Photobiomodulation augments the effects of mitochondrial transplantation in the treatment of spinal cord injury in rats by facilitating mitochondrial transfer to neurons via Connexin 36

• Published in: Bioengineering & translational medicine Vol. 8; no. 3; pp. e10473 - n/a
• Main Authors: Zhu, Zhijie, Li, Xin, Wang, Xuankang, Zuo, Xiaoshuang, Ma, Yangguang, Gao, Xue, Liang, Zhuowen, Zhang, Zhihao, Song, Zhiwen, Ding, Tan, Ju, Cheng, Li, Penghui, Li, Kun, Zhang, Jiawei, Quan, Huilin, Wang, Zhe, Hu, Xueyu
• Format: Journal Article
• Language: English
• Published: Hoboken, USA John Wiley & Sons, Inc 01-05-2023; Wiley
• Subjects: Adenosine triphosphate; Alzheimer's disease; Apoptosis; Blood platelets; connexin; Flow cytometry; Ganglia; In vivo methods and tests; Lasers; Metastasis; Mitochondria; mitochondrial transplantation; neuron; Neurons; Phosphorylation; photobiomodulation; Recovery; Spinal cord injuries; spinal cord injury; Transplantation; United States > US; China; photobiomodulation; spinal cord injury; neuron; connexin; mitochondrial transplantation
• ISSN: 2380-6761; 2380-6761
• DOI: 10.1002/btm2.10473

Mitochondrial transplantation is a promising treatment for spinal cord injury (SCI), but it has the disadvantage of low efficiency of mitochondrial transfer to targeted cells. Here, we demonstrated that Photobiomodulation (PBM) could promote the transfer process, thus augmenting the therapeutic effect of mitochondrial transplantation. In vivo experiments, motor function recovery, tissue repair, and neuronal apoptosis were evaluated in different treatment groups. Under the premise of mitochondrial transplantation, the expression of Connex36 (Cx36), the trend of mitochondria transferred to neurons, and its downstream effects, such as ATP production and antioxidant capacity, were evaluated after PBM intervention. In in vitro experiments, dorsal root ganglia (DRG) were cotreated with PBM and 18β‐GA (a Cx36 inhibitor). In vivo experiments showed that PBM combined with mitochondrial transplantation could increase ATP production and reduce oxidative stress and neuronal apoptosis levels, thereby promoting tissue repair and motor function recovery. In vitro experiments further verified that Cx36 mediated the transfer of mitochondria into neurons. PBM could facilitate this progress via Cx36 both in vivo and in vitro. The present study reports a potential method of using PBM to facilitate the transfer of mitochondria to neurons for the treatment of SCI.