Revascularization of ischemic tissues by PDGF-CC via effects on endothelial cells and their progenitors

Li, Xuri; Tjwa, Marc; Moons, Lieve; Fons, Pierre; Noël, Agnès; Ny, Annelii; Zhou, Jialing; Lennartsson, Johan; Li, Hong; Luttun, Aernout; Pontén, Annica; Devy, Laetitia; Bouché, Ann; Oh, Hideyasu; Manderveld, Ann; Blacher, Silvia; Communi, David; Savi, Pierre; Bono, Françoise; Dewerchin, Mieke; Foidart, Jean‐Michel; Autiero, Monica; Herbert, Jean‐Marc; Collen, Désiré; Heldin, Carl‐Henrik; Eriksson, Ulf; Carmeliet, Peter

doi:10.1172/jci19189

Cited by 151 publications

(73 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…We next examined whether PDGF-B regulates cell migration. PDGF and PDGFR may participate in cellular migration and PDGF-B is the strongest inducer in that process [45–47]. As expected, PDGF-B regulated cell migration and we confirmed this finding by an inhibition assay.…”

Section: Discussionsupporting

confidence: 86%

MLLT11/AF1q boosts oncogenic STAT3 activity through Src-PDGFR tyrosine kinase signaling

et al. 2016

View full text Add to dashboard Cite

Constitutive STAT3 activation by tyrosine phosphorylation of mutated or amplified tyrosine kinases (pYSTAT3) is critical for cancer initiation, progression, invasion, and motility of carcinoma cells. We showed that AF1q is associated with STAT3 signaling in breast cancer cells. In xenograft models, enhanced AF1q expression activated STAT3 and promoted tumor growth and metastasis in immunodeficient NSG mice. The cytokine secretory phenotype of MDA-MB-231LN breast cancer cells with altered AF1q expression revealed changes in expression of platelet-derived growth factor subunit B (PDGF-B). AF1q-induced PDGF-B stimulated motility, migration, and invasion of MDA-MB-231LN cells, and AF1q up-regulated platelet-derived growth factor receptor (PDGFR) signaling. Further, AF1q-induced PDGFR signaling enhanced STAT3 activity through Src kinase activation, which could be blocked by the Src kinase inhibitor PP1. Moreover, AF1q up-regulated tyrosine kinase signaling through PDGFR signaling, which was blockable by imatinib. In conclusion, we demonstrated that enhanced AF1q expression contributes to persistent and oncogenic pYSTAT3 levels in invasive carcinoma cells by activating Src kinase through activation of the PDGF-B/PDGFR cascade. Therefore, AF1q plays an essential role as a cofactor in PDGF-B-driven STAT3 signaling.

show abstract

Section: Discussionsupporting

confidence: 86%

MLLT11/AF1q boosts oncogenic STAT3 activity through Src-PDGFR tyrosine kinase signaling

et al. 2016

View full text Add to dashboard Cite

show abstract

“…Moreover, primary vascular SMCs have low proliferation potential and suffer from culture senescence. SMCs have been demonstrated to be differentiated from alternative cell sources such as bone-marrow mesenchymal stem cells [12, 13], endothelial progenitor cells [14], adipose-derived stem cells [15], among many other adult stem cells. However, the proliferation and differentiation capabilities of adult stem cells significantly decrease with aging donors.…”

Section: Discussionmentioning

confidence: 99%

Engineering vascular tissue with functional smooth muscle cells derived from human iPS cells and nanofibrous scaffolds

et al. 2014

View full text Add to dashboard Cite

Tissue-engineered blood vessels (TEBVs) are promising in the replacement of diseased vascular tissues. However, it remains a great challenge to obtain a sufficient number of functional smooth muscle cells (SMCs) in a clinical setting to construct patient-specific TEBVs. In addition, it is critical to develop a scaffold to accommodate these cells and retain their functional phenotype for the regeneration of TEBVs. In this study, human induced pluripotent stem cells (iPSCs) were established from primary human aortic fibroblasts, and characterized with the pluripotency markers expression and cells’ capabilities to differentiate into all three germ layer cells. A highly efficient method was then developed to induce these human iPSCs into proliferative SMCs. After multiple times of expansion, the expanded SMCs retained the potential to be induced into the functional contractile phenotype of mature SMCs, which was characterized by the contractile response to carbachol treatment, up-regulation of specific collagen genes under transforming growth factor β1 treatment, and up-regulation of specific matrix metalloproteinase genes under cytokine stimulation. We also developed an advanced macroporous and nanofibrous (NF) poly(L-lactic acid) (PLLA) scaffold with suitable pore size and interpore connectivity to seed these human iPSC-derived SMCs and maintain their differentiated phenotype. Subcutaneous implantation of the SMC-scaffold construct in nude mice demonstrated vascular tissue formation, with robust collagenous matrix deposition inside the scaffold and the maintenance of differentiated SMC phenotype. Taken together, this study established an exciting approach towards the construction of patient-specific TEBVs. We established patient-specific human iPSCs, derived proliferative SMCs fore expansion, turned on their mature contractile SMC phenotype, and developed an advanced scaffold for these cells to regenerate vascular tissue in vivo.

show abstract

“…PDGF also has an angiogenic activity in various models and induces angiogenic factors such as VEGF and FGF-2 17 35 36. Together, PDGF and PDGF-induced angiogenic molecules may contribute to inflammation-induced angiogenesis, an important mechanism supporting disease persistence in chronic inflammatory diseases.…”

Section: Discussionmentioning

confidence: 99%

Imatinib mesylate inhibits in vitro and ex vivo biological responses related to vascular occlusion in giant cell arteritis

Lozano

Segarra

García‐Martínez

et al. 2007

Annals of the Rheumatic Diseases

View full text Add to dashboard Cite

Objectives: Ischaemic complications occur in 15-20% of patients with giant cell arteritis (GCA). The aim of our study was to explore the effect of mesenchymal growth factors expressed in GCA lesions on myointimal cell responses related to the development of intimal hyperplasia and vessel occlusion. Methods: We developed a method to obtain primary human temporal artery derived myointimal cells (HTAMCs) based on the culture of temporal artery sections on Matrigel.

show abstract

Revascularization of ischemic tissues by PDGF-CC via effects on endothelial cells and their progenitors

Cited by 151 publications

References 53 publications

MLLT11/AF1q boosts oncogenic STAT3 activity through Src-PDGFR tyrosine kinase signaling

MLLT11/AF1q boosts oncogenic STAT3 activity through Src-PDGFR tyrosine kinase signaling

Engineering vascular tissue with functional smooth muscle cells derived from human iPS cells and nanofibrous scaffolds

Imatinib mesylate inhibits in vitro and ex vivo biological responses related to vascular occlusion in giant cell arteritis

Contact Info

Product

Resources

About