Review Article

The Influence of Intervertebral Disc Microenvironment on the Biological Behavior of Engrafted Mesenchymal Stem Cells

Table 2

Effects of hypoxia on the biological behavior of MSCs.

Cell sourcesYearTeamJournalResultsReference

BMSCs2004Risbud et al.SpineHypoxia (2% O2) and TGF-β1 induced the differentiation of BMSCs to a NP-like phenotype.[78]
2006Grayson et al.J Cell PhysiolHypoxia (2% O2) enhanced BMSC viability, proliferation, and expression of stemness genes (Oct4 and Rex-1) compared with normoxia.[72]
2007Grayson et al.Biochem Biophys Res CommunHypoxia (2% O2) promoted the proliferation of BMSCs and maintained their multilineage capabilities compared with normoxia.[73]
2008Kanichai et al.J Cell PhysiolHypoxia (2% O2) promoted the chondrogenic differentiation of BMSCs compared with normoxia.[81]
2009Felka et al.Osteoarthritis CartilageHypoxia (2% O2) reduced the negative effect of IL-1β on chondrogenic differentiation of BMSCs.[77]
2011Tsai et al.BloodHypoxia (1% O2) promoted BMSC proliferation and maintained their chondrogenic differentiation potential compared with normoxia.[74]
2011Müller et al.Cell TransplantHypoxia (4% O2) promoted chondrogenic differentiation of BMSCs compared with normoxia.[79]
2011Stoyanov et al.Eur Cell MaterHypoxia (2% O2) and GDF5 (100 ng/mL) promoted the differentiation of BMSCs to a NP-like phenotype.[80]
2011Raheja et al.Cell Biol IntHypoxia (1% O2) inhibited BMSC migration compared with normoxia.[76]
2018Wang et al.Stem Cells IntHypoxic preconditioning (CoCl2, 100 μM, 24 h) enhanced BMSC viability, migration, and expression of aggrecan and collagen-II but inhibited their proliferation.[75]
2021Peck et al.CartilageHypoxic preconditioning (2% O2) promoted BMSC viability and ECM production.[82]

AD-MSCs2012Chung et al.Res Vet SciHypoxia (1% and 5% O2) inhibited the proliferation of AD-MSCs and BMSCs compared with normoxia, and AD-MSCs exhibited higher proliferative potential than BMSCs.[91]
2013Portron et al.PLoS OneHypoxic preconditioning (5% O2) enhanced the chondrogenic differentiation of AD-MSCs in vitro but not in vivo.[84]
2014Choi et al.Journal of Asian Scientific ResearchHypoxia (2% O2) promoted AD-MSC viability and proliferation compared with normoxia.[86]
2015Fotia et al.CytotechnologyHypoxia (1% O2) promotes AD-MSC proliferation and expression of stemness genes (Nanog and Sox-2) compared with normoxia.[87]
2018Takahashi et al.Cell TransplantHypoxia (1% O2) inhibited AD-MSC viability but promoted their proliferation compared with normoxia.[89]
2019Deng et al.J Cell PhysiolHypoxia (5% O2) promoted AD-MSC proliferation and chondrogenic differentiation potential compared with normoxia.[90]
2020Hwang et al.Tissue Eng Regen MedHypoxic preconditioning (1% O2) promoted AD-MSC proliferation, migration, and chondrogenic differentiation.[83]
2021Govoni et al.Adv Med SciSevere hypoxic preconditioning (0.5% O2) promoted early chondrogenesis in AD-MSCs.[85]

NP-MSCs2013Li et al.Cells Tissues OrgansHypoxia (2% O2) inhibited the viability and proliferation of AD-MSCs and NP-MSCs but promoted their chondrogenic differentiation, and NPMSCs exhibited higher biological activity than AD-MSCs.[44]
2021He et al.AutophagyHypoxia (CoCl2) alleviated hydrostatic pressure-induced NP-MSC apoptosis.[92]

UC-MSCs2015Lee et al.Stem CellsHypoxia (2.2% O2) promoted UC-MSC proliferation and migration compared with normoxia.[93]

PMSCs2012Yang et al.The Spine JournalHypoxia (5% O2) promoted the early proliferation and differentiation of PMSCs into NP-like cells of compared with normoxia.[94]
2014Ni et al.The Spine JournalHypoxia (5% O2) promoted the proliferation and differentiation of PMSCs into NP-like cells of compared with normoxia.[95]
2016Choi et al.J Cell BiochemHypoxia (1% O2) promoted PMSC migration compared with normoxia.[96]
2017Li et al.The Journal of thoracic and cardiovascular surgeryHypoxia (CoCl2) promoted PMSC proliferation.[97]

AF-MSCs2017Kwon et al.Tissue Eng Regen MedHypoxia (5% O2) promoted AF-MSC proliferation and stemness maintenance compared with normoxia.[98]
2020Casciaro et al.Mech Ageing DevHypoxia (1% O2) promoted AF-MSC proliferation and stemness maintenance compared with normoxia.[99]

SMSCs2020Silva et al.Glycoconj JHypoxia (5% O2) promoted chondrogenic differentiation of SMSCs compared with normoxia.[101]

PB-MSCs2022Wang et al.Front EndocrinolHypoxia (5% O2) enhanced the proliferation, stemness, and multidirectional differentiation potential of PBSMCs compared with normoxia[100]

AD-MSCs: adipose-derived mesenchymal stem cells; AF-MSCs: amniotic fluid-derived mesenchymal stem cells; BMSCs: bone marrow-derived mesenchymal stem cells; ECM: extracellular matrix; IL-1β: interleukin-1β; IVD: intervertebral disc; NP: nucleus pulposus; NP-MSCs: nucleus pulposus-derived mesenchymal stem cells; PB-MSCs: peripheral blood-derived mesenchymal stem cells; PMSCs: placenta-derived mesenchymal stem cells; SMSCs: synovial-derived mesenchymal stem cells; TGF: transforming growth factor; UC-MSCs: umbilical cord-derived mesenchymal stem cells.