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Impaired endothelium-mesenchymal stem cells cross-talk in systemic sclerosis: a link between vascular and fibrotic
Introduction:
To assess if an impaired cross-talk between endothelial cells (ECs) and perivascular/multipotent mesenchymal stem cells (MSCs) might induce a perturbation of vascular repair and leading to a phenotypic switch of MSC toward myofibroblast in Systemic Sclerosis (SSc).
Methods:
We investigated different angiogenic and profibrotic molecules in a tridimentional matrigel assay, performing co-cultures with endothelial cells (ECs) and bone marrow derived MSCs from patients and healthy controls (HC). After 48 hours of co-culture, cells were sorted and analyzed for mRNA and protein expression.
Results:
ECs-SSc showed a decreased tube formation ability which is not improved by co-cultures with different MSCs. After sorting, we showed: i. an increased production of vascular endothelial growth factor A (VEGF-A) in SSc-MSCs when co-cultured with SSc-ECs; ii. an increased level of transforming growth factor beta (TGF-β) and platelet growth factor BB (PDGF-BB) in SSc-ECs when co-cultured with both HC- and SSc-MSCs; iii. an increase of TGF-β, PDGF-R, alpha smooth muscle actin (α-SMA) and collagen 1 (Col1) in both HC- and SSc-MSCs when co-cultured with SSc-ECs.
Conclusion:
We showed that during SSc, the ECs-MSCs crosstalk resulted in an altered expression of different molecules involved in the angiogenic processes, and mainly SSc-ECs seem to modulate the phenotypic switch of perivascular MSCs toward a myofibroblast population, thus supporting the fibrotic process.
Insights
Impaired communication between endothelial cells and mesenchymal stem cells in Systemic Sclerosis (SSc) promotes fibrosis. SSc endothelial cells drive stem cell transformation into myofibroblasts, hindering vascular repair.
Area of Science:
- Vascular Biology
- Stem Cell Biology
- Fibrosis Research
Background:
- Systemic Sclerosis (SSc) is characterized by vascular dysfunction and fibrosis.
- Impaired crosstalk between endothelial cells (ECs) and multipotent mesenchymal stem cells (MSCs) may contribute to SSc pathogenesis.
- This dysfunction might lead to MSCs transforming into myofibroblasts, exacerbating fibrotic processes.
Purpose of the Study:
- To investigate the impact of EC-MSC crosstalk on vascular repair in SSc.
- To determine if impaired EC-MSC communication induces MSCs to differentiate into myofibroblasts.
Main Methods:
- Co-culture of ECs and MSCs from SSc patients and healthy controls (HC) in a 3D matrigel assay.
- Analysis of angiogenic and profibrotic molecules via mRNA and protein expression after 48 hours.
- Cell sorting to isolate ECs and MSCs for differential analysis.
Main Results:
- ECs from SSc patients (SSc-ECs) exhibited reduced tube formation capacity.
- SSc-MSCs co-cultured with SSc-ECs showed increased vascular endothelial growth factor A (VEGF-A) production.
- SSc-ECs co-cultured with either HC-MSCs or SSc-MSCs displayed elevated transforming growth factor beta (TGF-β) and platelet growth factor BB (PDGF-BB).
- MSCs co-cultured with SSc-ECs showed increased TGF-β, PDGF-R, alpha smooth muscle actin (α-SMA), and collagen 1 (Col1).
Conclusions:
- EC-MSC crosstalk in SSc leads to altered expression of angiogenic molecules.
- SSc-ECs appear to drive the phenotypic switch of MSCs towards a myofibroblast population.
- This altered crosstalk contributes to the fibrotic process in Systemic Sclerosis.
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