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Article: Neurological Consequences of Sphingosine Phosphate Lyase Insufficiency.

Atreya, Krishan B / Saba, Julie D

2022 Volume 16, Page(s) 938693

Abstract: In 2017, an inborn error of metabolism caused by recessive mutations ... ...

Abstract	In 2017, an inborn error of metabolism caused by recessive mutations in
Language	English
Publishing date	2022-09-14
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2022.938693
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Article ; Online: Fifty years of lyase and a moment of truth: sphingosine phosphate lyase from discovery to disease.

Saba, Julie D

Journal of lipid research

2019 Volume 60, Issue 3, Page(s) 456–463

Abstract: Sphingosine phosphate lyase (SPL) is the final enzyme in the sphingolipid degradative pathway, catalyzing the irreversible cleavage of long-chain base phosphates (LCBPs) to yield a long-chain aldehyde and ethanolamine phosphate (EP). SPL guards the sole ... ...

Abstract	Sphingosine phosphate lyase (SPL) is the final enzyme in the sphingolipid degradative pathway, catalyzing the irreversible cleavage of long-chain base phosphates (LCBPs) to yield a long-chain aldehyde and ethanolamine phosphate (EP). SPL guards the sole exit point of sphingolipid metabolism. Its inactivation causes product depletion and accumulation of upstream sphingolipid intermediates. The main substrate of the reaction, sphingosine-1-phosphate (S1P), is a bioactive lipid that controls immune-cell trafficking, angiogenesis, cell transformation, and other fundamental processes. The products of the SPL reaction contribute to phospholipid biosynthesis and programmed cell-death activation. The main features of SPL enzyme activity were first described in detail by Stoffel et al. in 1969. The first SPL-encoding gene was cloned from budding yeast in 1997. Reverse and forward genetic strategies led to the rapid identification of other genes in the pathway and their homologs in other species. Genetic manipulation of SPL-encoding genes in model organisms has revealed the contribution of sphingolipid metabolism to development, physiology, and host-pathogen interactions. In 2017, recessive mutations in the human SPL gene
MeSH term(s)	Aldehyde-Lyases/metabolism ; Animals ; Disease ; Humans ; Phosphates/metabolism
Chemical Substances	Phosphates ; Aldehyde-Lyases (EC 4.1.2.-) ; sphingosine 1-phosphate lyase (aldolase) (EC 4.1.2.27)
Language	English
Publishing date	2019-01-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
DOI	10.1194/jlr.S091181
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Article ; Online: Analyzing Opposing Interactions Between Sphingosine 1-Phosphate Lyase and Influenza A Virus.

Wolf, Jennifer J / Saba, Julie D / Hahm, Bumsuk

DNA and cell biology

2022 Volume 41, Issue 4, Page(s) 331–335

Abstract: Sphingosine 1-phosphate lyase (SPL) is a critical component of sphingosine 1-phosphate (S1P) metabolism. SPL has been associated with several crucial cellular functions due to its role in S1P metabolism, but its role in viral infections is poorly ... ...

Abstract	Sphingosine 1-phosphate lyase (SPL) is a critical component of sphingosine 1-phosphate (S1P) metabolism. SPL has been associated with several crucial cellular functions due to its role in S1P metabolism, but its role in viral infections is poorly understood. Studies show that SPL has an antiviral function against influenza A virus (IAV) by interacting with IKKɛ, promoting the type I interferon (IFN) innate immune response to IAV infection. However, a more recent study has revealed that IAV NS1 protein hampers this by triggering ubiquitination and subsequent degradation of SPL, which reduces the type I IFN innate immune response. In this study, we describe SPL, the type I IFN response, and known interactions between SPL and IAV.
MeSH term(s)	Host-Pathogen Interactions ; Humans ; Immunity, Innate ; Influenza A virus ; Influenza, Human ; Lysophospholipids ; Sphingosine/analogs & derivatives
Chemical Substances	Lysophospholipids ; sphingosine 1-phosphate (26993-30-6) ; Sphingosine (NGZ37HRE42)
Language	English
Publishing date	2022-03-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	1024454-2
ISSN	1557-7430 ; 0198-0238 ; 1044-5498
ISSN (online)	1557-7430
ISSN	0198-0238 ; 1044-5498
DOI	10.1089/dna.2022.0071
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Article: The low down on sphingosine-1-phosphate lyase as a regulator of thymic egress.

Saba, Julie D

Journal of immunological sciences

2017 Volume 1, Issue 1, Page(s) 1–8

Abstract: After undergoing positive and negative selection in the thymus, surviving mature T cells egress from the thymic parenchyma and enter the bloodstream to participate in adaptive immunity. Thymic egress requires signals mediated by sphingosine-1-phosphate ( ... ...

Abstract	After undergoing positive and negative selection in the thymus, surviving mature T cells egress from the thymic parenchyma and enter the bloodstream to participate in adaptive immunity. Thymic egress requires signals mediated by sphingosine-1-phosphate (S1P), a bioactive lipid that serves as the ligand for a family of G protein-coupled receptors (S1P1-5) expressed on many cell types, including T cells. In the final stage of their development, T cells upregulate S1P1 expression on the cell surface, which enables them to recognize and respond to a chemotactic S1P gradient that lures them into the bloodstream. The gradient is generated by an S1P source close to the site of egress combined with an S1P sink generated by the actions of S1P catabolic enzymes including S1P lyase (SPL), the only enzyme that irreversibly degrades S1P. The requisite contribution of SPL to thymic egress is demonstrated by the profound lymphopenia observed in SPL knockout (KO) mice and wild type mice treated with SPL inhibitors. SPL is robustly expressed in thymic epithelial cells (TECs), which make up the stromal reticular network of the thymus. However, TEC SPL was recently found to be dispensable for thymic egress. In contrast, deletion of SPL in dendritic cells (DCs) - which represent only a small percent of thymic stroma - disrupts the S1P gradient and blocks thymic egress. These recent observations identify DCs as homeostatic regulators of thymic export through the actions of SPL, thereby adding one more piece to the complex puzzle of how S1P signaling contributes to the regulation of T cell trafficking.
Language	English
Publishing date	2017-12-06
Publishing country	United States
Document type	Journal Article
DOI	10.29245/2578-3009/2018/1.1103
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Article ; Online: A B cell-dependent mechanism restrains T cell transendothelial migration.

Saba, Julie D

Nature medicine

2015 Volume 21, Issue 5, Page(s) 424–426

MeSH term(s)	Animals ; Autoimmunity/immunology ; B-Lymphocytes/cytology ; Female ; Gene Expression Regulation ; Homeostasis ; Humans ; Inflammation/immunology ; Male ; T-Lymphocytes/cytology
Language	English
Publishing date	2015-05-07
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/nm.3858
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Zs.A 4212: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: AAV-SPL 2.0, a Modified Adeno-Associated Virus Gene Therapy Agent for the Treatment of Sphingosine Phosphate Lyase Insufficiency Syndrome.

Khan, Ranjha / Oskouian, Babak / Lee, Joanna Y / Hodgin, Jeffrey B / Yang, Yingbao / Tassew, Gizachew / Saba, Julie D

International journal of molecular sciences

2023 Volume 24, Issue 21

Abstract: Sphingosine-1-phosphate lyase insufficiency syndrome (SPLIS) is an inborn error of metabolism caused by inactivating mutations ... ...

Abstract	Sphingosine-1-phosphate lyase insufficiency syndrome (SPLIS) is an inborn error of metabolism caused by inactivating mutations in
MeSH term(s)	Animals ; Humans ; Mice ; Aldehyde-Lyases/genetics ; Aldehyde-Lyases/metabolism ; Dependovirus/genetics ; Dependovirus/metabolism ; Lysophospholipids/metabolism ; Mice, Knockout ; Parvovirinae/metabolism ; Phosphates ; Sphingosine/metabolism ; Genetic Therapy
Chemical Substances	Aldehyde-Lyases (EC 4.1.2.-) ; Lysophospholipids ; Phosphates ; Sphingosine (NGZ37HRE42) ; sphingosine 1-phosphate lyase (aldolase) (EC 4.1.2.27)
Language	English
Publishing date	2023-10-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms242115560
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Article ; Online: Sphingosine phosphate lyase insufficiency syndrome (SPLIS): A novel inborn error of sphingolipid metabolism.

Choi, Youn-Jeong / Saba, Julie D

Advances in biological regulation

2018 Volume 71, Page(s) 128–140

Abstract: Sphingosine-1-phosphate lyase (SPL) is an intracellular enzyme that controls the final step in the sphingolipid degradative pathway, the only biochemical pathway for removal of sphingolipids. Specifically, SPL catalyzes the cleavage of sphingosine 1- ... ...

Abstract	Sphingosine-1-phosphate lyase (SPL) is an intracellular enzyme that controls the final step in the sphingolipid degradative pathway, the only biochemical pathway for removal of sphingolipids. Specifically, SPL catalyzes the cleavage of sphingosine 1-phosphate (S1P) at the C2-3 carbon bond, resulting in its irreversible degradation to phosphoethanolamine (PE) and hexadecenal. The substrate of the reaction, S1P, is a bioactive sphingolipid metabolite that signals through a family of five G protein-coupled S1P receptors (S1PRs) to mediate biological activities including cell migration, cell survival/death/proliferation and cell extrusion, thereby contributing to development, physiological functions and - when improperly regulated - the pathophysiology of disease. In 2017, several groups including ours reported a novel childhood syndrome that featured a wide range of presentations including fetal hydrops, steroid-resistant nephrotic syndrome (SRNS), primary adrenal insufficiency (PAI), rapid or insidious neurological deterioration, immunodeficiency, acanthosis and endocrine abnormalities. In all cases, the disease was attributed to recessive mutations in the human SPL gene, SGPL1. We now refer to this condition as SPL Insufficiency Syndrome, or SPLIS. Some features of this new sphingolipidosis were predicted by the reported phenotypes of Sgpl1 homozygous null mice that serve as vertebrate SPLIS disease models. However, other SPLIS features reveal previously unrecognized roles for SPL in human physiology. In this review, we briefly summarize the biochemistry, functions and regulation of SPL, the main clinical and biochemical features of SPLIS and what is known about the pathophysiology of this condition from murine and cell models. Lastly, we consider potential therapeutic strategies for the treatment of SPLIS patients.
MeSH term(s)	Aldehyde-Lyases/deficiency ; Animals ; Cell Movement ; Disease Models, Animal ; Humans ; Lipid Metabolism, Inborn Errors/enzymology ; Lipid Metabolism, Inborn Errors/genetics ; Lipid Metabolism, Inborn Errors/pathology ; Lysophospholipids/genetics ; Lysophospholipids/metabolism ; Mice ; Mice, Mutant Strains ; Sphingosine/analogs & derivatives ; Sphingosine/genetics ; Sphingosine/metabolism ; Syndrome
Chemical Substances	Lysophospholipids ; sphingosine 1-phosphate (26993-30-6) ; Aldehyde-Lyases (EC 4.1.2.-) ; SGPL1 protein, human (EC 4.1.2.27) ; Sphingosine (NGZ37HRE42)
Language	English
Publishing date	2018-09-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2667413-0
ISSN	2212-4934 ; 2212-4926
ISSN (online)	2212-4934
ISSN	2212-4926
DOI	10.1016/j.jbior.2018.09.004
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Article ; Online: AF1q is a universal marker of neuroblastoma that sustains N-Myc expression and drives tumorigenesis.

Oskouian, Babak / Lee, Joanna Y / Asgharzadeh, Shahab / Khan, Ranjha / Zhang, Meng / Weisbrod, Julia R / Choi, Youn-Jeong / Puri, Latika / Aguilar, Ana E / Zhao, Piming / Saba, Julie D

Oncogene

2024 Volume 43, Issue 16, Page(s) 1203–1213

Abstract: Neuroblastoma is the most common extracranial malignant tumor of childhood, accounting for 15% of all pediatric cancer deaths. Despite significant advances in our understanding of neuroblastoma biology, five-year survival rates for high-risk disease ... ...

Abstract	Neuroblastoma is the most common extracranial malignant tumor of childhood, accounting for 15% of all pediatric cancer deaths. Despite significant advances in our understanding of neuroblastoma biology, five-year survival rates for high-risk disease remain less than 50%, highlighting the importance of identifying novel therapeutic targets to combat the disease. MYCN amplification is the most frequent and predictive molecular aberration correlating with poor outcome in neuroblastoma. N-Myc is a short-lived protein primarily due to its rapid proteasomal degradation, a potentially exploitable vulnerability in neuroblastoma. AF1q is an oncoprotein with established roles in leukemia and solid tumor progression. It is normally expressed in brain and sympathetic neurons and has been postulated to play a part in neural differentiation. However, no role for AF1q in tumors of neural origin has been reported. In this study, we found AF1q to be a universal marker of neuroblastoma tumors. Silencing AF1q in neuroblastoma cells caused proteasomal degradation of N-Myc through Ras/ERK and AKT/GSK3β pathways, activated p53 and blocked cell cycle progression, culminating in cell death via the intrinsic apoptotic pathway. Moreover, silencing AF1q attenuated neuroblastoma tumorigenicity in vivo signifying AF1q's importance in neuroblastoma oncogenesis. Our findings reveal AF1q to be a novel regulator of N-Myc and potential therapeutic target in neuroblastoma.
MeSH term(s)	Child ; Humans ; N-Myc Proto-Oncogene Protein/genetics ; N-Myc Proto-Oncogene Protein/metabolism ; Neuroblastoma/pathology ; Oncogene Proteins/metabolism ; Cell Transformation, Neoplastic ; Transcription Factors/metabolism ; Carcinogenesis/genetics ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic
Chemical Substances	N-Myc Proto-Oncogene Protein ; Oncogene Proteins ; Transcription Factors
Language	English
Publishing date	2024-02-27
Publishing country	England
Document type	Journal Article
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-024-02980-y
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Article ; Online: Gene therapy with AAV9-SGPL1 in an animal model of lung fibrosis.

Bhattacharyya, Aritra / Khan, Ranjha / Lee, Joanna Y / Tassew, Gizachew / Oskouian, Babak / Allende, Maria L / Proia, Richard L / Yin, Xiaoyang / Ortega, Javier G / Bhattacharya, Mallar / Saba, Julie D

The Journal of pathology

2024 Volume 263, Issue 1, Page(s) 22–31

Abstract: Idiopathic pulmonary fibrosis (IPF) is a progressive scarring disease of the lung that leads rapidly to respiratory failure. Novel approaches to treatment are urgently needed. The bioactive lipid sphingosine-1-phosphate (S1P) is increased in IPF lungs ... ...

Abstract	Idiopathic pulmonary fibrosis (IPF) is a progressive scarring disease of the lung that leads rapidly to respiratory failure. Novel approaches to treatment are urgently needed. The bioactive lipid sphingosine-1-phosphate (S1P) is increased in IPF lungs and promotes proinflammatory and profibrotic TGF-β signaling. Hence, decreasing lung S1P represents a potential therapeutic strategy for IPF. S1P is degraded by the intracellular enzyme S1P lyase (SPL). Here we find that a knock-in mouse with a missense SPL mutation mimicking human disease resulted in reduced SPL activity, increased S1P, increased TGF-β signaling, increased lung fibrosis, and higher mortality after injury compared to wild type (WT). We then tested adeno-associated virus 9 (AAV9)-mediated overexpression of human SGPL1 (AAV-SPL) in mice as a therapeutic modality. Intravenous treatment with AAV-SPL augmented lung SPL activity, attenuated S1P levels within the lungs, and decreased injury-induced fibrosis compared to controls treated with saline or only AAV. We confirmed that AAV-SPL treatment led to higher expression of SPL in the epithelial and fibroblast compartments during bleomycin-induced lung injury. Additionally, AAV-SPL decreased expression of the profibrotic cytokines TNFα and IL1β as well as markers of fibroblast activation, such as fibronectin (Fn1), Tgfb1, Acta2, and collagen genes in the lung. Taken together, our results provide proof of concept for the use of AAV-SPL as a therapeutic strategy for the treatment of IPF. © 2024 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.
MeSH term(s)	Humans ; Mice ; Animals ; Dependovirus/genetics ; Lung/metabolism ; Idiopathic Pulmonary Fibrosis/genetics ; Idiopathic Pulmonary Fibrosis/therapy ; Idiopathic Pulmonary Fibrosis/metabolism ; Bleomycin ; Models, Animal ; Genetic Therapy ; Aldehyde-Lyases/genetics ; Aldehyde-Lyases/metabolism ; Lysophospholipids ; Sphingosine/analogs & derivatives
Chemical Substances	Bleomycin (11056-06-7) ; sphingosine 1-phosphate (26993-30-6) ; SGPL1 protein, human (EC 4.1.2.27) ; Aldehyde-Lyases (EC 4.1.2.-) ; Lysophospholipids ; Sphingosine (NGZ37HRE42)
Language	English
Publishing date	2024-02-09
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3119-7
ISSN	1096-9896 ; 0022-3417
ISSN (online)	1096-9896
ISSN	0022-3417
DOI	10.1002/path.6256
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Article ; Online: AAV-SPL 2.0, a Modified Adeno-Associated Virus Gene Therapy Agent for the Treatment of Sphingosine Phosphate Lyase Insufficiency Syndrome

Ranjha Khan / Babak Oskouian / Joanna Y. Lee / Jeffrey B. Hodgin / Yingbao Yang / Gizachew Tassew / Julie D. Saba

International Journal of Molecular Sciences, Vol 24, Iss 21, p

2023 Volume 15560

Abstract: Sphingosine-1-phosphate lyase insufficiency syndrome (SPLIS) is an inborn error of metabolism caused by inactivating mutations in SGPL1 , the gene encoding sphingosine-1-phosphate lyase (SPL), an essential enzyme needed to degrade sphingolipids. SPLIS ... ...

Abstract	Sphingosine-1-phosphate lyase insufficiency syndrome (SPLIS) is an inborn error of metabolism caused by inactivating mutations in SGPL1 , the gene encoding sphingosine-1-phosphate lyase (SPL), an essential enzyme needed to degrade sphingolipids. SPLIS features include glomerulosclerosis, adrenal insufficiency, neurological defects, ichthyosis, and immune deficiency. Currently, there is no cure for SPLIS, and severely affected patients often die in the first years of life. We reported that adeno-associated virus (AAV) 9-mediated SGPL1 gene therapy (AAV-SPL) given to newborn Sgpl1 knockout mice that model SPLIS and die in the first few weeks of life prolonged their survival to 4.5 months and prevented or delayed the onset of SPLIS phenotypes. In this study, we tested the efficacy of a modified AAV-SPL, which we call AAV-SPL 2.0, in which the original cytomegalovirus (CMV) promoter driving the transgene is replaced with the synthetic “CAG” promoter used in several clinically approved gene therapy agents. AAV-SPL 2.0 infection of human embryonic kidney (HEK) cells led to 30% higher SPL expression and enzyme activity compared to AAV-SPL. Newborn Sgpl1 knockout mice receiving AAV-SPL 2.0 survived ≥ 5 months and showed normal neurodevelopment, 85% of normal weight gain over the first four months, and delayed onset of proteinuria. Over time, treated mice developed nephrosis and glomerulosclerosis, which likely resulted in their demise. Our overall findings show that AAV-SPL 2.0 performs equal to or better than AAV-SPL. However, improved kidney targeting may be necessary to achieve maximally optimized gene therapy as a potentially lifesaving SPLIS treatment.
Keywords	sphingosine phosphate lyase insufficiency syndrome ; Sgpl1 ; sphingolipid ; gene therapy ; AAV-SPL 2.0 ; adeno-associated virus ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	616
Language	English
Publishing date	2023-10-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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