Background:
Amniotic Fluid Derived Mesenchymal Stem Cells (AF-MSCs) are adult, fibroblast-
like, self-renewable, multipotent stem cells. During the last decade, the therapeutic potential of
AF-MSCs, based on their huge differentiation capacity and immunomodulatory characteristics, has
been extensively explored in animal models of degenerative and inflammatory diseases.
Objective:
In order to describe molecular mechanisms responsible for the therapeutic effects of AFMSCs,
we summarized current knowledge about phenotype, differentiation potential and immunosuppressive
properties of AF-MSCs.
Methods:
An extensive literature review was carried out in March 2018 across several databases
(MEDLINE, EMBASE, Google Scholar), from 1990 to present. Keywords used in the selection were:
“amniotic fluid derived mesenchymal stem cells”, “cell-therapy”, “degenerative diseases”, “inflammatory
diseases”, “regeneration”, “immunosuppression”. Studies that emphasized molecular and cellular
mechanisms responsible for AF-MSC-based therapy were analyzed in this review.
Results:
AF-MSCs have huge differentiation and immunosuppressive potential. AF-MSCs are capable
of generating cells of mesodermal origin (chondrocytes, osteocytes and adipocytes), neural cells, hepatocytes,
alveolar epithelial cells, insulin-producing cells, cardiomyocytes and germ cells. AF-MSCs, in
juxtacrine or paracrine manner, regulate proliferation, activation and effector function of immune cells.
Due to their huge differentiation capacity and immunosuppressive characteristic, transplantation of AFMSCs
showed beneficent effects in animal models of degenerative and inflammatory diseases of
nervous, respiratory, urogenital, cardiovascular and gastrointestinal system.
Conclusion:
Considering the fact that amniotic fluid is obtained through routine prenatal diagnosis,
with minimal invasive procedure and without ethical concerns, AF-MSCs represents a valuable source
for cell-based therapy of organ-specific or systemic degenerative and inflammatory diseases.
Skullcapflavone II Suppresses TNF-α/IFN-γ-Induced TARC, MDC, and CTSS Production in HaCaT Cells