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Oligodendrocyte Piezo2 is a regulator of age-dependent myelin integrity and dysregulated in multiple sclerosis - retina snRNA-seq data

ABSTRACT: Triggered by the relevance of Piezo mechanosensitive ion channels in different organs with functions beyond touch and pain sensation, we aimed to investigate Piezo2 in the central nervous system with a focus on the anterior visual system, especially because its role in the CNS lacks understanding. We found a bimodal expression pattern with Piezo1 in progenitors and Piezo2 in mature oligodendrocytes, which was conserved between mice and humans. Using two different OL-specific loss-of-function approaches, we found Piezo2 to be relevant for myelin compactness and white matter integrity in aged mice. Ultrastructural imaging was paired with snRNA-seq analysis and motor function testing that confirmed regulatory roles of Piezo2 in motor function and white matter integrity. We complemented our work with a validation study in human control and multiple sclerosis optic nerve tissue, and found Piezo2 to be downregulated in OLs towards the lesion rim.

ORGANISM(S): Mus musculus

PROVIDER: GSE304318 | GEO | 2026/06/03

REPOSITORIES: GEO

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Oligodendrocyte Piezo2 is a regulator of age-dependent myelin integrity and dysregulated in multiple sclerosis - ON snRNA-seq data

Project description:Triggered by the relevance of Piezo mechanosensitive ion channels in different organs with functions beyond touch and pain sensation, we aimed to investigate Piezo2 in the central nervous system with a focus on the anterior visual system, especially because its role in the CNS lacks understanding. We found a bimodal expression pattern with Piezo1 in progenitors and Piezo2 in mature oligodendrocytes, which was conserved between mice and humans. Using two different OL-specific loss-of-function approaches, we found Piezo2 to be relevant for myelin compactness and white matter integrity in aged mice. Ultrastructural imaging was paired with snRNA-seq analysis and motor function testing that confirmed regulatory roles of Piezo2 in motor function and white matter integrity. We complemented our work with a validation study in human control and multiple sclerosis optic nerve tissue, and found Piezo2 to be downregulated in OLs towards the lesion rim.

2026-06-03 | GSE304323 | GEO

Multisite phosphorylation by protein kinase A mediates modality-specific modulation of PIEZO2

Project description:Protein kinase A is a downstream effector of many inflammatory mediators that induce pain hypersensitivity by increasing the mechanosensitivity of nociceptive sensory afferent. Here we examine the molecular mechanism underlying protein kinase-Adependent modulation of the mechanically-activated ion channel PIEZO2, which confers mechanosensitivity to many nociceptors. Using phosphorylation site prediction algorithms, we identified multiple putative and highly conserved PKA phosphorylation sites located on intracellular intrinsically disordered regions of PIEZO2. Site-directed mutagenesis and patch-clamp recordings showed that substitution of one or multiple putative PKA sites within a single intracellular domains does not alter PKA-induced PIEZO2 sensitization, whereas mutation of a combination of nine putative sites located on four different intracellular regions completely abolishes PKA-dependent PIEZO2 modulation, suggesting that the effect requires multisite phosphorylation. By demonstrating that PIEZO1 is not modulated by PKA, our data also reveals a previously unrecognized functional difference between PIEZO1 and PIEZO2. Moreover, by demonstrating that PKA only modulates PIEZO2 currents evoked by focal mechanical indentation of the cell, but not currents evoked by pressure-induced membrane stretch, we provide evidence suggesting that PIEZO2 is a polymodal mechanosensor that engages different protein domains for detecting different types of mechanical stimuli.

2023-07-20 | PXD041372 | Pride

PIEZO2 mechanoreceptor-expressing fibroblasts in keloids cause short-term recurrence after surgical resection

Project description:Keloids are characterized by persistent scar tissue growth that causes abnormal sensory perceptions due to mechanical stress. But the molecular dysfunction and disease-specific cells that fashion keloid pathophysiology are still not evident. Here, we found a distinct subpopulation of fibroblasts with enhanced expression of PIEZO2 in the dermal layer of keloid patients experiencing dysesthesia, including pain and pressure-tactile itch. The PIEZO2-expressing fibroblasts exhibited a keloid-typical phenotype marked by increased extracellular matrix production signaling and higher levels of collagens such as COL1A1, COL1A2, and COL3A1 compared with other fibroblasts. Notably, patients with higher PIEZO2 expression tend to experience keloid recurrence more quickly after keloidectomy (4/5 vs. 0/5, p = 0.047) than those with lower PIEZO2 expression. Thus, the PIEZO2-positive fibroblasts are indicative cells that most accurately reflect the keloid characteristics, suggesting the driving role for the persistent growth of Keloids.

2025-06-20 | GSE274709 | GEO

Fibroblasts expressing PIEZO2 mechanoreceptor in keloids possibly cause alloknesis and short-term recurrence after surgical resection [scRNA-seq]

Project description:Keloids are scar tissue that can develop under tensile stress and manifest the tactile itch called alloknesis due to the heterogeneous course. But the molecular and cellular mechanisms underlying the pathology of keloid have been still unknown. Here, we found that unique fibroblast subpopulation that have dense-core granules with enhanced expression of PIEZO2 in the dermal layer of keloid tissue with alloknesis, a pressure-tactile itch. PIEZO2-expressed fibroblasts showed enhanced expression of COL1A1, COL1A2 and COL3A1. Gene expression profile analysis of fibrous disease tissues could distinguish the keloid cases by higher PIEZO2, which correlated with collagen COL1A1, COL1A2, and COL3A1 gene expression, not only from the keloid cases with lower PIEZO2 expression but also from the lymphedema cases where massive fibroblast proliferation appears. Notably, patients with the keloid accompanied by higher expression of PIEZO2 showed a significantly shorter time to recurrence after keloidectomy in patients with the keloids (4/5 vs. 0/5, p = 0.047). Thus, a unique subset of PIEZO2-positive fibroblasts may be involved in a keloid pathology and be a potent therapeutic target for the intractable keloids.

2025-06-20 | GSE266334 | GEO

Fibroblasts expressing PIEZO2 mechanoreceptor in keloids possibly cause alloknesis and short-term recurrence after surgical resection [RNA-seq]

2025-06-20 | GSE266338 | GEO

Piezo2 in sensory neurons regulates systemic and adipose tissue metabolism

Project description:Systemic metabolism ensures energy homeostasis through inter-organ crosstalk regulating thermogenic adipose tissue. Unlike the well-described inductive role of the sympathetic system, the inhibitory signal ensuring energy preservation remains poorly understood. Here, we show that, via the mechanosensor Piezo2, sensory neurons regulate morphological and physiological properties of brown and beige fat and prevent systemic hypermetabolism. Targeting runt-related transcription factor 3 (Runx3)/parvalbumin (PV) sensory neurons in independent genetic mouse models resulted in a systemic metabolic phenotype characterized by reduced body fat and increased insulin sensitivity and glucose tolerance. Deletion of Piezo2 in PV sensory neurons reproduced the phenotype, protected against high-fat-diet-induced obesity, and caused adipose tissue browning and beiging, likely driven by elevated norepinephrine levels. Finding that brown and beige fat are innervated by Runx3/PV sensory neurons expressing Piezo2 suggests a model in which mechanical signals, sensed by Piezo2 in sensory neurons, protect energy storage and prevent a systemic hypermetabolic phenotype.

2025-02-19 | GSE256369 | GEO

A key role of PIEZO2 mechanosensitive ion channel in adipose sensory innervation [scRNA-seq]

Project description:Compared to the well-established functions of sympathetic innervation, the role of sensory afferents in adipose tissues remains less understood. Recent work revealed the anatomical and physiological significance of adipose sensory innervation; however, its molecular underpinning remains unclear. Here, using organ-targeted single-cell RNA sequencing, we identified the mechanoreceptor PIEZO2 as one of the most prevalent receptors in fat-innervating dorsal root ganglia (DRG) neurons. Selective PIEZO2 deletion in fat-innervating neurons led to molecular alternations in adipose tissue similar to DRG ablation. Conversely, a gain-of-function PIEZO2 mutant shifted the adipose phenotypes in the opposite direction. These results indicate that PIEZO2 plays a major role in the sensory regulation of adipose tissues. This discovery opens new avenues for exploring mechanosensation in organs not traditionally considered mechanically active, such as the adipose tissues, and therefore sheds light on the broader significance of mechanosensation in regulating organ function and homeostasis.

2025-02-02 | GSE286425 | GEO

A key role of PIEZO2 mechanosensitive ion channel in adipose sensory innervation [bulk RNA-seq]

2025-02-02 | GSE286424 | GEO

Focal white matter lesions drive grey matter inflammation, neuronal dysfunction and synapse loss

Project description:Focal white matter lesions occur in most neurodegenerative disorders. Despite occurring early in disease, white matter lesions are considered either independent of, or secondary to, grey matter neuroinflammation, synapse loss and altered neuronal activity. Notably their functional impact on neuronal circuits has been understudied. To address this, we generated a focal white matter lesion in an anatomically well-defined circuit, in which white matter lesions occur in many neurodegenerative disorders. Here we show that focal white matter lesions evoke transient neuronal activity changes and microgliosis, with subsequent synapse loss and increased microglia engulfment in the grey matter, which is reversed if myelin regeneration completes. Grey matter microgliosis is often considered detrimental but we show that it is an integral part of the myelin regenerative process. When we prevent these transient changes in the grey matter, myelin regeneration is blocked in the white matter. Conversely, inducing myelin regeneration failure leads to chronic neuroinflammation in the grey matter, suggesting that myelin regeneration failure drives sustained grey matter microglial activation. This recapitulates the low-grade inflammation considered to be a dominant mechanism underlying neurodegeneration. Our findings reveal a form of regenerative plasticity coupling white matter integrity to grey matter function - a novel mechanism of neuroplasticity that may underlie multiple neurodegenerative conditions - and highlights the potential of targeting myelin regeneration to prevent chronic inflammation.

2026-02-05 | GSE311781 | GEO

Oligodendrocyte Progenitor Cell Transcriptome in White Matter Stroke

Project description:Tissue progenitors maintain the integrity of organ systems through aging and stress. The brain’s white matter regions experience ischemic lesions and age-dependent degeneration. Brain white matter contains progenitors, oligodendrocyte precursor cells (OPCs), which can repair some insults. The response of OPCs to white matter ischemia and aging is not known. We characterized the response of OPCs to white matter stroke using OPC reporter mice, cell migration tracking, OPC specific RNA sequencing, and mechanistic studies in candidate biochemical pathways in the aged brain. White matter stroke induces initial proliferation of local OPCs but blocks differentiation, shunting a portion into astrocytes. Candidate signaling pathways for this differentiation block including novel interactions of inhibin and matrilin-2 and new roles of NgR1 ligands following white matter stroke. Stroke induces inhibin expression in astrocytes and downregulates OPC matrilin-2 that contributes into OPC differentiation block. Antagonism of NgR1 ligands promotes OPC differentiation by attenuating the OPC astrocytic transformation and enhances functional recovery from stroke in aged animals.

2019-11-15 | GSE53737 | GEO

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