolment of neurotrophines in adaptation to the acidic microenvironment in degenerative conditions. These data could improve our knowledge about IVD cellularity and eventually lead to the development of pharmacological therapies.",
keywords = "intervertebral disc, mesenchymal stem cells, neural differentiation, neuroinflammation, nucleus pulposus cells",
author = "Navone, {Stefania E.} and Giovanni Marfia and Laura Canzi and Emilio Ciusani and Alessandra Canazza and Sergio Visintini and Rolando Campanella and Parati, {Eugenio A.}",
year = "2012",
month = "9",
doi = "10.1002/jor.22098",
language = "English",
volume = "30",
pages = "1470--1477",
journal = "Journal of Orthopaedic Research",
issn = "0736-0266",
publisher = "John Wiley and Sons Inc.",
number = "9",

}

TY - JOUR

T1 - Expression of neural and neurotrophic markers in nucleus pulposus cells isolated from degenerated intervertebral disc

AU - Navone, Stefania E.

AU - Marfia, Giovanni

AU - Canzi, Laura

AU - Ciusani, Emilio

AU - Canazza, Alessandra

AU - Visintini, Sergio

AU - Campanella, Rolando

AU - Parati, Eugenio A.

PY - 2012/9

Y1 - 2012/9

N2 - Intervertebral disc (IVD) degeneration is a common disorder of the lower spine. Since it is caused by loss of cellularity, there is interest in the comprehension of the cellular phenotypes. This study aimed to verify if stem cells isolated from nucleus pulposus of intervertebral discs (NPs-IVD), which may express neurogenic properties, may be implicated in IVD disease. NPs-IVD isolated from 14 human pathological discs were cultured under mesenchymal and neural differentiation. An induction of the neural markers GFAP, NF, MAP2, O4, and a decrement of the expression of the immature neural markers β-tubulin III, Nestin, NG2, occurred within the neural differentiation. The expression of TrkA and p75NGFR, the receptors of NGF, was not correlated with neural induction; in contrast, TrkB, the BDNF receptor, increased and was co-expressed with acid sensing ion channel 3 (ASIC3). In the same condition, neuroinflammatory markers were over-expressed. We confirm our hypothesis that stem cells within IVD degeneration acquire neurogenic phenotype, causing the induction of markers related to inflammatory condition. These cells could promote the enrolment of neurotrophines in adaptation to the acidic microenvironment in degenerative conditions. These data could improve our knowledge about IVD cellularity and eventually lead to the development of pharmacological therapies.

AB - Intervertebral disc (IVD) degeneration is a common disorder of the lower spine. Since it is caused by loss of cellularity, there is interest in the comprehension of the cellular phenotypes. This study aimed to verify if stem cells isolated from nucleus pulposus of intervertebral discs (NPs-IVD), which may express neurogenic properties, may be implicated in IVD disease. NPs-IVD isolated from 14 human pathological discs were cultured under mesenchymal and neural differentiation. An induction of the neural markers GFAP, NF, MAP2, O4, and a decrement of the expression of the immature neural markers β-tubulin III, Nestin, NG2, occurred within the neural differentiation. The expression of TrkA and p75NGFR, the receptors of NGF, was not correlated with neural induction; in contrast, TrkB, the BDNF receptor, increased and was co-expressed with acid sensing ion channel 3 (ASIC3). In the same condition, neuroinflammatory markers were over-expressed. We confirm our hypothesis that stem cells within IVD degeneration acquire neurogenic phenotype, causing the induction of markers related to inflammatory condition. These cells could promote the enrolment of neurotrophines in adaptation to the acidic microenvironment in degenerative conditions. These data could improve our knowledge about IVD cellularity and eventually lead to the development of pharmacological therapies.

KW - intervertebral disc

KW - mesenchymal stem cells

KW - neural differentiation

KW - neuroinflammation

KW - nucleus pulposus cells

UR - http://www.scopus.com/inward/record.url?scp=84863854306&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84863854306&partnerID=8YFLogxK

U2 - 10.1002/jor.22098

DO - 10.1002/jor.22098

M3 - Article

C2 - 22374745

AN - SCOPUS:84863854306

VL - 30

SP - 1470

EP - 1477

JO - Journal of Orthopaedic Research

JF - Journal of Orthopaedic Research

SN - 0736-0266

IS - 9

ER -