Table 1.
Molecular mechanism responsible for beneficial effects of MSCs and their secretome in glaucoma treatment.
| Type of MSCs or their secretome | Target cell | MSC-derived factor | Mechanism of action | Effect | Ref. |
|---|---|---|---|---|---|
| DP-MSCs; MSCsNGF | RGCs | NGF | Enhanced expression of Bcl-2 and attenuated expression of Bax in RGCs | Reduced apoptosis of RGCs | [5, 47, 48] |
| DP-MSCs; MSCsBDNF | RGCs | BDNF | Activation of c-jun and suppression of caspase-2 in RGCs | Increased survival of RGCs | [40, 47, 48] |
| BM-MSCs | RGCs | PDGF; CNTF | Increased phosphorylation and activation of STAT-3 | Reduced apoptotic loss of RGCs | [6, 50] |
| BM-MSC-Exos | RGCs | BDNF; NGF; PDGF | Trophic support; miR-17-92 and miR-21-dependent suppression of PTEN | Increased regeneration of RGCs | [5, 56–58] |
| AF-MSC-Exos | T cells | TGF-β; HGF | Suppression of Janus kinase/Stat pathways in inflammatory T cells | Attenuated inflammation in glaucomatous eyes | [5, 67, 68] |
| TM-MSCs; BM-MSC; BM-MSC-CM | TM cells | sox2; notch1; HIF-1 | Activation of autophagy-related mitogenic neuropeptide Apelin; decreased myosin phosphorylation; replacement of injured TM cells | Reduced apoptosis of TM cells; relaxation of TM cells; reduced aqueous humor outflow resistance; attenuated IOP | [9, 75, 76] |
Abbreviations: DP-MSCs: dental pulp-derived MSCs; NGF: nerve growth factor; MSCsNGF: NGF-overexpressing MSCs; RGCs: retinal ganglion cells; BDNF: brain-derived neurotrophic factor; MSCsBDNF: BDNF-overexpressing MSCs; BM-MSCs: bone marrow-derived MSCs; PDGF: platelet-derived growth factor; CNTF: ciliary neurotrophic factor; STAT-3: signal transducer and activator of transcription 3; Exos: exosomes; PTEN: phosphatase and tensin homolog; AF-MSCs: amniotic fluid-derived MSCs; TGF-β: transforming growth factor-β; HGF: hepatocyte growth factor; MSC-CM: MSC-derived conditioned medium; HIF-1: hypoxia-inducible factor 1; IOP: intraocular pressure.