ACP5: Its Structure, Distribution, Regulation and Novel Functions

Ren, Xiubao; Shan, Wenhua; Wei, Lulu; Gong, Chan‐Chan; Pei, Dong-Sheng

doi:10.2174/1871520618666180411123447

Cited by 17 publications

(15 citation statements)

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“…As outcomes in pulmonary brosis, especially IPF, remain poor despite the emergence of some new anti brotic agents, an improved understanding of factors that in uence gene expression and broblast differentiation is required. Although ACP5 has extensive pathophysiological functions depending on the cell type and disease 38,39 , to the best of our knowledge, our study provides for the rst direct experimental proof that ACP5 plays a crucial role in the pathogenesis of brosis. We detected a marked increase in the levels of ACP5 within human IPF samples compared to samples from control subjects.…”

Section: Discussionmentioning

confidence: 77%

Tartrate-resistant acid phosphatase 5 serves as a viable target against pulmonary fibrosis by modulating β-catenin signaling

Hu¹,

Yu²,

Wang³

et al. 2020

Preprint

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Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease with limited therapeutic options. Tartrate-resistant acid phosphatase 5 (ACP5) performs a variety of functions. However, its role in IPF remains unclear. Here, we demonstrated that the levels of ACP5 were increased in IPF patient samples and mice with bleomycin (BLM)-induced pulmonary fibrosis. In particular, higher levels of ACP5 were noted in the sera of IPF patients with a diffusing capacity of the lungs for carbon monoxide (DLCO) less than 40% of the predicted value. Additionally, Acp5 deficiency protected mice from BLM-induced lung injury and fibrosis and reduced the differentiation and proliferation of fibroblasts. Mechanistic studies revealed that Acp5 was upregulated by TGF-β1 in a TGFβR1/Smad3-dependent manner, after which Acp5 dephosphorylated p-β-catenin at Ser33 and Thr41, inhibiting the degradation of β-catenin and subsequently enhancing β-catenin signaling in the nucleus, which promoted the differentiation and proliferation of fibroblast. Notably, the treatment of mice with BLM-induced fibrosis with Acp5 siRNA-loaded liposomes robustly reversed lung fibrosis. Collectively, these data indicate that Acp5 plays an essential role in the initiation and progression of pulmonary fibrosis; therefore, strategies aimed at silencing Acp5 could be novel therapeutic approaches against pulmonary fibrosis in a clinical setting.

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Section: Discussionmentioning

confidence: 77%

Tartrate-resistant acid phosphatase 5 serves as a viable target against pulmonary fibrosis by modulating β-catenin signaling

Hu¹,

Yu²,

Wang³

et al. 2020

Preprint

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“…2a ). ACP5 is involved in osteoblast regulation and macrophage function, as well as reflecting bone resorption and osteoclast activity [28]. GPNMB has been linked to osteoblast differentiation [29].…”

Section: Resultsmentioning

confidence: 99%

Landscape of microenvironment in Randall’s plaque by single-cell sequencing

Duan

et al. 2021

Preprint

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Randall's plaque is significantly associated with the occurrence of nephrolithiasis. However, the microenvironment of Randall's plaque is poorly characterized. To investigate the microenvironment of Randall's plaque, we analyzed single-cell RNA data of 3 Randall's plaque and 3 normal renal papillae tissue and identified 11 different cell types. We screened differentially expressed genes among all cell types between Randall's plaque and normal renal papillae. The microenvironment showed two cell types with multiple stone formation-associated transcriptomic programs. Contrary to previous studies, we did not observe macrophage M1/M2 imbalance. Notably, we detected ossification-associated macrophage is enriched in Randall's plaque and validated GPNMB and ACP5 were potential biomarkers on the ossification-associated macrophage. We also identified an endothelial subset harboring active communication (COL15A1+ PCDH17+ endothelial, DPECs) with other cells. Together with Immunofluorescence, we validated ossification-associated macrophage and DPECs are enriched in Randall's plaque tissue. Finally, cell-to-cell communication revealed that Loop of Henle, DPECs, and osteoblasts-associated macrophages was the main source of SPP1 signaling. Our work will further the understanding of the microenvironment among Randall's plaque tissues and provide deep insight into immune modulation.

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“…In addition, AHR induced by IFNG maintains DCs in a tolerant phenotype, impairing antigen presentation (67). ACP5 is an evolutionarily conserved gene and encodes an iron-containing glycoprotein that catalyzes the conversion of orthophosphoric monoester to alcohol and orthophosphate (68). One of the most important positive regulators of ACP5 is IL4, which together with IFNG regulates the balance of Th2/Th1-type responses and avoids damage caused by excessive inflammatory responses (68,69).…”

Section: Discussionmentioning

confidence: 99%

Construction of Interferon-Gamma-Related Gene Signature to Characterize the Immune-Inflamed Phenotype of Glioblastoma and Predict Prognosis, Efficacy of Immunotherapy and Radiotherapy

et al. 2021

Front. Immunol.

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Interferon-gamma (IFNG) has profound impacts on tumor-immune interaction and is of great clinical significance for multiple cancers. Exploring the role of IFNG in glioblastoma (GBM) may optimize the current treatment paradigm of this disease. Here, multi-dimensional data of 429 GBM samples were collected. Various bioinformatics algorithms were employed to establish a gene signature that characterizes immunological features, genomic alterations, and clinical characteristics associated with the IFNG response. In this way, a novel IFNG-related gene signature (IFNGrGS, including TGFBI, IL4I1, ACP5, and LUM) has been constructed and validated. Samples with increased IFNGrGS scores were characterized by increased neutrophil and macrophage infiltration and exuberant innate immune responses, while the activated adaptive immune response may be frustrated by multiple immunosuppressive mechanisms. Notably, the IFNG pathway as well as its antagonistic pathways including IL4, IL10, TGF-beta, and VEGF converged on the expression of immune checkpoints. Besides, gene mutations involved in the microenvironment were associated with the IFNGrGS-based stratification, where the heterogeneous prognostic significance of EGFR mutation may be related to the different degrees of IFNG response. Moreover, the IFNGrGS score had solid prognostic value and the potential to screen ICB and radiotherapy sensitive populations. Collectively, our study provided insights into the role of IFNG on the GBM immune microenvironment and offered feasible information for optimizing the treatment of GBM.

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ACP5: Its Structure, Distribution, Regulation and Novel Functions

Cited by 17 publications

References 0 publications

Tartrate-resistant acid phosphatase 5 serves as a viable target against pulmonary fibrosis by modulating β-catenin signaling

Tartrate-resistant acid phosphatase 5 serves as a viable target against pulmonary fibrosis by modulating β-catenin signaling

Landscape of microenvironment in Randall’s plaque by single-cell sequencing

Construction of Interferon-Gamma-Related Gene Signature to Characterize the Immune-Inflamed Phenotype of Glioblastoma and Predict Prognosis, Efficacy of Immunotherapy and Radiotherapy

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