Combined treatment of human mesenchymal stem cells and green tea extract on retinal ganglion cell regeneration in rats after optic nerve injury

• Published in: Experimental eye research Vol. 239; p. 109787
• Main Authors: Yang, Qichen, Xu, Yanxuan, Bin, Xin, Chan, Kwok Ping, Chen, Shaowan, Qian, Zhen, Yao, Yao, Yuan, Xiang-Ling, Qiu, Kunliang, Huang, Yuqiang, Ng, Tsz Kin
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.02.2024
• Subjects: Animals; Axons - metabolism; Cell Survival - physiology; Green tea extract; Humans; Mesenchymal Stem Cells; Nerve Regeneration - physiology; Neuroprotection; Optic Nerve Injuries - metabolism; Optic Nerve Injuries - therapy; Optic nerve injury; Osteogenesis; Rats; Retinal ganglion cells; Retinal Ganglion Cells - metabolism; Tea - metabolism; Retinal ganglion cells; Green tea extract; Neuroprotection; Optic nerve injury; Mesenchymal stem cells
• ISSN: 0014-4835; 1096-0007
• DOI: 10.1016/j.exer.2024.109787

Retinal ganglion cell (RGC) death and axonal loss cause irreversible vision loss upon optic nerve (ON) injury. We have independently demonstrated that mesenchymal stem cells (MSCs) and green tea extract (GTE) promote RGC survival and axonal regeneration in rats with ON injury. Here we aimed to evaluate the combined treatment effect of human bone marrow-derived MSCs (hBM-MSCs) and GTE on RGC survival and axonal regeneration after ON injury. Combined treatment of hBM-MSCs and GTE promoted RGC survival and neurite outgrowth/axonal regeneration in ex vivo retinal explant culture and in rats after ON injury. GTE increased Stat3 activation in the retina after combined treatment, and enhanced brain-derived neurotrophic factor secretion from hBM-MSCs. Treatment of 10 μg/mL GTE would not induce hBM-MSC apoptosis, but inhibited their proliferation, migration, and adipogenic and osteogenic differentiation in vitro with reducing matrix metalloproteinase secretions. In summary, this study revealed that GTE can enhance RGC protective effect of hBM-MSCs, suggesting that stem cell priming could be a prospective strategy enhancing the properties of stem cells for ON injury treatment. •Combined treatment of hBM-MSCs and GTE can enhance RGC survival and axonal regeneration in rats after ON injury.•Combined treatment of hBM-MSCs and GTE can increase STAT3 activation and BDNF secretion.•GTE does not cause hBM-MSC apoptosis, but inhibits migration, proliferation, and adipogenic and osteogenic differentiation.