A platform for research: civil engineering, architecture and urbanism
A platform for research: civil engineering, architecture and urbanism
Reversing Persistent PTEN Activation after Traumatic Brain Injury Fuels Long‐Term Axonal Regeneration via Akt/mTORC1 Signaling Cascade
https://orcid.org/0000-0002-0009-4225
https://orcid.org/0000-0001-8586-7532
https://orcid.org/0009-0005-2909-6506
https://orcid.org/0000-0003-1703-6504
https://orcid.org/0009-0007-9982-645X
https://orcid.org/0000-0002-7689-435X
https://orcid.org/0000-0003-2444-2332
https://orcid.org/0009-0006-2028-8138
https://orcid.org/0009-0006-6096-2633
https://orcid.org/0000-0002-0962-7702
https://orcid.org/0000-0002-4915-9819
AbstractTraumatic brain injury (TBI) often leads to enduring axonal damage and persistent neurological deficits. While PTEN's role in neuronal growth is recognized, its long‐term activation changes post‐TBI and its effects on sensory‐motor circuits are not well understood. Here, it is demonstrated that the neuronal knockout of PTEN (PTEN‐nKO) significantly enhances both structural and functional recovery over the long term after TBI. Importantly, in vivo, DTI‐MRI revealed that PTEN‐nKO promotes white matter repair post‐TBI. Additionally, calcium imaging and electromyographic recordings indicated that PTEN‐nKO facilitates cortical remapping and restores sensory‐motor pathways. Mechanistically, PTEN negatively regulates the Akt/mTOR pathway by inhibiting Akt, thereby suppressing mTOR. Raptor is a key component of mTORC1 and its suppression impedes axonal regeneration. The restoration of white matter integrity and the improvements in neural function observed in PTEN‐nKO TBI‐treated mice are reversed by a PTEN/Raptor double knockout (PTEN/Raptor D‐nKO), suggesting that mTORC1 acts as a key mediator. These findings highlight persistent alterations in the PTEN/Akt/mTORC1 axis are critical for neural circuit remodeling and cortical remapping post‐TBI, offering new insights into TBI pathophysiology and potential therapeutic targets.
Reversing Persistent PTEN Activation after Traumatic Brain Injury Fuels Long‐Term Axonal Regeneration via Akt/mTORC1 Signaling Cascade
https://orcid.org/0000-0002-0009-4225
https://orcid.org/0000-0001-8586-7532
https://orcid.org/0009-0005-2909-6506
https://orcid.org/0000-0003-1703-6504
https://orcid.org/0009-0007-9982-645X
https://orcid.org/0000-0002-7689-435X
https://orcid.org/0000-0003-2444-2332
https://orcid.org/0009-0006-2028-8138
https://orcid.org/0009-0006-6096-2633
https://orcid.org/0000-0002-0962-7702
https://orcid.org/0000-0002-4915-9819
AbstractTraumatic brain injury (TBI) often leads to enduring axonal damage and persistent neurological deficits. While PTEN's role in neuronal growth is recognized, its long‐term activation changes post‐TBI and its effects on sensory‐motor circuits are not well understood. Here, it is demonstrated that the neuronal knockout of PTEN (PTEN‐nKO) significantly enhances both structural and functional recovery over the long term after TBI. Importantly, in vivo, DTI‐MRI revealed that PTEN‐nKO promotes white matter repair post‐TBI. Additionally, calcium imaging and electromyographic recordings indicated that PTEN‐nKO facilitates cortical remapping and restores sensory‐motor pathways. Mechanistically, PTEN negatively regulates the Akt/mTOR pathway by inhibiting Akt, thereby suppressing mTOR. Raptor is a key component of mTORC1 and its suppression impedes axonal regeneration. The restoration of white matter integrity and the improvements in neural function observed in PTEN‐nKO TBI‐treated mice are reversed by a PTEN/Raptor double knockout (PTEN/Raptor D‐nKO), suggesting that mTORC1 acts as a key mediator. These findings highlight persistent alterations in the PTEN/Akt/mTORC1 axis are critical for neural circuit remodeling and cortical remapping post‐TBI, offering new insights into TBI pathophysiology and potential therapeutic targets.
Reversing Persistent PTEN Activation after Traumatic Brain Injury Fuels Long‐Term Axonal Regeneration via Akt/mTORC1 Signaling Cascade
https://orcid.org/0000-0002-0009-4225
https://orcid.org/0000-0001-8586-7532
https://orcid.org/0009-0005-2909-6506
https://orcid.org/0000-0003-1703-6504
https://orcid.org/0009-0007-9982-645X
https://orcid.org/0000-0002-7689-435X
https://orcid.org/0000-0003-2444-2332
https://orcid.org/0009-0006-2028-8138
https://orcid.org/0009-0006-6096-2633
https://orcid.org/0000-0002-0962-7702
https://orcid.org/0000-0002-4915-9819
AbstractTraumatic brain injury (TBI) often leads to enduring axonal damage and persistent neurological deficits. While PTEN's role in neuronal growth is recognized, its long‐term activation changes post‐TBI and its effects on sensory‐motor circuits are not well understood. Here, it is demonstrated that the neuronal knockout of PTEN (PTEN‐nKO) significantly enhances both structural and functional recovery over the long term after TBI. Importantly, in vivo, DTI‐MRI revealed that PTEN‐nKO promotes white matter repair post‐TBI. Additionally, calcium imaging and electromyographic recordings indicated that PTEN‐nKO facilitates cortical remapping and restores sensory‐motor pathways. Mechanistically, PTEN negatively regulates the Akt/mTOR pathway by inhibiting Akt, thereby suppressing mTOR. Raptor is a key component of mTORC1 and its suppression impedes axonal regeneration. The restoration of white matter integrity and the improvements in neural function observed in PTEN‐nKO TBI‐treated mice are reversed by a PTEN/Raptor double knockout (PTEN/Raptor D‐nKO), suggesting that mTORC1 acts as a key mediator. These findings highlight persistent alterations in the PTEN/Akt/mTORC1 axis are critical for neural circuit remodeling and cortical remapping post‐TBI, offering new insights into TBI pathophysiology and potential therapeutic targets.
Reversing Persistent PTEN Activation after Traumatic Brain Injury Fuels Long‐Term Axonal Regeneration via Akt/mTORC1 Signaling Cascade
Advanced Science
Shi, Ziyu (author) / Mao, Leilei (author) / Chen, Shuning (author) / Du, Zhuoying (author) / Xiang, Jiakun (author) / Shi, Minghong (author) / Wang, Yana (author) / Wang, Yuqing (author) / Chen, Xingdong (author) / Xu, Zhi‐Xiang (author)
Advanced Science ; 12
2025-02-01
Article (Journal)
Electronic Resource
English
Text comprehension after traumatic brain injury: Missing the gist?
| British Library Conference Proceedings | 2005
Nano‐Engineering in Traumatic Brain Injury
| Wiley | 2023
Neurocritical Care for Traumatic Brain Injury
| British Library Online Contents | 2016