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Journal articles on the topic 'NG2/CSPG4'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Schiffer, Davide, Marta Mellai, Renzo Boldorini, Ilaria Bisogno, Silvia Grifoni, Cristiano Corona, Luca Bertero, Paola Cassoni, Cristina Casalone, and Laura Annovazzi. "The Significance of Chondroitin Sulfate Proteoglycan 4 (CSPG4) in Human Gliomas." International Journal of Molecular Sciences 19, no. 9 (September 12, 2018): 2724. http://dx.doi.org/10.3390/ijms19092724.

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Neuron glial antigen 2 (NG2) is a chondroitin sulphate proteoglycan 4 (CSPG4) that occurs in developing and adult central nervous systems (CNSs) as a marker of oligodendrocyte precursor cells (OPCs) together with platelet-derived growth factor receptor α (PDGFRα). It behaves variably in different pathological conditions, and is possibly involved in the origin and progression of human gliomas. In the latter, NG2/CSPG4 induces cell proliferation and migration, is highly expressed in pericytes, and plays a role in neoangiogenesis. NG2/CSPG4 expression has been demonstrated in oligodendrogliomas, astrocytomas, and glioblastomas (GB), and it correlates with malignancy. In rat tumors transplacentally induced by N-ethyl-N-nitrosourea (ENU), NG2/CSPG4 expression correlates with PDGFRα, Olig2, Sox10, and Nkx2.2, and with new vessel formation. In this review, we attempt to summarize the normal and pathogenic functions of NG2/CSPG4, as well as its potential as a therapeutic target.

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2

Zhang, Hongyu, Zhenyu Wu, Deyu Hu, Min Yan, Jing Sun, Jiejuan Lai, and Lianhua Bai. "Immunotherapeutic Targeting of NG2/CSPG4 in Solid Organ Cancers." Vaccines 10, no. 7 (June 26, 2022): 1023. http://dx.doi.org/10.3390/vaccines10071023.

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: Neuro-glia antigen 2/chondroitin sulfate proteoglycan 4 (NG2/CSPG4, also called MCSP, HMW-MAA, MSK16, MCSPG, MEL-CSPG, or gp240) is a large cell-surface antigen and an unusual cell membrane integral glycoprotein frequently expressed on undifferentiated precursor cells in multiple solid organ cancers, including cancers of the liver, pancreas, lungs, and kidneys. It is a valuable molecule involved in cancer cell adhesion, invasion, spreading, angiogenesis, complement inhibition, and signaling. Although the biological significance underlying NG2/CSPG4 proteoglycan involvement in cancer progression needs to be better defined, based on the current evidence, NG2/CSPG4+ cells, such as pericytes (PCs, NG2+/CD146+/PDGFR-β+) and cancer stem cells (CSCs), are closely associated with the liver malignancy, hepatocellular carcinoma (HCC), pancreatic malignancy, and pancreatic ductal adenocarcinoma (PDAC) as well as poor prognoses. Importantly, with a unique method, we successfully purified NG2/CSPG4-expressing cells from human HCC and PDAC vasculature tissue blocks (by core needle biopsy). The cells appeared to be spheres that stably expanded in cultures. As such, these cells have the potential to be used as sources of target antigens. Herein, we provide new information on the possibilities of frequently selecting NG2/CSPG4 as a solid organ cancer biomarker or exploiting expressing cells such as CSCs, or the PG/chondroitin sulfate chain of NG2/CSPG4 on the cell membrane as specific antigens for the development of antibody- and vaccine-based immunotherapeutic approaches to treat these cancers.

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Mellai, Marta, Laura Annovazzi, Ilaria Bisogno, Cristiano Corona, Paola Crociara, Barbara Iulini, Paola Cassoni, Cristina Casalone, Renzo Boldorini, and Davide Schiffer. "Chondroitin Sulphate Proteoglycan 4 (NG2/CSPG4) Localization in Low- and High-Grade Gliomas." Cells 9, no. 6 (June 24, 2020): 1538. http://dx.doi.org/10.3390/cells9061538.

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Background: Neuron glial antigen 2 or chondroitin sulphate proteoglycan 4 (NG2/CSPG4) is expressed by immature precursors/progenitor cells and is possibly involved in malignant cell transformation. The aim of this study was to investigate its role on the progression and survival of sixty-one adult gliomas and nine glioblastoma (GB)-derived cell lines. Methods: NG2/CSPG4 protein expression was assessed by immunohistochemistry and immunofluorescence. Genetic and epigenetic alterations were detected by molecular genetic techniques. Results: NG2/CSPG4 was frequently expressed in IDH-mutant/1p19q-codel oligodendrogliomas (59.1%) and IDH-wild type GBs (40%) and rarely expressed in IDH-mutant or IDH-wild type astrocytomas (14.3%). Besides tumor cells, NG2/CSPG4 immunoreactivity was found in the cytoplasm and/or cell membranes of reactive astrocytes and vascular pericytes/endothelial cells. In GB-derived neurospheres, it was variably detected according to the number of passages of the in vitro culture. In GB-derived adherent cells, a diffuse positivity was found in most cells. NG2/CSPG4 expression was significantly associated with EGFR gene amplification (p = 0.0005) and poor prognosis (p = 0.016) in astrocytic tumors. Conclusion: The immunoreactivity of NG2/CSPG4 provides information on the timing of the neoplastic transformation and could have prognostic and therapeutic relevance as a promising tumor-associated antigen for antibody-based immunotherapy in patients with malignant gliomas.

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4

Arnesen, Victoria Smith, Susina Suntharalingam, Żaneta Matuszek, Shahin Sarowar, Stian Knappskog, Stein Atle Lie, David R. Liu, Mohummad Aminur Rahman, and Martha Chekenya. "Abstract 3996: A novel 13-basepair deletion in CSPG4/NG2 abrogates protein expression, glioblastoma proliferation and invasion in vitro and in vivo in mice." Cancer Research 82, no. 12_Supplement (June 15, 2022): 3996. http://dx.doi.org/10.1158/1538-7445.am2022-3996.

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Abstract Introduction: Glioblastoma (GBM) is the most frequent treatment resistant and poor prognosis primary brain tumor. Age-adjusted incidence among Caucasians is approx. twice that of Africans. Genetic changes in ethnicity may represent druggable targets for development of new treatments for GBM. Chondroitin sulfate proteoglycan 4 (CSPG4) with sequence homology to neuron-glial-2 (NG2), henceforth CSPG4/NG2, is a transmembrane proteoglycan that is upregulated in GBM, resulting in leaky neovasculature and high cell proliferation, and is independently prognostic for poor survival. Mechanisms regulating CSPG4/NG2 expression remain to be elucidated. Experiments: Tumor-derived DNA whole exome sequences (WES) from mixed American GBM patients (n=300) collected into the TCGA database and blood-derived DNA WES from controls (n = 2504) in the 1000 Genome database were analyzed for mutations in the CSPG4 gene by GATK-3.5. We used prime editing (PE) to introduce a 13-base pair (bp) deletion through design of PE guide RNA (n=27), screening GBM cells (n=14) for CSPG4/NG2 expression, transfecting and expanding PE cells, confirming editing using Sanger sequencing. We functionally characterized the mutation in PE cells and transplanted in orthotopic PDX mouse models compared to wild type (WT) and Cas9 control cells. Western blotting, BrdU proliferation assays, clonogenic- and wound healing assays were used to investigate function. Gelatin zymography assessed CSPG4/NG2 matrix metalloproteinase (MMP) cross-talk during invasion on mixed extracellular matrix- or collagen IV- coated transwells. Results: A novel 13bp frameshift deletion in exon 3 of the CSPG4 gene was identified from WES of GBM samples deposited in TCGA. The mutation was cancer specific (p<0.001). Comparison of frequency in various ethnicities revealed the mutation to be more frequent among African American GBM patients (p=0.019). We generated 3 clones heterozygous for the CSPG4/NG2 deletion in patient derived GBMs. A homozygous deletion was lethal to the cells. The 13bp deletion reduced CSPG4/NG2 expression by approx. 60%, slowed tumor cell proliferation compared to both WT (p<0.001) and Cas9 cells (p<0.0001). PE cells had significantly reduced colony formation (p<0.001), scratch wound healing (p<0.001), had a weaker invasive phenotype when challenged with collagen IV (p<0.001), and reduced cleavage of collagen I by MMP2 that was corroborated by RNAseq gene expression. Reduced growth of PE cells in vivo was verified by multiplex immunohistochemistry on ex vivo brain sections and identified biomarkers for differential tumor development. Tumor growth was reduced in vivo in mice. Conclusions: We identified a novel 13bp deletion in CSPG4/NG2 with phenotypic effect that could be used as a future molecular target in GBM treatment, and present the first successful application of PE in human GBM cells. Citation Format: Victoria Smith Arnesen, Susina Suntharalingam, Żaneta Matuszek, Shahin Sarowar, Stian Knappskog, Stein Atle Lie, David R. Liu, Mohummad Aminur Rahman, Martha Chekenya. A novel 13-basepair deletion in CSPG4/NG2 abrogates protein expression, glioblastoma proliferation and invasion in vitro and in vivo in mice [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 3996.

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5

Yang, Le, Hang Zhang, Chengbin Dong, Wenhui Yue, Renmin Xue, Fuquan Liu, Lin Yang, and Liying Li. "Neuron-Glial Antigen 2 Participates in Liver Fibrosis via Regulating the Differentiation of Bone Marrow Mesenchymal Stem Cell to Myofibroblast." International Journal of Molecular Sciences 24, no. 2 (January 7, 2023): 1177. http://dx.doi.org/10.3390/ijms24021177.

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Neuron-glial antigen 2 (NG2, gene name: Cspg4) has been characterized as an important factor in many diseases. However, the pathophysiological relevance of NG2 in liver disease specifically regarding bone marrow mesenchymal stem cell (BMSC) differentiation to myofibroblast (MF) and the molecular details remain unknown. Human liver tissues were obtained from patients with different chronic liver diseases, and mouse liver injury models were induced by feeding a methionine-choline-deficient and high-fat diet, carbon tetrachloride administration, or bile duct ligation operation. NG2 expression was increased in human and mouse fibrotic liver and positively correlated with MF markers α-smooth muscle actin (αSMA) and other fibrotic markers in the liver. There was a co-localization between NG2 and αSMA, NG2 and EGFP (BMSC-derived MF) in the fibrotic liver determined by immunofluorescence analysis. In vitro, TGFβ1-treated BMSC showed a progressive increase in NG2 levels, which were mainly expressed on the membrane surface. Interestingly, there was a translocation of NG2 from the cell membrane into cytoplasm after the transfection of Cspg4 siRNA in TGFβ1-treated BMSC. siRNA-mediated inhibition of Cspg4 abrogated the TGFβ1-induced BMSC differentiation to MF. Importantly, inhibition of NG2 in vivo significantly attenuated the extent of liver fibrosis in methionine-choline-deficient and high fat (MCDHF) mice, as demonstrated by the decreased mRNA expression of fibrotic parameters, collagen deposition, serum transaminase levels, liver steatosis and inflammation after the administration of Cspg4 siRNA in MCDHF mice. We identify the positive regulation of NG2 in BMSC differentiation to MF during liver fibrosis, which may provide a promising target for the treatment of liver disease.

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6

Finocchiaro, Gaetano, and Serena Pellegatta. "NG2/CSPG4 in glioblastoma: about flexibility." Neuro-Oncology 21, no. 6 (March 28, 2019): 697–98. http://dx.doi.org/10.1093/neuonc/noz055.

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7

Tsidulko, Alexandra Y., Galina M. Kazanskaya, Diana V. Kostromskaya, Svetlana V. Aidagulova, Roman S. Kiselev, Alexandr M. Volkov, Vyacheslav V. Kobozev, Alexei S. Gaitan, Alexei L. Krivoshapkin, and Elvira V. Grigorieva. "Prognostic relevance of NG2/CSPG4, CD44 and Ki-67 in patients with glioblastoma." Tumor Biology 39, no. 9 (September 2017): 101042831772428. http://dx.doi.org/10.1177/1010428317724282.

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Neuron-glial antigen 2 (NG2, also known as CSPG4) and hyaluronic acid receptor CD44 are chondroitin sulphate proteoglycans actively involved in brain development and its malignant transformation. Here, we aimed to compare prognostic significances of NG2, CD44 and Ki-67 expression in glioblastoma multiforme patients. Totally, 45 tissue samples and 83 paraffin-embedded tissues for 75 patients were analysed. The prognostic values of the genes were analysed using Kaplan–Meier survival curves. Grade III gliomas showed 2-fold difference in NG2 expression between anaplastic astrocytoma and oligoastrocytoma (10.1 ± 3.5 and 25.5 ± 14.5, respectively). For grade IV gliomas, upregulated NG2 expression (21.0 ± 6.8) was associated with poor glioblastoma multiforme prognosis (overall survival < 12 months) compared with glioblastoma multiforme patients with good prognosis (4.4 ± 3.2; overall survival > 12 months). Multivariate survival analysis using Cox proportional hazards model confirmed that high NG2 expression was associated with low survival of the patients (hazard ratio: 3.43; 95% confidence interval: 1.18–9.93; p = 0.02), whereas age (hazard ratio: 1.02; 95% confidence interval: 0.96–1.09; p = 0.42), tumour resection (hazard ratio: 1.03; 95% confidence interval: 0.98–1.08; p = 0.25) and sex (hazard ratio: 0.62; 95% confidence interval: 0.21–1.86; p = 0.40) did not show significant association with prognosis. Although the positive correlation was shown for NG2 and CD44 expression in the glioblastomas (Pearson coefficient = 0.954), Kaplan–Meier and multivariate survival analyses did not revealed a significant association of the increased CD44 expression (hazard ratio: 2.18; 95% confidence interval: 0.50–9.43; p = 0.30) or high Ki-67 proliferation index (hazard ratio: 1.10; 95% confidence interval: 1.02–1.20; p = 0.02) with the disease prognosis. The results suggest that upregulation of NG2/CSPG4 rather than changes in CD44 or Ki-67 expression is associated with low overall survival in glioblastoma multiforme patients, supporting NG2/CSPG4 as a potential prognostic marker in glioblastoma.

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8

Jamil, Nuor S. M., Asim Azfer, Harrison Worrell, and Donald M. Salter. "Functional roles of CSPG4/NG2 in chondrosarcoma." International Journal of Experimental Pathology 97, no. 2 (April 2016): 178–86. http://dx.doi.org/10.1111/iep.12189.

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9

Nicolosi, Pier Andrea, Alice Dallatomasina, and Roberto Perris. "Theranostic Impact of NG2/CSPG4 Proteoglycan in Cancer." Theranostics 5, no. 5 (2015): 530–44. http://dx.doi.org/10.7150/thno.10824.

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10

Tamburini, Elisa, Alice Dallatomasina, Jade Quartararo, Barbara Cortelazzi, Domenica Mangieri, Mirca Lazzaretti, and Roberto Perris. "Structural deciphering of the NG2/CSPG4 proteoglycan multifunctionality." FASEB Journal 33, no. 3 (December 14, 2018): 3112–28. http://dx.doi.org/10.1096/fj.201801670r.

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11

Schäfer, Michael K. E., and Irmgard Tegeder. "NG2/CSPG4 and progranulin in the posttraumatic glial scar." Matrix Biology 68-69 (August 2018): 571–88. http://dx.doi.org/10.1016/j.matbio.2017.10.002.

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12

Jamil, N. S., A. Azfer, H. E. Sarah, and D. M. Salter. "NG2/CSPG4 regulates aggrecanase and MMP expression in human chondrocytes." Osteoarthritis and Cartilage 20 (April 2012): S44. http://dx.doi.org/10.1016/j.joca.2012.02.585.

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13

Jamil⁎, N. S., S. E. Howie, A. Azfer, and D. Salter. "NG2/CSPG4 regulates aggrecanase and MMP expression in human chondrocytes." Bone 50 (May 2012): S98. http://dx.doi.org/10.1016/j.bone.2012.02.294.

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14

Fenton, Moon, Maura Gasparetto, Chang-Sook Hong, XinHui Wang, Clay Smith, Theresa Whiteside, Soldano Ferrone, and Michael Boyiadzis. "Identification of Chondroitin Sulfate Proteoglycan-4 In Acute Myeloid Leukemia Using Monoclonal Antibody 225.28." Blood 118, no. 21 (November 18, 2011): 4885. http://dx.doi.org/10.1182/blood.v118.21.4885.4885.

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Abstract Abstract 4885 Chondroitin sulfate proteoglycan-4 (CSPG4) is a membrane-bound proteoglycan that is expressed on the surface of differentiated malignant cells, progenitor cells, and cancer initiating cells in various types of solid tumors. CSPG4 is highly conserved through evolution; its structure, amino acid sequence and functional properties show a high degree of homology with its rat counterpart, named neuron-glial antigen 2 (NG2). CSPG4 has been shown to be involved in the activation of several signaling pathways that play an important role in tumor progression. Because of its high levels of expression on malignant cells and its restricted distribution in normal tissues, CSPG4 is potential candidate tumor marker and target for immune- and targeted therapy. CSPG4 has been shown previously to be expressed on AML cells using an antibody raised against the rat counterpart and levels of expression were correlated with the clinical course of the disease. In this report we extend these findings by identifying a monoclonal antibody (mAb) directed at a human CSPG4 epitope and then used this antibody to examine co-expression with other common markers in AML as well as important molecular/cytogenetic abnormalities. Initially we screened a panel of 15 CSPG4-specific mAb which recognize 7 distinct epitopes for reactivity with leukemic blasts. mAb 225.28 was shown to have the highest reactivity and was selected for further studies. CSPG4 expression using mb225.28 was detected in 18/18 peripheral blood samples containing AML blasts at levels ranging from 0.2% to 98%. 7 samples showed less than 10% CSPG4 positive cells, 2 showed 10 – 20% positivity, 4 showed 20 – 30% positivity, and 5 showed greater than 30% positivity. CSPG-4 expression was not confined to any single blast sub-population defined by co-staining with CD34, CD117 and CD33. The expression of CSPG4 was shown on leukemic cells with mixed lineage leukemia (MLL) gene rearrangements, FTL3 mutation, NPM1 mutation, and complex cytogenetic abnormalities. These results indicate that the expression of CSPG4 is not restricted to any sub-type of AML or confined to one developmental compartment and using the mAb 225.28 CSPG4 may constitute a potential marker for AML. Disclosures: No relevant conflicts of interest to declare.

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15

Heywood, Richard M., and Colin Watts. "NG2/CSPG4 promotes proliferation and resistance to therapy in glioblastoma multiforme." Annals of Medicine and Surgery 3, no. 1 (March 2014): 18. http://dx.doi.org/10.1016/j.amsu.2014.01.003.

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16

Poli, Aurélie, Jian Wang, Olivia Domingues, Jesús Planagumà, Tao Yan, Cecilie Brekke Rygh, Kai Ove Skaftnesmo, et al. "Targeting glioblastoma with NK cells and mAb against NG2/CSPG4 prolongs animal survival." Oncotarget 4, no. 9 (September 9, 2013): 1527–46. http://dx.doi.org/10.18632/oncotarget.1291.

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17

Gotoh, Hitoshi, William M. Wood, Kiran D. Patel, Daniel C. Factor, Linda L. Boshans, Tadashi Nomura, Paul J. Tesar, Katsuhiko Ono, and Akiko Nishiyama. "NG2 expression in NG2 glia is regulated by binding of SoxE and bHLH transcription factors to a Cspg4 intronic enhancer." Glia 66, no. 12 (October 10, 2018): 2684–99. http://dx.doi.org/10.1002/glia.23521.

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18

Girolamo, Francesco, Alice Dallatomasina, Marco Rizzi, Mariella Errede, Thomas Wälchli, Maria Teresa Mucignat, Karl Frei, Luisa Roncali, Roberto Perris, and Daniela Virgintino. "Diversified Expression of NG2/CSPG4 Isoforms in Glioblastoma and Human Foetal Brain Identifies Pericyte Subsets." PLoS ONE 8, no. 12 (December 26, 2013): e84883. http://dx.doi.org/10.1371/journal.pone.0084883.

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19

Sato, Shingo, Yuning J. Tang, Qingxia Wei, Makoto Hirata, Angela Weng, Ilkyu Han, Atsushi Okawa, et al. "Mesenchymal Tumors Can Derive from Ng2/Cspg4-Expressing Pericytes with β-Catenin Modulating the Neoplastic Phenotype." Cell Reports 16, no. 4 (July 2016): 917–27. http://dx.doi.org/10.1016/j.celrep.2016.06.058.

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20

Rivera, Andrea D., Irene Chacon-De-La-Rocha, Francesca Pieropan, Maria Papanikolau, Kasum Azim, and Arthur M. Butt. "Keeping the ageing brain wired: a role for purine signalling in regulating cellular metabolism in oligodendrocyte progenitors." Pflügers Archiv - European Journal of Physiology 473, no. 5 (March 13, 2021): 775–83. http://dx.doi.org/10.1007/s00424-021-02544-z.

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AbstractWhite matter (WM) is a highly prominent feature in the human cerebrum and is comprised of bundles of myelinated axons that form the connectome of the brain. Myelin is formed by oligodendrocytes and is essential for rapid neuronal electrical communication that underlies the massive computing power of the human brain. Oligodendrocytes are generated throughout life by oligodendrocyte precursor cells (OPCs), which are identified by expression of the chondroitin sulphate proteoglycan NG2 (Cspg4), and are often termed NG2-glia. Adult NG2+ OPCs are slowly proliferating cells that have the stem cell–like property of self-renewal and differentiation into a pool of ‘late OPCs’ or ‘differentiation committed’ OPCs(COPs) identified by specific expression of the G-protein-coupled receptor GPR17, which are capable of differentiation into myelinating oligodendrocytes. In the adult brain, these reservoirs of OPCs and COPs ensure rapid myelination of new neuronal connections formed in response to neuronal signalling, which underpins learning and cognitive function. However, there is an age-related decline in myelination that is associated with a loss of neuronal function and cognitive decline. The underlying causes of myelin loss in ageing are manifold, but a key factor is the decay in OPC ‘stemness’ and a decline in their replenishment of COPs, which results in the ultimate failure of myelin regeneration. These changes in ageing OPCs are underpinned by dysregulation of neuronal signalling and OPC metabolic function. Here, we highlight the role of purine signalling in regulating OPC self-renewal and the potential importance of GPR17 and the P2X7 receptor subtype in age-related changes in OPC metabolism. Moreover, age is the main factor in the failure of myelination in chronic multiple sclerosis and myelin loss in Alzheimer’s disease, hence understanding the importance of purine signalling in OPC regeneration and myelination is critical for developing new strategies for promoting repair in age-dependent neuropathology.

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21

Wang, Jian, Agnete Svendsen, Justyna Kmiecik, Heike Immervoll, Kai Ove Skaftnesmo, Jesús Planagumà, Rolf Kåre Reed, et al. "Targeting the NG2/CSPG4 Proteoglycan Retards Tumour Growth and Angiogenesis in Preclinical Models of GBM and Melanoma." PLoS ONE 6, no. 7 (July 29, 2011): e23062. http://dx.doi.org/10.1371/journal.pone.0023062.

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Svendsen, Agnete, Joost J. C. Verhoeff, Heike Immervoll, Jan C. Brøgger, Justyna Kmiecik, Aurelie Poli, Inger A. Netland, et al. "Expression of the progenitor marker NG2/CSPG4 predicts poor survival and resistance to ionising radiation in glioblastoma." Acta Neuropathologica 122, no. 4 (August 24, 2011): 495–510. http://dx.doi.org/10.1007/s00401-011-0867-2.

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23

Cattaruzza, S., P. A. Nicolosi, P. Braghetta, L. Pazzaglia, M. S. Benassi, P. Picci, K. Lacrima, et al. "NG2/CSPG4-collagen type VI interplays putatively involved in the microenvironmental control of tumour engraftment and local expansion." Journal of Molecular Cell Biology 5, no. 3 (April 3, 2013): 176–93. http://dx.doi.org/10.1093/jmcb/mjt010.

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24

Hsu, Shu-Hsuan Claire, Puviindran Nadesan, Vijitha Puviindran, William B. Stallcup, David G. Kirsch, and Benjamin A. Alman. "Effects of chondroitin sulfate proteoglycan 4 (NG2/CSPG4) on soft-tissue sarcoma growth depend on tumor developmental stage." Journal of Biological Chemistry 293, no. 7 (December 1, 2017): 2466–75. http://dx.doi.org/10.1074/jbc.m117.805051.

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25

Jung, Bongnam, Thomas D. Arnold, Elisabeth Raschperger, Konstantin Gaengel, and Christer Betsholtz. "Visualization of vascular mural cells in developing brain using genetically labeled transgenic reporter mice." Journal of Cerebral Blood Flow & Metabolism 38, no. 3 (March 9, 2017): 456–68. http://dx.doi.org/10.1177/0271678x17697720.

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The establishment of a fully functional blood vascular system requires elaborate angiogenic and vascular maturation events in order to fulfill organ-specific anatomical and physiological needs. Although vascular mural cells, i.e. pericytes and vascular smooth muscle cells, are known to play fundamental roles during these processes, their characteristics during vascular development remain incompletely understood. In this report, we utilized transgenic reporter mice in which mural cells are genetically labeled to examine developing vascular mural cells in the central nervous system (CNS). We found platelet-derived growth factor receptor β gene ( Pdgfrb)-driven EGFP reporter expression as a suitable marker for vascular mural cells at the earliest stages of mouse brain vascularization. Furthermore, the combination of Pdgfrb and NG2 gene (Cspg4) driven reporter expression increased the specificity of brain vascular mural cell labeling at later stages. The expression of other known pericyte markers revealed time-, region- and marker-specific patterns, suggesting heterogeneity in mural cell maturation. We conclude that transgenic reporter mice provide an important tool to explore the development of CNS pericytes in health and disease.

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Wilms, Christina, Klaudia Lepka, Felix Häberlein, Steven Edwards, Jörg Felsberg, Linda Pudelko, Tobias T. Lindenberg, et al. "Glutaredoxin 2 promotes SP-1-dependent CSPG4 transcription and migration of wound healing NG2 glia and glioma cells: Enzymatic Taoism." Redox Biology 49 (February 2022): 102221. http://dx.doi.org/10.1016/j.redox.2021.102221.

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Mitsou, Ioli, Hinke A. B. Multhaupt, and John R. Couchman. "Proteoglycans, ion channels and cell–matrix adhesion." Biochemical Journal 474, no. 12 (May 25, 2017): 1965–79. http://dx.doi.org/10.1042/bcj20160747.

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Cell surface proteoglycans comprise a transmembrane or membrane-associated core protein to which one or more glycosaminoglycan chains are covalently attached. They are ubiquitous receptors on nearly all animal cell surfaces. In mammals, the cell surface proteoglycans include the six glypicans, CD44, NG2 (CSPG4), neuropilin-1 and four syndecans. A single syndecan is present in invertebrates such as nematodes and insects. Uniquely, syndecans are receptors for many classes of proteins that can bind to the heparan sulphate chains present on syndecan core proteins. These range from cytokines, chemokines, growth factors and morphogens to enzymes and extracellular matrix (ECM) glycoproteins and collagens. Extracellular interactions with other receptors, such as some integrins, are mediated by the core protein. This places syndecans at the nexus of many cellular responses to extracellular cues in development, maintenance, repair and disease. The cytoplasmic domains of syndecans, while having no intrinsic kinase activity, can nevertheless signal through binding proteins. All syndecans appear to be connected to the actin cytoskeleton and can therefore contribute to cell adhesion, notably to the ECM and migration. Recent data now suggest that syndecans can regulate stretch-activated ion channels. The structure and function of the syndecans and the ion channels are reviewed here, along with an analysis of ion channel functions in cell–matrix adhesion. This area sheds new light on the syndecans, not least since evidence suggests that this is an evolutionarily conserved relationship that is also potentially important in the progression of some common diseases where syndecans are implicated.

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28

Reed, David A., Yan Zhao, Mina Bagheri Varzaneh, Jun Soo Shin, Jacob Rozynek, Michael Miloro, and Michael Han. "NG2/CSPG4 regulates cartilage degeneration during TMJ osteoarthritis." Frontiers in Dental Medicine 3 (October 25, 2022). http://dx.doi.org/10.3389/fdmed.2022.1004942.

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Changes in the mechanical homeostasis of the temporomandibular joint (TMJ) can lead to the initiation and progression of degenerative arthropathies such as osteoarthritis (OA). Cells sense and engage with their mechanical microenvironment through interactions with the extracellular matrix. In the mandibular condylar cartilage, the pericellular microenvironment is composed of type VI collagen. NG2/CSPG4 is a transmembrane proteoglycan that binds with type VI collagen, and has been implicated in the cell stress response through mechanical loading-sensitive signaling networks including ERK 1/2. The objective of this study is to define the role of NG2/CSPG4 in the initiation and progression of TMJ OA and to determine if NG2/CSPG4 engages ERK 1/2 in a mechanical loading dependent manner. In vivo, we induced TMJ OA in control and NG2/CSPG4 knockout mice using a surgical destabilization approach. In control mice, NG2/CSPG4 is depleted during the early stages of TMJ OA and NG2/CSPG4 knockout mice have more severe cartilage degeneration, elevated expression of key OA proteases, and suppression of OA matrix synthesis genes. In vitro, we characterized the transcriptome and protein from control and NG2/CSPG4 knockout cells and found significant dysregulation of the ERK 1/2 signaling axis. To characterize the mechanobiological response of NG2/CSPG4, we applied mechanical loads on cell-agarose-collagen scaffolds using a compression bioreactor and illustrate that NG2/CSPG4 knockout cells fail to mechanically activate ERK 1/2 and are associated with changes in the expression of the same key OA biomarkers measured in vivo. Together, these findings implicate NG2/CSPG4 in the mechanical homeostasis of TMJ cartilage and in the progression of degenerative arthropathies including OA.

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Liu, Yang, Grace Hammel, Minjun Shi, Zhijian Cheng, Sandra Zivkovic, Xiaoqi Wang, Pingyi Xu, et al. "Myelin Debris Stimulates NG2/CSPG4 Expression in Bone Marrow-Derived Macrophages in the Injured Spinal Cord." Frontiers in Cellular Neuroscience 15 (March 19, 2021). http://dx.doi.org/10.3389/fncel.2021.651827.

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Although the increased expression of members of the chondroitin sulfate proteoglycan family, such as neuron-glial antigen 2 (NG2), have been well documented after an injury to the spinal cord, a complete picture as to the cellular origins and function of this NG2 expression has yet to be made. Using a spinal cord injury (SCI) mouse model, we describe that some infiltrated bone marrow-derived macrophages (BMDMΦ) are early contributors to NG2/CSPG4 expression and secretion after SCI. We demonstrate for the first time that a lesion-related form of cellular debris generated from damaged myelin sheaths can increase NG2/CSPG4 expression in BMDMΦ, which then exhibit enhanced proliferation and decreased phagocytic capacity. These results suggest that BMDMΦ may play a much more nuanced role in secondary spinal cord injury than previously thought, including acting as early contributors to the NG2 component of the glial scar.

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Rippe, Catarina, Björn Morén, Li Liu, Karin G. Stenkula, Johan Mustaniemi, Malin Wennström, and Karl Swärd. "NG2/CSPG4, CD146/MCAM and VAP1/AOC3 are regulated by myocardin-related transcription factors in smooth muscle cells." Scientific Reports 11, no. 1 (March 16, 2021). http://dx.doi.org/10.1038/s41598-021-85335-x.

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AbstractThe present work addressed the hypothesis that NG2/CSPG4, CD146/MCAM, and VAP1/AOC3 are target genes of myocardin-related transcription factors (MRTFs: myocardin/MYOCD, MRTF-A/MKL1, MRTF-B/MKL2) and serum response factor (SRF). Using a bioinformatics approach, we found that CSPG4, MCAM, and AOC3 correlate with MYOCD, MRTF-A/MKL1, and SRF across human tissues. No other transcription factor correlated as strongly with these transcripts as SRF. Overexpression of MRTFs increased both mRNA and protein levels of CSPG4, MCAM, and AOC3 in cultured human smooth muscle cells (SMCs). Imaging confirmed increased staining for CSPG4, MCAM, and AOC3 in MRTF-A/MKL1-transduced cells. MRTFs exert their effects through SRF, and the MCAM and AOC3 gene loci contained binding sites for SRF. SRF silencing reduced the transcript levels of these genes, and time-courses of induction paralleled the direct target ACTA2. MRTF-A/MKL1 increased the activity of promoter reporters for MCAM and AOC3, and transcriptional activation further depended on the chromatin remodeling enzyme KDM3A. CSPG4, MCAM, and AOC3 responded to the MRTF-SRF inhibitor CCG-1423, to actin dynamics, and to ternary complex factors. Coincidental detection of these proteins should reflect MRTF-SRF activity, and beyond SMCs, we observed co-expression of CD146/MCAM, NG2/CSPG4, and VAP1/AOC3 in pericytes and endothelial cells in the human brain. This work identifies highly responsive vascular target genes of MRTF-SRF signaling that are regulated via a mechanism involving KDM3A.

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Ampofo, Emmanuel, Beate M. Schmitt, Michael D. Menger, and Matthias W. Laschke. "The regulatory mechanisms of NG2/CSPG4 expression." Cellular & Molecular Biology Letters 22, no. 1 (February 28, 2017). http://dx.doi.org/10.1186/s11658-017-0035-3.

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Ping Bie, Hongyu Zhang. "NG2/CSPG4 Proteoglycan as a Novel Prognostic Indicator and Therapeutic Target in Malignant Cancer." Journal of Stem Cell Research & Therapy 04, no. 02 (2014). http://dx.doi.org/10.4172/2157-7633.1000171.

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"Correction: Diversified Expression of NG2/CSPG4 Isoforms in Glioblastoma and Human Foetal Brain Identifies Pericyte Subsets." PLoS ONE 9, no. 4 (April 9, 2014): e95120. http://dx.doi.org/10.1371/journal.pone.0095120.

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Kabdesh, Ilyas M., Svetlana S. Arkhipova, Yana O. Mukhamedshina, Victoria James, Albert A. Rizvanov, and Yuri A. Chelyshev. "The Function of NG2/CSPG4-expressing Cells in the Rat Spinal Cord Injury: An Immunoelectron Microscopy Study." Neuroscience, June 2021. http://dx.doi.org/10.1016/j.neuroscience.2021.05.031.

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Otsu, Masahiro, Zubair Ahmed, and Daniel Fulton. "Generation of Multipotential NG2 Progenitors From Mouse Embryonic Stem Cell-Derived Neural Stem Cells." Frontiers in Cell and Developmental Biology 9 (August 24, 2021). http://dx.doi.org/10.3389/fcell.2021.688283.

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Embryonic stem cells (ESC) have the potential to generate homogeneous immature cells like stem/progenitor cells, which appear to be difficult to isolate and expand from primary tissue samples. In this study, we developed a simple method to generate homogeneous immature oligodendrocyte (OL) lineage cells from mouse ESC-derived neural stem cell (NSC). NSC converted to NG2+/OLIG2+double positive progenitors (NOP) after culturing in serum-free media for a week. NOP expressed Prox1, but not Gpr17 gene, highlighting their immature phenotype. Interestingly, FACS analysis revealed that NOP expressed proteins for NG2, but not PDGFRɑ, distinguishing them from primary OL progenitor cells (OPC). Nevertheless, NOP expressed various OL lineage marker genes including Cspg4, Pdgfrα, Olig1/2, and Sox9/10, but not Plp1 genes, and, when cultured in OL differentiation conditions, initiated transcription of Gpr17 and Plp1 genes, and expression of PDGFRα proteins, implying that NOP converted into a matured OPC phenotype. Unexpectedly, NOP remained multipotential, being able to differentiate into neurons as well as astrocytes under appropriate conditions. Moreover, NOP-derived OPC myelinated axons with a lower efficiency when compared with primary OPC. Taken together, these data demonstrate that NOP are an intermediate progenitor cell distinguishable from both NSC and primary OPC. Based on this profile, NOP may be useful for modeling mechanisms influencing the earliest stages of oligogenesis, and exploring the cellular and molecular responses of the earliest OL progenitors to conditions that impair myelination in the developing nervous system.

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Behrangi, Newshan, Peter Lorenz, and Markus Kipp. "Oligodendrocyte Lineage Marker Expression in eGFP-GFAP Transgenic Mice." Journal of Molecular Neuroscience, December 21, 2020. http://dx.doi.org/10.1007/s12031-020-01771-w.

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AbstractOligodendrocytes, the myelinating cells of the central nervous system, orchestrate several key cellular functions in the brain and spinal cord, including axon insulation, energy transfer to neurons, and, eventually, modulation of immune responses. There is growing interest for obtaining reliable markers that can specifically label oligodendroglia and their progeny. In many studies, anti-CC1 antibodies, presumably recognizing the protein adenomatous polyposis coli (APC), are used to label mature, myelinating oligodendrocytes. However, it has been discussed whether anti-CC1 antibodies could recognize as well, under pathological conditions, other cell populations, particularly astrocytes. In this study, we used transgenic mice in which astrocytes are labeled by the enhanced green fluorescent protein (eGFP) under the control of the human glial fibrillary acidic protein (GFAP) promoter. By detailed co-localization studies we were able to demonstrate that a significant proportion of eGFP-expressing cells co-express markers of the oligodendrocyte lineage, such as the transcription factor Oligodendrocyte Transcription Factor 2 (OLIG2); the NG2 proteoglycan, also known as chrondroitin sulfate proteoglycan 4 (CSPG4); or APC. The current finding that the GFAP promoter drives transgene expression in cells of the oligodendrocyte lineage should be considered when interpreting results from co-localization studies.

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Kirkwood, Phoebe M., Douglas A. Gibson, Isaac Shaw, Ross Dobie, Olympia Kelepouri, Neil C. Henderson, and Philippa TK Saunders. "Single cell RNA sequencing and lineage tracing confirm mesenchyme to epithelial transformation (MET) contributes to repair of the endometrium at menstruation." eLife 11 (December 16, 2022). http://dx.doi.org/10.7554/elife.77663.

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The human endometrium experiences repetitive cycles of tissue wounding characterised by piecemeal shedding of the surface epithelium and rapid restoration of tissue homeostasis. In this study we used a mouse model of endometrial repair and three transgenic lines of mice to investigate whether epithelial cells that become incorporated into the newly formed luminal epithelium have their origins in one or more of the mesenchymal cell types present in the stromal compartment of the endometrium. Using scRNAseq we identified a novel population of PDGFRb+ mesenchymal stromal cells that developed a unique transcriptomic signature in response to endometrial breakdown/repair. These cells expressed genes usually considered specific to epithelial cells and in silico trajectory analysis suggested they were stromal fibroblasts in transition to becoming epithelial cells. To confirm our hypothesis we used a lineage tracing strategy to compare the fate of stromal fibroblasts (PDGFRa+) and stromal perivascular cells (NG2/CSPG4+). We demonstrated that stromal fibroblasts can undergo a mesenchyme to epithelial transformation and become incorporated into the re-epithelialised luminal surface of the repaired tissue. This study is the first to discover a novel population of wound-responsive, plastic endometrial stromal fibroblasts that contribute to the rapid restoration of an intact luminal epithelium during endometrial repair. These findings form a platform for comparisons both to endometrial pathologies which involve a fibrotic response (Asherman’s syndrome, endometriosis) as well as other mucosal tissues which have a variable response to wounding.

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Farnedi, Anna, Silvia Rossi, Nicoletta Bertani, Mariolina Gulli, Enrico Maria Silini, Maria Teresa Mucignat, Tito Poli, et al. "Proteoglycan-based diversification of disease outcome in head and neck cancer patients identifies NG2/CSPG4 and syndecan-2 as unique relapse and overall survival predicting factors." BMC Cancer 15, no. 1 (May 3, 2015). http://dx.doi.org/10.1186/s12885-015-1336-4.

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Lopes, Bruno A., Caroline Pires Poubel, Cristiane Esteves Teixeira, Aurélie Caye-Eude, Hélène Cavé, Claus Meyer, Rolf Marschalek, Mariana Boroni, and Mariana Emerenciano. "Novel Diagnostic and Therapeutic Options for KMT2A-Rearranged Acute Leukemias." Frontiers in Pharmacology 13 (June 6, 2022). http://dx.doi.org/10.3389/fphar.2022.749472.

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The KMT2A (MLL) gene rearrangements (KMT2A-r) are associated with a diverse spectrum of acute leukemias. Although most KMT2A-r are restricted to nine partner genes, we have recently revealed that KMT2A-USP2 fusions are often missed during FISH screening of these genetic alterations. Therefore, complementary methods are important for appropriate detection of any KMT2A-r. Here we use a machine learning model to unravel the most appropriate markers for prediction of KMT2A-r in various types of acute leukemia. A Random Forest and LightGBM classifier was trained to predict KMT2A-r in patients with acute leukemia. Our results revealed a set of 20 genes capable of accurately estimating KMT2A-r. The SKIDA1 (AUC: 0.839; CI: 0.799–0.879) and LAMP5 (AUC: 0.746; CI: 0.685–0.806) overexpression were the better markers associated with KMT2A-r compared to CSPG4 (also named NG2; AUC: 0.722; CI: 0.659–0.784), regardless of the type of acute leukemia. Of importance, high expression levels of LAMP5 estimated the occurrence of all KMT2A-USP2 fusions. Also, we performed drug sensitivity analysis using IC50 data from 345 drugs available in the GDSC database to identify which ones could be used to treat KMT2A-r leukemia. We observed that KMT2A-r cell lines were more sensitive to 5-Fluorouracil (5FU), Gemcitabine (both antimetabolite chemotherapy drugs), WHI-P97 (JAK-3 inhibitor), Foretinib (MET/VEGFR inhibitor), SNX-2112 (Hsp90 inhibitor), AZD6482 (PI3Kβ inhibitor), KU-60019 (ATM kinase inhibitor), and Pevonedistat (NEDD8-activating enzyme (NAE) inhibitor). Moreover, IC50 data from analyses of ex-vivo drug sensitivity to small-molecule inhibitors reveals that Foretinib is a promising drug option for AML patients carrying FLT3 activating mutations. Thus, we provide novel and accurate options for the diagnostic screening and therapy of KMT2A-r leukemia, regardless of leukemia subtype.

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