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Clinical and pathological findings in neurolymphomatosis: preliminary association with gene expression profiles in sural nerves.

ABSTRACT: Clinical and pathological findings in neurolymphomatosis: preliminary association with gene expression profiles in sural nerves.

PROVIDER: PRJNA880872 | ENA |

REPOSITORIES: ENA

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Clinical and pathological findings in neurolymphomatosis: preliminary association with gene expression profiles in sural nerves.

Project description:Although inflammation appears to play a role in neurolymphomatosis (NL), the mechanisms leading to degeneration in the peripheral nervous system are poorly understood. The purpose of this exploratory study was to identify molecular pathways underlying NL pathogenesis, combining clinical and neuropathological investigation with gene expression (GE) studies. Based on the neuropathic symptoms and signs, NL patients were classified into three forms of neuropathy: chronic symmetrical sensorimotor polyneuropathy (SMPN, n=3), multiple mononeuropathy (MN, n=4) and acute motor-sensory axonal neuropathy (AMSAN, n=1). Predominantly diffuse malignant cells infiltration of epineurium was present in chronic SMPN, whereas endoneurial perivascular cells invasion was observed in MN. In contrast, diffuse endoneurium malignant cells localization occurred in AMSAN. We identified alterations in the expression of 1266 genes, with 115 up-regulated and 1151 down-regulated genes, which were mainly associated with ribosomal proteins (RP) and olfactory receptors (OR) signaling pathways, respectively. Among the top up-regulated genes were actin alpha 1 skeletal muscle (ACTA1) and desmin (DES). Similarly, in NL nerves ACTA1, DES and several RPs were highly expressed, associated with endothelial cells and pericytes abnormalities. Peripheral nerve involvement may be due to conversion towards a more aggressive phenotype, potentially explaining the poor prognosis. The candidate genes reported in this study may be a source of clinical biomarkers for NL.

2022-09-16 | GSE213455 | GEO

Small RNA sequencing of human sural nerves

Project description:Small RNA (miRNA) sequencing of human sural nerves with (n=6) and without (n=6) diabetic peripheral neuropathy

2026-07-21 | GSE324215 | GEO

Small RNA sequencing of human sural nerves

Project description:Small RNA sequencing of human sural nerves

| PRJNA1434182 | ENA

Perirenal Adipose Afferent Nerves Sustain Pathological High Blood Pressure

Project description:Perirenal Adipose Afferent Nerves Sustain Pathological High Blood Pressure

| PRJNA674829 | ENA

Clinical and pathological findings in neurolymphomatosis: Preliminary association with gene expression profiles in sural nerves.

Project description: Not available

| S-EPMC9549065 | biostudies-literature

Perirenal Adipose Afferent Nerves Sustain Pathological High Blood Pressure

Project description:Hypertension is a pathological condition of persistent high blood pressure (BP) of which the underlying mechanisms remain largely obscure. Here, we show that the afferent nerves in perirenal adipose tissue are a regulatory site in triggering and maintaining pathological high BP, without affecting physiological BP. Bilateral perirenal adipose tissue (PRAT) ablation leads to a long-term and effective reduction of BP in spontaneous hypertensive rats (SHR) and high fat and high salt diet fed rats, but has no effect on normal BP in control Wistar-Kyoto or control SD rats. Moreover, gain- and loss-of-function studies show that augmented activities of L1-L2 dorsal root ganglia (DRG) neurons are responsible for hypertension in SHR. Further, L1-L2 DRG neuron transcriptomics uncovers significant changes in neuron development, remodeling, and plasticity. Importantly, calcitonin gene-related peptide (CGRP), a systemic vasodilator, is induced after PRAT ablation. We went on to show that CGRP antagonist blocks the BP-lowering effect of PRAT ablation. CGRP is therefore a key endogenous suppressor of hypertension that is sequestered by anti-hypertensive PRAT in SHRs. Taken together, we identify PRAT afferent nerves as a pathological node of hypertension that sustains high BP via suppressing CGRP, thereby providing a therapeutic target to tackle primary hypertension.

2022-05-10 | GSE160914 | GEO

Multi-omic characterization of human sural nerves across polyneuropathies [Xenium]

Project description:Multi-omic characterization of human sural nerves across polyneuropathies [Xenium]

| PRJNA1207203 | ENA

Multi-omic characterization of human sural nerves across polyneuropathies [snRNA-seq]

Project description:Multi-omic characterization of human sural nerves across polyneuropathies [snRNA-seq]

| PRJNA1207198 | ENA

Using Next-Generation Sequencing Transcriptomics to Determine Markers of Post-traumatic Symptoms - preliminary findings from a post-deployment cohort

Project description:Using Next-Generation Sequencing Transcriptomics to Determine Markers of Post-traumatic Symptoms - preliminary findings from a post-deployment cohort

| PRJNA430870 | ENA

Complement profiling on sural nerves of patients with chronic inflammatory demyelinating polyneuropathy

Project description:Overall, 55 sural nerve biopsies from patients with CIDP (n=36) and CIDP-variants (n=18) were included into the study. Immunohistochemical analysis of the sural nerve specimens showed an aberrant deposition of terminal complement complex C5b-9 on endoneural capillaries in 52 (94%) of patients in addition to endoneural CD8+ T cell- and CD68+ macrophage infiltration. Gene expression studies showed an increase of factors C3 and C6 compared to NDCs with no difference in regard to clinical phenotype, whereas levels of IL6 or TNF-alpha were not significantly elevated. Our proteomic profiling approach revealed the statistically significant dysregulation of 50 proteins, which based on their respective functions suggest altered mitochondrial activity, perturbed cytoskeleton, and increased oxidative stress. The majority of patients with high to moderate complement deposition presented with a progressive disease course, however without any correlation with disease severity as measured by INCAT or MRC at baseline and follow-up. Our combined data supports the role of complement in CIDP pathogenesis. Based on these findings, we propose to further evaluate complement inhibition therapies as new targeted treatment option for patients with CIDP.

2025-09-29 | PXD056286 | Pride

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