The importance of physioxia in mesenchymal stem cell chondrogenesis and the mechanisms controlling its response

Girish Pattappa, Brian Johnstone, Johannes Zellner, Denitsa Docheva, Peter Angele

Research output: Contribution to journalReview article

2 Citations (Scopus)

Abstract

Articular cartilage covers the surface of synovial joints and enables joint movement. However, it is susceptible to progressive degeneration with age that can be accelerated by either previous joint injury or meniscectomy. This degenerative disease is known as osteoarthritis (OA) and it greatly affects the adult population. Cell-based tissue engineering provides a possible solution for treating OA at its earliest stages, particularly focal cartilage lesions. A candidate cell type for treating these focal defects are Mesenchymal Stem Cells (MSCs). However, present methods for differentiating these cells towards the chondrogenic lineage lead to hypertrophic chondrocytes and bone formation in vivo. Environmental stimuli that can stabilise the articular chondrocyte phenotype without compromising tissue formation have been extensively investigated. One factor that has generated intensive investigation in MSC chondrogenesis is low oxygen tension or physioxia (2–5% oxygen). In vivo articular cartilage resides at oxygen tensions between 1–4%, and in vitro results suggest that these conditions are beneficial for MSC expansion and chondrogenesis, particularly in suppressing the cartilage hypertrophy. This review will summarise the current literature regarding the effects of physioxia on MSC chondrogenesis with an emphasis on the pathways that control tissue formation and cartilage hypertrophy.

Original languageEnglish (US)
Article number484
JournalInternational Journal of Molecular Sciences
Volume20
Issue number3
DOIs
StatePublished - Feb 1 2019

Fingerprint

Chondrogenesis
cartilage
stem cells
Cartilage
Stem cells
Mesenchymal Stromal Cells
Joints
oxygen tension
Articular Cartilage
Chondrocytes
Oxygen
Osteoarthritis
Hypertrophy
cells
Tissue
osteogenesis
Tissue Engineering
Osteogenesis
phenotype
degeneration

Keywords

  • Cartilage
  • Chondrogenesis
  • Early osteoarthritis
  • Hypertrophy
  • Hypoxia
  • Hypoxia inducible factors
  • Mesenchymal stem cells

ASJC Scopus subject areas

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry

Cite this

The importance of physioxia in mesenchymal stem cell chondrogenesis and the mechanisms controlling its response. / Pattappa, Girish; Johnstone, Brian; Zellner, Johannes; Docheva, Denitsa; Angele, Peter.

In: International Journal of Molecular Sciences, Vol. 20, No. 3, 484, 01.02.2019.

Research output: Contribution to journalReview article

@article{52e63eb352134cf1adeda40ad22f3e36,
title = "The importance of physioxia in mesenchymal stem cell chondrogenesis and the mechanisms controlling its response",
abstract = "Articular cartilage covers the surface of synovial joints and enables joint movement. However, it is susceptible to progressive degeneration with age that can be accelerated by either previous joint injury or meniscectomy. This degenerative disease is known as osteoarthritis (OA) and it greatly affects the adult population. Cell-based tissue engineering provides a possible solution for treating OA at its earliest stages, particularly focal cartilage lesions. A candidate cell type for treating these focal defects are Mesenchymal Stem Cells (MSCs). However, present methods for differentiating these cells towards the chondrogenic lineage lead to hypertrophic chondrocytes and bone formation in vivo. Environmental stimuli that can stabilise the articular chondrocyte phenotype without compromising tissue formation have been extensively investigated. One factor that has generated intensive investigation in MSC chondrogenesis is low oxygen tension or physioxia (2–5{\%} oxygen). In vivo articular cartilage resides at oxygen tensions between 1–4{\%}, and in vitro results suggest that these conditions are beneficial for MSC expansion and chondrogenesis, particularly in suppressing the cartilage hypertrophy. This review will summarise the current literature regarding the effects of physioxia on MSC chondrogenesis with an emphasis on the pathways that control tissue formation and cartilage hypertrophy.",
keywords = "Cartilage, Chondrogenesis, Early osteoarthritis, Hypertrophy, Hypoxia, Hypoxia inducible factors, Mesenchymal stem cells",
author = "Girish Pattappa and Brian Johnstone and Johannes Zellner and Denitsa Docheva and Peter Angele",
year = "2019",
month = "2",
day = "1",
doi = "10.3390/ijms20030484",
language = "English (US)",
volume = "20",
journal = "International Journal of Molecular Sciences",
issn = "1661-6596",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "3",

}

TY - JOUR

T1 - The importance of physioxia in mesenchymal stem cell chondrogenesis and the mechanisms controlling its response

AU - Pattappa, Girish

AU - Johnstone, Brian

AU - Zellner, Johannes

AU - Docheva, Denitsa

AU - Angele, Peter

PY - 2019/2/1

Y1 - 2019/2/1

N2 - Articular cartilage covers the surface of synovial joints and enables joint movement. However, it is susceptible to progressive degeneration with age that can be accelerated by either previous joint injury or meniscectomy. This degenerative disease is known as osteoarthritis (OA) and it greatly affects the adult population. Cell-based tissue engineering provides a possible solution for treating OA at its earliest stages, particularly focal cartilage lesions. A candidate cell type for treating these focal defects are Mesenchymal Stem Cells (MSCs). However, present methods for differentiating these cells towards the chondrogenic lineage lead to hypertrophic chondrocytes and bone formation in vivo. Environmental stimuli that can stabilise the articular chondrocyte phenotype without compromising tissue formation have been extensively investigated. One factor that has generated intensive investigation in MSC chondrogenesis is low oxygen tension or physioxia (2–5% oxygen). In vivo articular cartilage resides at oxygen tensions between 1–4%, and in vitro results suggest that these conditions are beneficial for MSC expansion and chondrogenesis, particularly in suppressing the cartilage hypertrophy. This review will summarise the current literature regarding the effects of physioxia on MSC chondrogenesis with an emphasis on the pathways that control tissue formation and cartilage hypertrophy.

AB - Articular cartilage covers the surface of synovial joints and enables joint movement. However, it is susceptible to progressive degeneration with age that can be accelerated by either previous joint injury or meniscectomy. This degenerative disease is known as osteoarthritis (OA) and it greatly affects the adult population. Cell-based tissue engineering provides a possible solution for treating OA at its earliest stages, particularly focal cartilage lesions. A candidate cell type for treating these focal defects are Mesenchymal Stem Cells (MSCs). However, present methods for differentiating these cells towards the chondrogenic lineage lead to hypertrophic chondrocytes and bone formation in vivo. Environmental stimuli that can stabilise the articular chondrocyte phenotype without compromising tissue formation have been extensively investigated. One factor that has generated intensive investigation in MSC chondrogenesis is low oxygen tension or physioxia (2–5% oxygen). In vivo articular cartilage resides at oxygen tensions between 1–4%, and in vitro results suggest that these conditions are beneficial for MSC expansion and chondrogenesis, particularly in suppressing the cartilage hypertrophy. This review will summarise the current literature regarding the effects of physioxia on MSC chondrogenesis with an emphasis on the pathways that control tissue formation and cartilage hypertrophy.

KW - Cartilage

KW - Chondrogenesis

KW - Early osteoarthritis

KW - Hypertrophy

KW - Hypoxia

KW - Hypoxia inducible factors

KW - Mesenchymal stem cells

UR - http://www.scopus.com/inward/record.url?scp=85060519346&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85060519346&partnerID=8YFLogxK

U2 - 10.3390/ijms20030484

DO - 10.3390/ijms20030484

M3 - Review article

VL - 20

JO - International Journal of Molecular Sciences

JF - International Journal of Molecular Sciences

SN - 1661-6596

IS - 3

M1 - 484

ER -