Table 1.
Factors inducing ASC differentiation towards endothelial cells.
| Factor | Source of ASC | Authors | Details |
|---|---|---|---|
| Semisolid methylcellulose medium | Human | [34] | Expression of CD31 and vWf and formation of vessel-like structures in vitro. In vivo neovascularization. Dedifferentiation of mature adipocytes into ECs. |
| Endothelial cell growth medium containing VEGF and IGF | Human | [35] | Expression of CD31 and vWf in vitro. Increased capillary density and blood flow in ischemic hindlimb in vivo. |
| Endothelial cell growth medium containing VEGF and FGF-2, Matrigel coating | Human | [4] | Ac-LDL uptake in vitro. Expression of CD31, VE-cadherin and eNOS in vitro and in vivo. Improved blood perfusion in vivo. Blockade of PI3K inhibits differentiation. |
| Endothelial cell growth medium containing FGF-2 | Rat | [51] | Ac-LDL uptake; expression of CD31, vWf and eNOS; and formation of tube-like structures on Matrigel in vitro. Blockade of FGF-2 inhibits differentiation. |
| Endothelial cell growth medium containing VEGF | Pig | [52] | Endothelial cell morphology and increase in ERK phosphorylation in vitro. ERK inhibition decreases the expression of CD31 and VE-cadherin. Blockade of VEGFR2 inhibits ERK. |
| Endothelial cell growth medium containing VEGF, FGF-2, EGF and IGF-1 | Human | [53] | Change in morphology; induced expression of CD31, vWf and eNOS; and formation of cord-like structures on Matrigel in vitro. Improved fat graft retention and neovascularization in vivo. |
| Endothelial cell growth supplement, shear force | Human | [54] | Ac-LDL uptake and expression of CD31 in vitro. No expression of eNOS or vWf. |
| Shear stress + VEGF | Human | [55] | Expression of CD31, VE-cadherin, vWf, eNOS and VEGFR1 and -2 in vitro. |
| Added FGF-2 or FGF-2 + VEGF | Human | [56] | Expression of CD31, vWf, eNOS and VE-cadherin and formation of capillary-like structures on Matrigel in vitro. Blockade of FGF receptor inhibits differentiation. |
| Hypoxia in combination with leptin and VEGF | Human | [57] | Expression of CD31, VE-cadherin, vWf, VEGR2 and eNOS and increased sprout formation on Matrigel in vitro. Blockade of AKT inhibits differentiation. |
| HUVEC priming | Human | [58] | Change in morphology and increased expression of CD31, vWf and eNOS. Formation of capillary-like tube networks on Matrigel. |
| 3D cell culturing | Human | [49] | Formation of 3D cell mass induced hypoxia and expression of VEGF, IL-8 and CD31 among other angiogenic factors. Formation of vascular structures in vivo when implanted in mice. |
| Silencing of MMP-2 and MMP-14 | Pig | [50] | Increased expression of CD31 and VE-cadherin, formation of capillary tubes and ac-LDL uptake in vitro. Decreased cleavage of VEGFR2. |