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http://purl.uniprot.org/citations/24624965http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24624965http://www.w3.org/2000/01/rdf-schema#comment"

Background

Stem cell-fate is highly regulated by stem cell niche, which is composed of a distinct microenvironment, including neighboring cells, signals and extracellular matrix. Bone marrow-derived mesenchymal stem cells (BM-MSCs) are multipotent stem cells and are potentially applicable in wide variety of pathological conditions. However, the niche microenvironment for BM-MSCs maintenance has not been clearly characterized. Accumulating evidence indicated that heparan sulfate glycosaminoglycans (HS-GAGs) modulate the self-renewal and differentiation of BM-MSCs, while overexpression of heparanase (HPSE1) resulted in the change of histological profile of bone marrow. Here, we inhibited the enzymatic activity of cell-autonomous HPSE1 in BM-MSCs to clarify the physiological role of HPSE1 in BM-MSCs.

Results

Isolated mouse BM-MSCs express HPSE1 as indicated by the existence of its mRNA and protein, which includes latent form and enzymatically active HPSE1. During in vitro osteo-differentiations, although the expression levels of Hpse1 fluctuated, enzymatic inhibition did not affect osteogenic differentiation, which might due to increased expression level of matrix metalloproteinase 9 (Mmp9). However, cell proliferation and colony formation efficiency were decreased when HPSE1 was enzymatically inhibited. HPSE1 inhibition potentiated SDF-1/CXCR4 signaling axis and in turn augmented the migratory/anchoring behavior of BM-MSCs. We further demonstrated that inhibition of HPSE1 decreased the accumulation of acetylation marks on histone H4 lysine residues suggesting that HPSE1 also modulates the chromatin remodeling.

Conclusions

Our findings indicated cell-autonomous HPSE1 modulates clonogenicity, proliferative potential and migration of BM-MSCs and suggested the HS-GAGs may contribute to the niche microenvironment of BM-MSCs."xsd:string
http://purl.uniprot.org/citations/24624965http://purl.org/dc/terms/identifier"doi:10.1186/1423-0127-21-21"xsd:string
http://purl.uniprot.org/citations/24624965http://purl.uniprot.org/core/author"Lin S.P."xsd:string
http://purl.uniprot.org/citations/24624965http://purl.uniprot.org/core/author"Lee Y.H."xsd:string
http://purl.uniprot.org/citations/24624965http://purl.uniprot.org/core/author"Cheng C.C."xsd:string
http://purl.uniprot.org/citations/24624965http://purl.uniprot.org/core/author"Huangfu W.C."xsd:string
http://purl.uniprot.org/citations/24624965http://purl.uniprot.org/core/author"Liu I.H."xsd:string
http://purl.uniprot.org/citations/24624965http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/24624965http://purl.uniprot.org/core/name"J Biomed Sci"xsd:string
http://purl.uniprot.org/citations/24624965http://purl.uniprot.org/core/pages"21"xsd:string
http://purl.uniprot.org/citations/24624965http://purl.uniprot.org/core/title"Cell-autonomous heparanase modulates self-renewal and migration in bone marrow-derived mesenchymal stem cells."xsd:string
http://purl.uniprot.org/citations/24624965http://purl.uniprot.org/core/volume"21"xsd:string
http://purl.uniprot.org/citations/24624965http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/24624965
http://purl.uniprot.org/citations/24624965http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/24624965
http://purl.uniprot.org/uniprot/#_Q6YGZ1-mappedCitation-24624965http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24624965
http://purl.uniprot.org/uniprot/Q6YGZ1http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/24624965