Hyaluronic acid drives mesenchymal stromal cell-derived extracellular matrix assembly by promoting fibronectin fibrillogenesis

2021 ◽  
Author(s):  
Marisa Assunção ◽  
Chi Him Kendrick Yiu ◽  
Ho-Ying Wan ◽  
Dan Wang ◽  
Dai Fei Elmer Ker ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Hyaluronic Acid ◽  
Mesenchymal Stromal Cell ◽  
Stromal Cell ◽  
Matrix Assembly ◽  
Fibronectin Deposition

Hyaluronic acid (HA) is present at sites of ongoing fibronectin fibrillogenesis (fibrillar adhesions) and necessary for efficient fibronectin fibrillogenesis. As a result, fibronectin deposition can be enhanced by exogenous HA.

Clumps of a mesenchymal stromal cell/extracellular matrix complex can be a novel tissue engineering therapy for bone regeneration

Cytotherapy ◽  
2015 ◽  
Vol 17 (7) ◽  
pp. 860-873 ◽  
Author(s):  
Mizuho Kittaka ◽  
Mikihito Kajiya ◽  
Hideki Shiba ◽  
Manabu Takewaki ◽  
Kei Takeshita ◽  
...  
Keyword(s):  
Tissue Engineering ◽  
Extracellular Matrix ◽  
Bone Regeneration ◽  
Mesenchymal Stromal Cell ◽  
Stromal Cell

scholarly journals Fibronectin Deposition Participates in Extracellular Matrix Assembly and Vascular Morphogenesis

PLoS ONE ◽  
2016 ◽  
Vol 11 (1) ◽  
pp. e0147600 ◽  
Author(s):  
Abigail Hielscher ◽  
Kim Ellis ◽  
Connie Qiu ◽  
Josh Porterfield ◽  
Sharon Gerecht
Keyword(s):  
Extracellular Matrix ◽  
Matrix Assembly ◽  
Vascular Morphogenesis ◽  
Fibronectin Deposition

scholarly journals pVHL Function Is Essential for Endothelial Extracellular Matrix Deposition

2006 ◽  
Vol 26 (7) ◽  
pp. 2519-2530 ◽  
Author(s):  
Nan Tang ◽  
Fiona Mack ◽  
Volker H. Haase ◽  
M. Celeste Simon ◽  
Randall S. Johnson
Keyword(s):  
Extracellular Matrix ◽  
Endothelial Cells ◽  
Critical Role ◽  
Matrix Assembly ◽  
Developmental Defects ◽  
Vhl Gene ◽  
Matrix Deposition ◽  
Fibronectin Deposition

ABSTRACT The tumor suppressor von Hippel-Lindau protein (pVHL) is critical for cellular molecular oxygen sensing, acting to target degradation of the hypoxia-inducible factor alpha transcription factor subunits under normoxic conditions. We have found that independent of its function in regulating hypoxic response, the VHL gene plays a critical role in embryonic endothelium development through regulation of vascular extracellular matrix assembly. We created mice lacking the VHL gene in endothelial cells; these conditional null mice died at the same stage as homozygous VHL-null mice, with similar vascular developmental defects. These included defective vasculogenesis in the placental labyrinth, a collapsed endocardium, and impaired vessel network patterning. The defects in embryonic vascularization were correlated with a diminished vascular fibronectin deposition in vivo and defective endothelial extracellular fibronectin assembly in vitro. We found that the impaired migration and adhesion of VHL-null endothelial cells can be partially rescued by the addition of back exogenous fibronectin, which indicates that pVHL regulation of fibronectin deposition plays an important functional role in vascular patterning and maintenance of vascular integrity.

Synthetic extracellular matrix mimic hydrogel improves efficacy of mesenchymal stromal cell therapy for ischemic cardiomyopathy

2018 ◽  
Vol 70 ◽  
pp. 71-83 ◽  
Author(s):  
Maria Chiara Ciuffreda ◽  
Giuseppe Malpasso ◽  
Cindy Chokoza ◽  
Deon Bezuidenhout ◽  
Kyle P. Goetsch ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cell Therapy ◽  
Mesenchymal Stromal Cell ◽  
Ischemic Cardiomyopathy ◽  
Stromal Cell

A novel role for alpha 3 beta 1 integrins in extracellular matrix assembly

1995 ◽  
Vol 108 (6) ◽  
pp. 2511-2523 ◽  
Author(s):  
C. Wu ◽  
A.E. Chung ◽  
J.A. McDonald
Keyword(s):  
Extracellular Matrix ◽  
Cell Adhesion ◽  
Binding Activity ◽  
Integrin Subunit ◽  
Pericellular Matrix ◽  
Matrix Assembly ◽  
Amino Terminal ◽  
Beta 1 Integrin ◽  
Fibronectin Deposition

To study the biological role of alpha 3 beta 1 integrins in cell adhesion, migration, and in the deposition of extracellular matrix, we stably expressed the human alpha 3 integrin subunit in the alpha 4, alpha 5 integrin deficient CHO cell line B2. The expression of alpha 3 beta 1 integrins enhanced cell adhesion on entactin (also known as nidogen), but not on fibronectin. Using recombinant GST-fusion proteins that span the entire length of the entactin molecule, we located cell adhesive activity to the G2 domain of entactin. These results suggest that the alpha 3 beta 1 integrin functions as an adhesion receptor interacting with the G2 domain of entactin. On the other hand, the expression of alpha 3 beta 1 integrins did not confer the ability to migrate on entactin. Strikingly, the expression of alpha 3 beta 1 dramatically increased the deposition of entactin and fibronectin into the pericellular matrix. This was accompanied by increased binding activity of the 29 kDa amino-terminal domain of fibronectin. Thus, similar to alpha 5 beta 1 integrins, alpha 3 beta 1 integrins can play an important role in modulating the assembly of pericellular matrices. However, unlike fibronectin deposition supported by alpha 5 beta 1, alpha 3 beta 1 supported fibronectin deposition into pericellular matrix was not inhibited by antibodies binding to the RGD containing cell adhesion domain of fibronectin, demonstrating that the two processes are mechanistically distinct. The role of alpha 3 beta 1 in pericellular matrix assembly potentially implicates this receptor in the assembly and/or recognition of entactin-containing pericellular matrices, an observation consistent with its apparent role in the renal glomerulus of the mammalian kidney.

scholarly journals Mesenchymal Stromal Cell-Produced Components of Extracellular Matrix Potentiate Multipotent Stem Cell Response to Differentiation Stimuli

2020 ◽  
Vol 8 ◽  
Author(s):  
Ekaterina Novoseletskaya ◽  
Olga Grigorieva ◽  
Peter Nimiritsky ◽  
Nataliya Basalova ◽  
Roman Eremichev ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Stem Cell ◽  
Cell Response ◽  
Mesenchymal Stromal Cell ◽  
Stromal Cell ◽  
Multipotent Stem Cell

Mesenchymal stromal cell-derived extracellular matrix influences gene expression of chondrocytes

2013 ◽  
Vol 5 (2) ◽  
pp. 025003 ◽  
Author(s):  
Shraddha Thakkar ◽  
Corina A Ghebes ◽  
Maqsood Ahmed ◽  
Cindy Kelder ◽  
Clemens A van Blitterswijk ◽  
...  
Keyword(s):  
Gene Expression ◽  
Extracellular Matrix ◽  
Mesenchymal Stromal Cell ◽  
Stromal Cell

scholarly journals Pharmacological inhibition of longevity regulator PAPP-A restrains mesenchymal stromal cell activity

2020 ◽  
Author(s):  
Mary Mohrin ◽  
Justin Liu ◽  
Jose Zavala-Solorio ◽  
Sakshi Bhargava ◽  
John Maxwell Trumble ◽  
...  
Keyword(s):  
Gene Expression ◽  
Bone Marrow ◽  
Extracellular Matrix ◽  
Mesenchymal Stromal Cell ◽  
Stromal Cell ◽  
Cell Activity ◽  
Short Term Treatment ◽  
Matrix Gene ◽  
Age Related ◽  
Igf Signaling

AbstractReducing insulin-like growth factor (IGF) signaling is one of the best conserved and characterized mechanisms to extend longevity. Pregnancy associated plasma protein A (PAPP-A) is a secreted metalloprotease that increases IGF availability by cleaving IGF binding proteins. PAPP-A inhibition reduces local IGF signaling, limits the progression of multiple age-related diseases, and extends lifespan, but the mechanisms behind these pleiotropic effects remains unknown. Here, we developed and utilized a PAPP-A neutralizing antibody to discover that adulthood inhibition of this protease reduced collagen and extracellular matrix (ECM) gene expression in multiple tissues in mice. Using bone marrow to explore this effect, we identified mesenchymal stromal cells (MSCs) as the source of PAPP-A and primary responders to PAPP-A inhibition. Short-term treatment with anti-PAPP-A reduced IGF signaling in MSCs, altered MSC expression of collagen/ECM, and decreased MSC number. This affected MSC-dependent functions, decreasing myelopoiesis and osteogenesis. Our data demonstrate that PAPP-A inhibition reduces the activity and number of IGF-dependent mesenchymal progenitor cells and their differentiated progeny, and that this reduction leads to functional changes at the tissue level. MSC-like cells are present in virtually all tissues, and aberrant collagen and ECM production from mesenchymal cells drives aspects of aging and age-related diseases, thus this may be a mechanism by which PAPP-A deficiency enhances lifespan and healthspan.SummaryInhibition of PAPP-A, a regulator of IGF signaling, decreases multi-tissue collagen and extracellular matrix gene expression and modulates mesenchymal stromal cell activity in murine bone marrow.

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