Table 1.
Cell-based therapies for treatment of AA
| Cell source | Cells | Species | Model | Delivery | Outcome | Ref. |
|---|---|---|---|---|---|---|
| BM-MSCs | 1 × 106 | Mouse | Angiotensin II | IV |
AAA diameter ↓ IL-6 and MCP-1 ↓ MMP-2 and -9 ↓ M1 macrophages infiltration ↓ IGF-1 and TIMP-2 ↑ Preserved elastin structure |
[37, 38] |
| BM-MSCs or VSMCs | 1 × 106 | Guinea pig | Xenograft rat model | Catheter |
AAA expansion ↓ MMP-9 ↓ Macrophages infiltration ↓ BM-MSCs had more powerfully than VSMCs |
[39] |
| Male or female BM-MSCs | 3 × 106 | Mouse | Elastase | IV |
In female MSCs AAA growth ↓ TNF-α, IL-1β, and MCP-1 ↓ Female MSCs most strongly attenuated AAA growth |
[40] |
| AD-MSCs | 4 × 106 | Rat | CaCl2 | Carotid artery injected |
Elastin expression in SMCs ↑ Reconstruction of elastic fiber |
[41] |
| Muse cells | 2 × 104 | Mouse | CaCl2 and elastase | IV |
AAA dilation ↓ Preserved elastic fibers Spontaneous differentiation into ECs and SMCs |
[42] |
| SPCs | 1 × 107 | Rabbit | CaCl2 and elastase | Subadventitially injected |
In LOX gene-modified SPCs AAA progression ↓ MMP-2 and -9 ↓ Preserved elastin structure |
[43] |
| UC-MSCs | 1 × 106 | Mouse | Elastase | IV |
AAA formation ↓ HMGB1 and IL-17 ↓ MMP2 and MMP9 ↓ |
[44] |
| AD-MSCs | 1 × 106 | Mouse | Elastase | IV |
AAA expansion ↓ Aortic site CD206+ M2 macrophages ↑ Tregs ↑ CD4+CD28− T cells ↓ CD8+CD28+ T cells ↓ Ly6G/C+ neutrophils ↓ Circulating CD115+CXCR1−LY6C+ activated monocytes ↓ |
[43] |
| UC-MSCs | 1 × 106 | Rat | Elastase | IV |
AAA expansion ↓ Elastin degradation ↓ MMPs, TNF-α ↓ Preserved and/or restored VSMC contractile phenotype |
[45] |
| Allogeneic BM-MSCs | 1 × 106 | Mouse | Angiotensin II | IV |
Aortic diameter ↓ MMP-2 and -9, IL-6, MCP-1 ↓ M1 macrophages infiltration ↓ IGF-1, TIMP-2 ↑ Preserved elastin structure |
[46] |
| UC-MSCs | 1 × 106 | Mouse | Elastase | IV |
TAA formation and expansion ↓ Infiltration of macrophages, T cells, neutrophils ↓ miRNA-10a, -29b, 24 ↑ CXCL-13/BCA-1, CXCL12, CXCL10, CCL5, and IL27 ↓ IL-10 ↑ |
[44] |
| VSMCs or iPSC-SMP | 5 × 105 | Mouse | Elastase | Porous collagen scaffolds |
In the SMC-seeded scaffold group AAA expansion ↓ In both the SMC- and iPSC-SMP-seeded scaffold groups SMC retention ↑ Macrophage invasion ↓ |
[47] |
| AD-MSCs | 1 × 106 | Pig | Collagenase and elastase | Gel foam |
AAA dilation ↓ Collagen and elastin ↑ α-SMA ↑ VEGF, TIMP1, and MMP3 ↑ |
[48] |
| M2 macrophages differentiated from J774A.1 cell line | 1 × 106 | Mouse | Angiotensin II | IP |
Aneurysmal expansion ↓ M1/M2 ratio ↓ IL-1β, IL-6, and MCP-1 ↓ IL-4 and IL-10 ↑ Elastin degradation ↓ Injected cells maintained the M2 phenotype throughout 28 days |
[49] |
Abbreviations: AAA Abdominal aortic aneurysm, AD Adipose derived, BM Bone marrow, MSCs Mesenchymal stem cells, VSMCs Vascular smooth muscle cells, iPSC-SMP pluripotent stem cell-derived smooth muscle progenitor cells, IV Intravenous injection; IP Intraperitoneal injection, α-SMA α-smooth muscle actin, HMGB1 High mobility group box 1, IGF-1 Insulin-like growth factor-1, IL Interleukin, MCP-1 Monocyte chemoattractant protein-1, MMP Matrix metalloproteinase, Muse cells Multilineage-differentiating stress-enduring cells, SPCs Smooth muscle progenitor cells, TAA Thoracic aortic aneurysm, TIMP Tissue inhibitor of metalloproteinase, TNF-α Tumor necrosis factor-α, UC Umbilical cord, VEGF Vascular endothelial growth factor