PXD067597

PXD067597 is an original dataset announced via ProteomeXchange.

Title	Therapeutic effects of neuronal PTEN-knockout reveal a critical role of mitochondrial dysfunction in sustaining locomotor deficits chronically after spinal cord injury
Description	Neuron-specific PTEN-knockout has demonstrated an ability to induce axon regeneration after spinal cord injury (SCI) as well as restore motor functions through regeneration-independent mechanisms. To better understand the biological effects of neuron-specific PTEN-KO, PTENflox mice (Male/Female mix) were treated with spinal cord injections of a retrogradely transported adeno-associated virus (AAVrg) to deliver Cre-recombinase under a Synapsin1 (Syn1) promoter. Naïve, SCI-eGFP, and SCI-Cre-eGFP groups were compared for analyses. AAVrg’s were delivered immediately after SCI and spinal cords were harvested 6 weeks post 100 kDyn contusion. Protein homogenates obtained from whole-spinal cord samples above, and including, the lesion were assessed for total- and phospho-proteomics. Amongst the largest observations from total proteomics, we observed a major injury-induced decrease in mitochondrial proteins, with a notable loss of Complex I subunits, chronically after SCI. In contrast, amongst the largest treatment mediated effects in total proteomics was a PTEN-KO induce increase in mitochondrial peptides, also notably reversing the loss of Complex I mediated subunits. Next, we replicated our experimental model and isolated mitochondria from whole spinal-cord extracts and evaluated for respiratory functions through the electron transport chain which revealed a global decrease in mitochondrial respiration chronically after SCI. PTEN-KO reversed mitochondrial dysfunctions observed chronically after injury. Notably, the largest treatment effect was observed in Complex I mediated respiration, validating the predictions made from total proteomics. To determine the extent that specifically targeting mitochondrial functions can mediate improvements chronically after SCI, we injured mice using a 90 kDyn contusion and injected an AAVrg to overexpress PGC1α as a master regulator of mitochondria and metabolism.
HostingRepository	PRIDE
AnnounceDate	2026-06-11
AnnouncementXML	Submission_2026-06-10_16:00:20.293.xml
DigitalObjectIdentifier
ReviewLevel	Peer-reviewed dataset
DatasetOrigin	Original dataset
RepositorySupport	Unsupported dataset by repository
PrimarySubmitter	Carlos Gartner
SpeciesList	scientific name: Mus musculus (Mouse); NCBI TaxID: NEWT:10090;
ModificationList	iodoacetamide derivatized residue
Instrument	TripleTOF 6600

Revision	Datetime	Status	ChangeLog Entry
0	2025-08-22 01:45:34	ID requested
⏵ 1	2026-06-10 16:00:20	announced

Dataset with its publication pending

submitter keyword: Chronic Spinal Cord Injury

Mitochondria

PTEN

PGC1α

mass spectrometry

SWATH

Calvin Vary
contact affiliation	MaineHealth Institute for Research, Director, Proteomics and Lipidomics Core
contact email	calvin.vary@mainehealth.org
lab head
Carlos Gartner
contact affiliation	MaineHealth Institute for Research
contact email	gusti.gartner@gmail.com
dataset submitter

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PRIDE project URI

• PRIDE
  1. PXD067597
     1. Label: PRIDE project
     2. Name: Therapeutic effects of neuronal PTEN-knockout reveal a critical role of mitochondrial dysfunction in sustaining locomotor deficits chronically after spinal cord injury