Dataset Information

TMT-based quantitative proteomic analysis of serum from patients with postherpetic neuralgia reveals a key role of Endoglin in neuropathic pain via TGF-β/Smad2 signaling

ABSTRACT: This dataset comprises a Tandem Mass Tag (TMT)-based quantitative proteomic analysis of serum samples from patients with postherpetic neuralgia (PHN) compared to healthy control subjects. The study aimed to identify differentially expressed proteins involved in the pathogenesis of neuropathic pain. Peripheral blood serum was collected from three PHN patients and three age- and sex-matched healthy volunteers. Proteins were digested with trypsin, labeled with TMT isobaric tags, and fractionated by reversed-phase liquid chromatography. The peptides were analyzed by liquid chromatography-tandem mass spectrometry (LC-MS/MS) on a SCIEX TripleTOF 5600+ instrument. Our analysis identified 127 differentially expressed proteins (79 down-regulated and 48 up-regulated in the PHN group). Notably, Endoglin (CD105), a key endothelial cell membrane glycoprotein, was one of the significantly down-regulated proteins. This discovery was subsequently validated by ELISA in a larger cohort (n=30 per group). The proteomic profiling presented in this dataset led to the mechanistic hypothesis that reduced Endoglin expression contributes to neuropathic pain by disrupting the blood-spinal cord barrier (BSCB) integrity via inhibition of the TGF-β/Smad2 signaling pathway. This hypothesis was successfully confirmed in a spared nerve injury (SNI) rat model through behavioral, biochemical, and histological experiments, as detailed in our associated manuscript. This dataset provides the foundational proteomic evidence for the role of Endoglin in neuropathic pain and serves as a valuable resource for identifying potential biomarkers and therapeutic targets.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Blood Cell, Blood Serum

DISEASE(S): Herpes Zoster Oticus

SUBMITTER: Zhou FeiRan

LAB HEAD: Ying Zhang

PROVIDER: PXD067890 | Pride | 2025-10-06

REPOSITORIES: Pride

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Publications

Endoglin alleviates neuropathic pain by protecting the blood-spinal cord barrier through the TGF-β/Smad2 signaling pathway.

Liao SiJing S Zhou Fei-Ran FR Li Qun Q Jin Tao T Xiang Gui-Fang GF Wang Xin X Liu Yan Y Zhu Hq H Liu Qing Q Liu Yuexin Y Zhang Ying Y

Frontiers in molecular neuroscience 20250915

<h4>Introduction</h4>Central neuroinflammation is pivotal in neuropathic pain pathogenesis, with blood-spinal cord barrier (BSCB) dysfunction recognized as a trigger for neuroinflammation and pain, though molecular mechanisms remain poorly understood.<h4>Methods</h4>Through comparative clinical studies measuring serum endoglin in postherpetic neuralgia (PHN) patients versus healthy controls, and animal investigations using spared nerve injury (SNI) rat models with recombinant endoglin interventi ...[more]

PMID: 41030313

Similar Datasets

Project description:Peripheral nerve injury alters the expression of hundreds of proteins in dorsal root ganglia (DRG). Targeting some of these proteins has led to successful treatments for acute pain, but not for sustained postoperative neuropathic pain. The latter may require targeting multiple proteins. Since a single microRNA (miR) can affect the expression of multiple proteins, here, we describe an approach to identify chronic neuropathic pain-relevant miRs. We used two variants of the spared nerve injury (SNI): Sural-SNI and Tibial-SNI and found distinct pain phenotypes between the two. Both models induced strong mechanical allodynia, but only Sural-SNI rats maintained strong mechanical and cold allodynia, as previously reported. In contrast, we found that Tibial-SNI rats recovered from mechanical allodynia and never developed cold allodynia. Since both models involve nerve injury, we increased the probability of identifying differentially regulated miRs that correlated with the quality and magnitude of neuropathic pain and decreased the probability of detecting miRs that are solely involved in neuronal regeneration. We found seven such miRs in L3-L5 DRG. The expression of these miRs increased in Tibial-SNI. These miRs displayed a lower level of expression in Sural-SNI, with four having levels lower than those in sham animals. Bioinformatics analysis of how these miRs could affect the expression of some ion channels supports the view that, following a peripheral nerve injury, the increase of the 7 miRs may contribute to the recovery from neuropathic pain while the decrease of four of them may contribute to the development of chronic neuropathic pain. The approach used resulted in the identification of a small number of potentially neuropathic pain relevant miRs. Additional studies are required to investigate whether manipulating the expression of the identified miRs in primary sensory neurons can prevent or ameliorate chronic neuropathic pain following peripheral nerve injuries. To identify the miRs that were differentially dysregulated between Tibial-SNI and Sural-SNI, we first performed 12 microarrays in a limited number of samples (in four individual DRGs per group: Sham, Tibial-SNI and Sural-SNI; two L3-DRG and two L4-DRG). Then, miRs identified as having differential expression were corroborated with real time qRT-PCR in RNA isolated from individual DRGs (L3, L4 and L5) derived from 4 rats per group (not presented here, but in the manuscript).

			Action	DRS
	P0791S_.msf	Msf
	P0791S_.msfView	Msf
	P0791S_.pdResult	Other
	P0791S_.pdResultView	Other
	P0791S_.pdStudy	Other