Low-Density Lipoprotein Receptor-Related Protein 1 (LRP1) Is a Negative Regulator of Oligodendrocyte Progenitor Cell Differentiation in the Adult Mouse Brain

Auderset, Loic; Pitman, Kimberley A; Cullen, Carlie L.; Pepper, Renee E; Taylor, Bruce; Foa, Lisa; Young, Karen

doi:10.3389/fcell.2020.564351

Cited by 23 publications

(21 citation statements)

References 119 publications

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“…For the focus of this review, particularly interesting is the observation that transport defects and intracellular accumulation of cholesterol are accompanied by myelin defects in many disorders. For example, the low-density lipoprotein receptor-related protein-1 (Lrp1), a member of the LDL receptor family with prominent functions also in endocytosis, regulates cholesterol homeostasis in OLs [16] and the differentiation of OL progenitor cells (OPs) [17]. This protein can be defective in some demyelinating diseases, such as peroxisome biogenesis disorders.…”

Section: Cholesterol In Myelinationmentioning

confidence: 99%

Myelin Defects in Niemann–Pick Type C Disease: Mechanisms and Possible Therapeutic Perspectives

Bernardo

Nuccio

Visentin

et al. 2021

IJMS

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Niemann–Pick type C (NPC) disease is a wide-spectrum clinical condition classified as a neurovisceral disorder affecting mainly the liver and the brain. It is caused by mutations in one of two genes, NPC1 and NPC2, coding for proteins located in the lysosomes. NPC proteins are deputed to transport cholesterol within lysosomes or between late endosome/lysosome systems and other cellular compartments, such as the endoplasmic reticulum and plasma membrane. The first trait of NPC is the accumulation of unesterified cholesterol and other lipids, like sphingosine and glycosphingolipids, in the late endosomal and lysosomal compartments, which causes the blockade of autophagic flux and the impairment of mitochondrial functions. In the brain, the main consequences of NPC are cerebellar neurodegeneration, neuroinflammation, and myelin defects. This review will focus on myelin defects and the pivotal importance of cholesterol for myelination and will offer an overview of the molecular targets and the pharmacological strategies so far proposed, or an object of clinical trials for NPC. Finally, it will summarize recent data on a new and promising pharmacological perspective involving A2A adenosine receptor stimulation in genetic and pharmacological NPC dysmyelination models.

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Section: Cholesterol In Myelinationmentioning

confidence: 99%

Myelin Defects in Niemann–Pick Type C Disease: Mechanisms and Possible Therapeutic Perspectives

Bernardo

Nuccio

Visentin

et al. 2021

IJMS

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“…AST and VMO1 participate in the adaptive response of Daphnia pulex to environmental temperature changes ( Schwerin et al, 2009 ). LDLR is an important regulator of cell differentiation and proliferation ( Tsukamoto et al, 2012 ; Auderset et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Single-Cell Ribonucleic Acid Sequencing Clarifies Cold Tolerance Mechanisms in the Pacific White Shrimp (Litopenaeus Vannamei)

et al. 2022

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To characterize the cold tolerance mechanism of the Pacific white shrimp (Litopenaeus vannamei), we performed single-cell RNA sequencing (scRNA-seq) of ∼5185 hepatopancreas cells from cold-tolerant (Lv-T) and common (Lv-C) L. vannamei at preferred and low temperatures (28°C and 10°C, respectively). The cells fell into 10 clusters and 4 cell types: embryonic, resorptive, blister-like, and fibrillar. We identified differentially expressed genes between Lv-T and Lv-C, which were mainly associated with the terms “immune system,” “cytoskeleton,” “antioxidant system,” “digestive enzyme,” and “detoxification,” as well as the pathways “metabolic pathways of oxidative phosphorylation,” “metabolism of xenobiotics by cytochrome P450,” “chemical carcinogenesis,” “drug metabolism-cytochrome P450,” and “fatty acid metabolism.” Reconstruction of fibrillar cell trajectories showed that, under low temperature stress, hepatopancreas cells had two distinct fates, cell fate 1 and cell fate 2. Cell fate 1 was mainly involved in signal transduction and sensory organ development. Cell fate 2 was mainly involved in metabolic processes. This study preliminarily clarifies the molecular mechanisms underlying cold tolerance in L. vannamei, which will be useful for the breeding of shrimp with greater cold tolerance.

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“…Primary mixed glial cultures were prepared from P0-5 Pdgfrα-histGFP mice as previously described 98 . Briefly, cortices were dissected into sterile Earle’s Balanced Salt Solution (EBSS, Invitrogen, 14155–063), diced into small pieces and digested in 0.25% (w/v) trypsin (Sigma, T4799) in EBSS at 37 °C for 50 min before the addition of 10% foetal calf serum (FCS, Invitrogen, 10099–141) and 0.12 mg/ml DNAse 1 (Sigma, 5025).…”

Section: Methodsmentioning

confidence: 99%

“…GFP + OPCs were isolated from primary mixed glial cultures at 7 days in vitro (7DIV) by fluorescence-activated cell sorting (FACS) 99 or immunopanning 98 . In brief, cells were detached by exposure to 50% (v/v) TrypLE (Thermo Fisher Scientific, 12604013) in EBSS, the trypsin inactivated by the addition of FCS, and the cells resuspended in 50% (v/v) FCS in EBSS and passed through a 40 µm cell sieve.…”

Section: Methodsmentioning

confidence: 99%

Protocadherin 15 suppresses oligodendrocyte progenitor cell proliferation and promotes motility through distinct signalling pathways

et al. 2022

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Oligodendrocyte progenitor cells (OPCs) express protocadherin 15 (Pcdh15), a member of the cadherin superfamily of transmembrane proteins. Little is known about the function of Pcdh15 in the central nervous system (CNS), however, Pcdh15 expression can predict glioma aggression and promote the separation of embryonic human OPCs immediately following a cell division. Herein, we show that Pcdh15 knockdown significantly increases extracellular signal-related kinase (ERK) phosphorylation and activation to enhance OPC proliferation in vitro. Furthermore, Pcdh15 knockdown elevates Cdc42-Arp2/3 signalling and impairs actin kinetics, reducing the frequency of lamellipodial extrusion and slowing filopodial withdrawal. Pcdh15 knockdown also reduces the number of processes supported by each OPC and new process generation. Our data indicate that Pcdh15 is a critical regulator of OPC proliferation and process motility, behaviours that characterise the function of these cells in the healthy CNS, and provide mechanistic insight into the role that Pcdh15 might play in glioma progression.

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Low-Density Lipoprotein Receptor-Related Protein 1 (LRP1) Is a Negative Regulator of Oligodendrocyte Progenitor Cell Differentiation in the Adult Mouse Brain

Cited by 23 publications

References 119 publications

Myelin Defects in Niemann–Pick Type C Disease: Mechanisms and Possible Therapeutic Perspectives

Myelin Defects in Niemann–Pick Type C Disease: Mechanisms and Possible Therapeutic Perspectives

Single-Cell Ribonucleic Acid Sequencing Clarifies Cold Tolerance Mechanisms in the Pacific White Shrimp (Litopenaeus Vannamei)

Protocadherin 15 suppresses oligodendrocyte progenitor cell proliferation and promotes motility through distinct signalling pathways

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