Abstract
Astrogliosis following spinal cord injury (SCI) was considered as a negative factor for neural regeneration. We found that miR-21 was significantly upregulated after SCI. So, we aim to determine whether miR-21 acts in a positive manner post SCI. In vitro, we measured the proliferation, apoptosis and cytokine secretion of primary cultured astrocytes after modulating the expression of miR-21 by western blot, RT-PCR and immunofluorescence. In vivo, we performed a modified Allen’s weight drop model. Manipulation of the miR-21 expression level was achieved by interfering with antagomir and agomir. Clinic score was evaluated and recorded every day. Then, western blot, immunohistochemistry, TUNEL assay and ELISA were performed to detect pathological and functional alterations. Our results demonstrate that miR-21 can modulate the secretion, proliferation and apoptosis of astrocytes to promote recovery after SCI both in vivo and in vitro. These effects are likely mediated through transforming growth factor beta mediated targeting of the PI3K/Akt/mTOR pathway. These data suggest that miR-21 can regulate astrocytic function, then promote the functional recovery after SCI. We therefore highlight the positive effects of miR-21 after SCI.
Highlights
Spinal cord injury (SCI) is the most severe complication of spine trauma because it causes serious physical and psychological harm
After verification and we hypothesized that miR-21 might serve as an important candidate of astrogliosis regulator, as it was significantly upregulated after spinal cord injury (SCI)
The immunohistochemistry analysis confirmed the significantly elevated protein levels of transforming growth factor-beta1 (TGF-β1) (Fig. 1D), glial fibrillary acidic protein (GFAP) (Fig. 1E), and chondroitin sulfate proteoglycans (CSPGs) (Fig. 1F) in the SCI sections compared to the sham counterparts
Summary
Spinal cord injury (SCI) is the most severe complication of spine trauma because it causes serious physical and psychological harm. Many studies have suggested that astrogliosis following SCI resulted in local tissue hypertrophic response, limited inflammation, and subsequential formation of glial scars that may act as a physical barrier for axon regeneration [1, 2]. Astrocytes become activated, characterized by increased expression of glial fibrillary acidic protein (GFAP). They become hypertrophic and hyperplasia occurs around the lesion site. Secretion of neurotrophins such as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) has been identified in astrocytes [11] In this regard, we hypothesized that astrocytes might play a dual role in axon regeneration during both acute and chronic stages of SCI
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