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Origin of the continental-scale Tan-Lu fault zone (TLFZ), East China, remains controversial. About 550 km sinistral offset of the Dabie orogenic belt (DOB) and Sulu orogenic belt (SOB) is shown along the NE-NNEstriking TLFZ. Syn-collisional, sinistral ductile shear belts in the TLFZ have been identified. Thirteen phengite bulk separates from the mylonites were dated by the 40 Ar/ 39 Ar method. They gave cooling ages of the 198-181 Ma for the shear belts along the eastern margin of the DOB and 221-210 Ma from the western margin of the SOB. Distribution of the foreland basin deposits suggests that sinistral offset of the DOB and SOB by the TLFZ took place prior to deposition of the Upper Triassic strata. The marginal structures around the DOB and SOB support syn-collisional faulting, and indicate anticlockwise rotation of the DOB during the displacement. The folding and thrust faulting related to crustal subduction, coeval with the TanLu faulting, is older than the foreland basin deposition related to the orogenic exhumation. Several lines of evidence demonstrate that the TLFZ was developed as a syncollisional transform fault during latest Middle to earliest Late Triassic time when the DOB and SOB experienced crustal subduction of the South China Block (SCB). Eastward increase of the crustal subduction rates is believed to be responsible for the sinistral transform faulting.

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Acute traumatic spinal cord injury is a devastating event without effective therapeutic approach. The feeble plasticity of spinal cord microvascular endothelial cells (SCMECs) after trauma is one of the major causes for the exacerbation of spinal cord injury. Therefore, improving the plasticity and regeneration of SCMECs is crucial to promote recovery after spinal cord injury. For the present study, we explored the influence of exosomes derived from neural stem cells (NSCs-Exos) on the spinal cord microvascular regeneration after spinal cord injury and determined the underlying mechanisms. After the primary NSCs and SCMECs were extracted, exosomes were isolated from NSCs conditioned medium and used to co-incubated with the SCMECs in vitro, and then the effect of exosomes on the angiogenic activities of SCMECs was measured. The candidate molecules involved in the NSCs-Exos-mediated angiogenesis were screened using Western blotting. The effect of NSCs-Exos on angiogenesis and spinal cord functional recovery after injury in vivo was analyzed. The results demonstrated that NSCs-Exos could enhance the angiogenic activities of SCMECs, and were highly enriched in VEGF-A. The level of VEGF-A was downregulated in NSCsshVEGF-A-Exos and the pro-angiogenic effects on cocultured SCMECs were inhibited. Furthermore, NSCs-Exos significantly accelerated the microvascular regeneration, reduced the spinal cord cavity, and improved the Basso mouse scale scores in spinal cord injury mice. This work provides the evidence of the underlying mechanism of NSCs-Exos-mediated angiogenesis and suggests a novel therapeutic target for spinal cord injury. Impact statement The feeble plasticity of SCMECs after trauma is one of the major causes for the exacerbation of SCI. Therefore, improving the regeneration ability of SCMECs is crucial to promote spinal cord functional recovery after injury. Our current study uncovered that NSCs-Exos could promote SCMECs migration, tube formation and proliferation in vitro, and further identified that exosomal VEGF-A mediated the pro-angiogenic effect. Furthermore, we observed a remarkable microvascular density increase, spinal cord cavity shrinkage, and motor function recovery in SCI mice treated with NSCs-Exos, which confirmed the therapeutic effects of NSCs-Exos to alleviate SCI. Downregulating VEGF-A partially abolished these effects of NSCs-Exos. This is the first study to reveal that NSCs-Exos has the pro-angiogenic effect on SCMECs by transferring VEGF-A and promote microvascular regeneration and tissue healing, indicating that NSCs-Exos can become a promising therapeutic bioagent for facilitating the functional recovery of SCI.