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Article ; Online: The Pathophysiological Role of Thymosin β4 in the Kidney Glomerulus.

Mason, William J / Vasilopoulou, Elisavet

International journal of molecular sciences

2023 Volume 24, Issue 9

Abstract: Diseases affecting the glomerulus, the filtration unit of the kidney, are a major cause of chronic kidney disease. Glomerular disease is characterised by injury of glomerular cells and is often accompanied by an inflammatory response that drives disease ... ...

Abstract	Diseases affecting the glomerulus, the filtration unit of the kidney, are a major cause of chronic kidney disease. Glomerular disease is characterised by injury of glomerular cells and is often accompanied by an inflammatory response that drives disease progression. New strategies are needed to slow the progression to end-stage kidney disease, which requires dialysis or transplantation. Thymosin β4 (Tβ4), an endogenous peptide that sequesters G-actin, has shown potent anti-inflammatory function in experimental models of heart, kidney, liver, lung, and eye injury. In this review, we discuss the role of endogenous and exogenous Tβ4 in glomerular disease progression and the current understanding of the underlying mechanisms.
MeSH term(s)	Humans ; Disease Progression ; Kidney Glomerulus ; Renal Dialysis ; Renal Insufficiency, Chronic ; Thymosin
Chemical Substances	Thymosin (61512-21-8) ; thymosin beta(4) (549LM7U24W) ; TMSB4X protein, human
Language	English
Publishing date	2023-04-22
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24097684
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Article ; Online: The Pathophysiological Role of Thymosin β4 in the Kidney Glomerulus

William J. Mason / Elisavet Vasilopoulou

International Journal of Molecular Sciences, Vol 24, Iss 7684, p

2023 Volume 7684

Abstract	Diseases affecting the glomerulus, the filtration unit of the kidney, are a major cause of chronic kidney disease. Glomerular disease is characterised by injury of glomerular cells and is often accompanied by an inflammatory response that drives disease progression. New strategies are needed to slow the progression to end-stage kidney disease, which requires dialysis or transplantation. Thymosin β4 (Tβ4), an endogenous peptide that sequesters G-actin, has shown potent anti-inflammatory function in experimental models of heart, kidney, liver, lung, and eye injury. In this review, we discuss the role of endogenous and exogenous Tβ4 in glomerular disease progression and the current understanding of the underlying mechanisms.
Keywords	thymosin β4 ; glomerulus ; podocyte ; macrophage ; chronic kidney disease ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Language	English
Publishing date	2023-04-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Isolating and Culturing Mouse Podocyte Cells to Study Diabetic Nephropathy.

Vasilopoulou, Elisavet

Methods in molecular biology (Clifton, N.J.)

2019 Volume 2067, Page(s) 53–59

Abstract: Diabetic nephropathy is associated with injury and loss of podocytes, specialized epithelial cells that are critical for glomerular filtration. This chapter describes a method of isolating and culturing podocyte cells from mouse adult kidneys. In this ... ...

Abstract	Diabetic nephropathy is associated with injury and loss of podocytes, specialized epithelial cells that are critical for glomerular filtration. This chapter describes a method of isolating and culturing podocyte cells from mouse adult kidneys. In this way, podocytes with genetic modifications can be obtained from transgenic animals and they can be used to study the effects of the diabetic environment in vitro.
MeSH term(s)	Animals ; Cells, Cultured ; Diabetic Nephropathies/genetics ; Diabetic Nephropathies/pathology ; Disease Models, Animal ; Humans ; Immunomagnetic Separation ; Mice ; Mice, Transgenic ; Podocytes/pathology ; Primary Cell Culture/methods ; Signal Transduction
Language	English
Publishing date	2019-12-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-9841-8_5
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Article ; Online: Thymosin-β4: A key modifier of renal disease.

Vasilopoulou, Elisavet / Riley, Paul R / Long, David A

Expert opinion on biological therapy

2018 Volume 18, Issue sup1, Page(s) 185–192

Abstract: Introduction: There is an urgent need for new treatments for chronic kidney disease (CKD). Thymosin-β4 is a peptide that reduces inflammation and fibrosis and has the potential to restore endothelial and epithelial cell injury, biological processes ... ...

Abstract	Introduction: There is an urgent need for new treatments for chronic kidney disease (CKD). Thymosin-β4 is a peptide that reduces inflammation and fibrosis and has the potential to restore endothelial and epithelial cell injury, biological processes involved in the pathophysiology of CKD. Therefore, thymosin-β4 could be a novel therapeutic direction for CKD. Areas covered: Here, we review the current evidence on the actions of thymosin-β4 in the kidney in health and disease. Using transgenic mice, two recent studies have demonstrated that endogenous thymosin-β4 is dispensable for healthy kidneys. In contrast, lack of endogenous thymosin-β4 exacerbates mouse models of glomerular disease and angiotensin-II-induced renal injury. Administration of exogenous thymosin-β4, or its metabolite, Ac-SDKP, has shown therapeutic benefits in a range of experimental models of kidney disease. Expert opinion: The studies conducted so far reveal a protective role for thymosin-β4 in the kidney and have shown promising results for the therapeutic potential of exogenous thymosin-β4 in CKD. Further studies should explore the mechanisms by which thymosin-β4 modulates kidney function in different types of CKD. Ac-SDKP treatment has beneficial effects in many experimental models of kidney disease, thus supporting its potential use as a new treatment strategy.
MeSH term(s)	Animals ; Disease Models, Animal ; Fibrosis/pathology ; Fibrosis/prevention & control ; Humans ; Inflammation/drug therapy ; Inflammation/pathology ; Kidney/drug effects ; Kidney/pathology ; Mice ; Mice, Transgenic ; Renal Insufficiency, Chronic/drug therapy ; Renal Insufficiency, Chronic/pathology ; Thymosin/physiology ; Thymosin/therapeutic use
Chemical Substances	thymosin beta(4) (549LM7U24W) ; Thymosin (61512-21-8)
Language	English
Publishing date	2018-05-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2052501-1
ISSN	1744-7682 ; 1471-2598
ISSN (online)	1744-7682
ISSN	1471-2598
DOI	10.1080/14712598.2018.1473371
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Article ; Online: Systemic gene therapy with thymosin β4 alleviates glomerular injury in mice.

Mason, William J / Jafree, Daniyal J / Pomeranz, Gideon / Kolatsi-Joannou, Maria / Rottner, Antje K / Pacheco, Sabrina / Moulding, Dale A / Wolf, Anja / Kupatt, Christian / Peppiatt-Wildman, Claire / Papakrivopoulou, Eugenia / Riley, Paul R / Long, David A / Vasilopoulou, Elisavet

Scientific reports

2022 Volume 12, Issue 1, Page(s) 12172

Abstract: Plasma ultrafiltration in the kidney occurs across glomerular capillaries, which are surrounded by epithelial cells called podocytes. Podocytes have a unique shape maintained by a complex cytoskeleton, which becomes disrupted in glomerular disease ... ...

Abstract	Plasma ultrafiltration in the kidney occurs across glomerular capillaries, which are surrounded by epithelial cells called podocytes. Podocytes have a unique shape maintained by a complex cytoskeleton, which becomes disrupted in glomerular disease resulting in defective filtration and albuminuria. Lack of endogenous thymosin β4 (TB4), an actin sequestering peptide, exacerbates glomerular injury and disrupts the organisation of the podocyte actin cytoskeleton, however, the potential of exogenous TB4 therapy to improve podocyte injury is unknown. Here, we have used Adriamycin (ADR), a toxin which injures podocytes and damages the glomerular filtration barrier leading to albuminuria in mice. Through interrogating single-cell RNA-sequencing data of isolated glomeruli we demonstrate that ADR injury results in reduced levels of podocyte TB4. Administration of an adeno-associated viral vector encoding TB4 increased the circulating level of TB4 and prevented ADR-induced podocyte loss and albuminuria. ADR injury was associated with disorganisation of the podocyte actin cytoskeleton in vitro, which was ameliorated by treatment with exogenous TB4. Collectively, we propose that systemic gene therapy with TB4 prevents podocyte injury and maintains glomerular filtration via protection of the podocyte cytoskeleton thus presenting a novel treatment strategy for glomerular disease.
MeSH term(s)	Albuminuria ; Animals ; Cells, Cultured ; Doxorubicin ; Genetic Therapy ; Kidney Diseases ; Kidney Glomerulus ; Mice ; Podocytes ; Thymosin
Chemical Substances	thymosin beta(4) (549LM7U24W) ; Thymosin (61512-21-8) ; Doxorubicin (80168379AG)
Language	English
Publishing date	2022-07-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-16287-z
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Article ; Online: The role of thymosin-β4 in kidney disease.

Vasilopoulou, Elisavet / Winyard, Paul J D / Riley, Paul R / Long, David A

Expert opinion on biological therapy

2015 Volume 15 Suppl 1, Page(s) S187–90

Abstract: Therapies that modulate inflammation and fibrosis have the potential to reduce the morbidity and mortality associated with chronic kidney disease (CKD). A promising avenue may be manipulating thymosin-β4, a naturally occurring peptide, which is the major ...

Abstract	Therapies that modulate inflammation and fibrosis have the potential to reduce the morbidity and mortality associated with chronic kidney disease (CKD). A promising avenue may be manipulating thymosin-β4, a naturally occurring peptide, which is the major G-actin sequestering protein in mammalian cells and a regulator of inflammation and fibrosis. Thymosin-β4 is already being tested in clinical trials for heart disease and wound healing. This editorial outlines the evidence that thymosin-β4 may also have therapeutic benefit in CKD.
MeSH term(s)	Adult ; Animals ; Fibrosis/drug therapy ; Fibrosis/genetics ; Humans ; Inflammation/drug therapy ; Inflammation/genetics ; Kidney/drug effects ; Kidney/pathology ; Mice ; Rats ; Renal Insufficiency, Chronic/drug therapy ; Renal Insufficiency, Chronic/genetics ; Thymosin/physiology ; Thymosin/therapeutic use ; Wound Healing/drug effects ; Wound Healing/genetics
Chemical Substances	thymosin beta(4) (549LM7U24W) ; Thymosin (61512-21-8)
Language	English
Publishing date	2015
Publishing country	England
Document type	Editorial ; Research Support, Non-U.S. Gov't
ZDB-ID	2052501-1
ISSN	1744-7682 ; 1471-2598
ISSN (online)	1744-7682
ISSN	1471-2598
DOI	10.1517/14712598.2015.1009891
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Article ; Online: The role of the placenta in thyroid hormone delivery to the fetus.

Chan, Shiao Y / Vasilopoulou, Elisavet / Kilby, Mark D

Nature clinical practice. Endocrinology & metabolism

2008 Volume 5, Issue 1, Page(s) 45–54

Abstract: The transplacental passage of thyroid hormones from the maternal circulation to the fetal circulation within the human hemochorial placenta is important for normal fetal development, particularly the development of the central nervous system. The role of ...

Abstract	The transplacental passage of thyroid hormones from the maternal circulation to the fetal circulation within the human hemochorial placenta is important for normal fetal development, particularly the development of the central nervous system. The role of maternal thyroid hormones is particularly important in the first half of pregnancy, before the onset of endogenous thyroid hormone production in the fetus. The human placenta regulates the quantity and composition of different forms of transported thyroid hormones to ensure that the requisite levels are present in the fetus for each stage of development. Transplacental thyroid hormone supply to the fetus is modulated by several factors, including the following proteins: plasma membrane transporters, which regulate the passage of thyroid hormones in and out of cells; iodothyronine deiodinases, which metabolize thyroid hormones; and proteins within trophoblast cells, which bind thyroid hormones. In pathological situations of either maternal or fetal thyroid hormone deficiency during pregnancy, the placenta seems to lack the full compensatory mechanisms necessary to optimize maternal-fetal transfer of thyroid hormones. Inadequate passage of thyroid hormones can lead to suboptimal fetal thyroid hormone levels, which might contribute to the neurodevelopmental delay associated with such conditions. Thus, maintaining normal maternal thyroid hormone status is likely to be the primary factor in ensuring adequate transplacental thyroid hormone passage and appropriate iodide supply to the fetus.
MeSH term(s)	Female ; Fetus/metabolism ; Humans ; Maternal-Fetal Exchange/physiology ; Placenta/metabolism ; Placenta/physiology ; Pregnancy ; Thyroid Hormones/metabolism
Chemical Substances	Thyroid Hormones
Language	English
Publishing date	2008-12-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2228540-4
ISSN	1745-8374 ; 1745-8366
ISSN (online)	1745-8374
ISSN	1745-8366
DOI	10.1038/ncpendmet1026
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Article ; Online: Loss of endogenous thymosin β

Vasilopoulou, Elisavet / Kolatsi-Joannou, Maria / Lindenmeyer, Maja T / White, Kathryn E / Robson, Michael G / Cohen, Clemens D / Sebire, Neil J / Riley, Paul R / Winyard, Paul J / Long, David A

Kidney international

2016 Volume 90, Issue 5, Page(s) 1056–1070

Abstract: Glomerular disease is characterized by morphologic changes in podocyte cells accompanied by inflammation and fibrosis. Thymosin ... ...

Abstract	Glomerular disease is characterized by morphologic changes in podocyte cells accompanied by inflammation and fibrosis. Thymosin β
MeSH term(s)	Animals ; Cell Movement ; Cells, Cultured ; Cytoskeleton/metabolism ; Fibrosis ; Glomerulonephritis/metabolism ; Glomerulonephritis/pathology ; Kidney Glomerulus/pathology ; Macrophages ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Podocytes/metabolism ; Thymosin/metabolism
Chemical Substances	thymosin beta(4) (549LM7U24W) ; Thymosin (61512-21-8)
Language	English
Publishing date	2016-08-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2016.06.032
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Article ; Online: Vangl2, a planar cell polarity molecule, is implicated in irreversible and reversible kidney glomerular injury.

Papakrivopoulou, Eugenia / Vasilopoulou, Elisavet / Lindenmeyer, Maja T / Pacheco, Sabrina / Brzóska, Hortensja Ł / Price, Karen L / Kolatsi-Joannou, Maria / White, Kathryn E / Henderson, Deborah J / Dean, Charlotte H / Cohen, Clemens D / Salama, Alan D / Woolf, Adrian S / Long, David A

The Journal of pathology

2018 Volume 246, Issue 4, Page(s) 485–496

Abstract: Planar cell polarity (PCP) pathways control the orientation and alignment of epithelial cells within tissues. Van Gogh-like 2 (Vangl2) is a key PCP protein that is required for the normal differentiation of kidney glomeruli and tubules. Vangl2 has also ... ...

Abstract	Planar cell polarity (PCP) pathways control the orientation and alignment of epithelial cells within tissues. Van Gogh-like 2 (Vangl2) is a key PCP protein that is required for the normal differentiation of kidney glomeruli and tubules. Vangl2 has also been implicated in modifying the course of acquired glomerular disease, and here, we further explored how Vangl2 impacts on glomerular pathobiology in this context. Targeted genetic deletion of Vangl2 in mouse glomerular epithelial podocytes enhanced the severity of not only irreversible accelerated nephrotoxic nephritis but also lipopolysaccharide-induced reversible glomerular damage. In each proteinuric model, genetic deletion of Vangl2 in podocytes was associated with an increased ratio of active-MMP9 to inactive MMP9, an enzyme involved in tissue remodelling. In addition, by interrogating microarray data from two cohorts of renal patients, we report increased VANGL2 transcript levels in the glomeruli of individuals with focal segmental glomerulosclerosis, suggesting that the molecule may also be involved in certain human glomerular diseases. These observations support the conclusion that Vangl2 modulates glomerular injury, at least in part by acting as a brake on MMP9, a potentially harmful endogenous enzyme. © 2018 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.
MeSH term(s)	Adult ; Animals ; Case-Control Studies ; Cell Polarity ; Cells, Cultured ; Disease Models, Animal ; Enzyme Activation ; Female ; Glomerulosclerosis, Focal Segmental/genetics ; Glomerulosclerosis, Focal Segmental/metabolism ; Glomerulosclerosis, Focal Segmental/pathology ; Glomerulosclerosis, Focal Segmental/physiopathology ; Humans ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Kidney Glomerulus/metabolism ; Kidney Glomerulus/pathology ; Kidney Glomerulus/physiopathology ; Male ; Matrix Metalloproteinase 9/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Middle Aged ; Nephrosis, Lipoid/genetics ; Nephrosis, Lipoid/metabolism ; Nephrosis, Lipoid/pathology ; Nephrosis, Lipoid/physiopathology ; Nerve Tissue Proteins/deficiency ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Podocytes/metabolism ; Podocytes/pathology ; Signal Transduction ; Young Adult
Chemical Substances	Intracellular Signaling Peptides and Proteins ; Ltap protein, mouse ; Membrane Proteins ; Nerve Tissue Proteins ; VANGL2 protein, human ; Matrix Metalloproteinase 9 (EC 3.4.24.35) ; Mmp9 protein, mouse (EC 3.4.24.35)
Language	English
Publishing date	2018-08-17
Publishing country	England
Document type	Journal Article ; 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.5158
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Article ; Online: Monocarboxylate transporter 8 modulates the viability and invasive capacity of human placental cells and fetoplacental growth in mice.

Vasilopoulou, Elisavet / Loubière, Laurence S / Heuer, Heike / Trajkovic-Arsic, Marija / Darras, Veerle M / Visser, Theo J / Lash, Gendie E / Whitley, Guy S / McCabe, Christopher J / Franklyn, Jayne A / Kilby, Mark D / Chan, Shiao Y

PloS one

2013 Volume 8, Issue 6, Page(s) e65402

Abstract: Monocarboxylate transporter 8 (MCT8) is a well-established thyroid hormone (TH) transporter. In humans, MCT8 mutations result in changes in circulating TH concentrations and X-linked severe global neurodevelopmental delay. MCT8 is expressed in the human ... ...

Abstract	Monocarboxylate transporter 8 (MCT8) is a well-established thyroid hormone (TH) transporter. In humans, MCT8 mutations result in changes in circulating TH concentrations and X-linked severe global neurodevelopmental delay. MCT8 is expressed in the human placenta throughout gestation, with increased expression in trophoblast cells from growth-restricted pregnancies. We postulate that MCT8 plays an important role in placental development and transplacental TH transport. We investigated the effect of altering MCT8 expression in human trophoblast in vitro and in a Mct8 knockout mouse model. Silencing of endogenous MCT8 reduced T3 uptake into human extravillous trophoblast-like cells (SGHPL-4; 40%, P<0.05) and primary cytotrophoblast (15%, P<0.05). MCT8 over-expression transiently increased T3 uptake (SGHPL-4∶30%, P<0.05; cytotrophoblast: 15%, P<0.05). Silencing MCT8 did not significantly affect SGHPL-4 invasion, but with MCT8 over-expression T3 treatment promoted invasion compared with no T3 (3.3-fold; P<0.05). Furthermore, MCT8 silencing increased cytotrophoblast viability (∼20%, P<0.05) and MCT8 over-expression reduced cytotrophoblast viability independently of T3 (∼20%, P<0.05). In vivo, Mct8 knockout reduced fetal:placental weight ratios compared with wild-type controls at gestational day 18 (25%, P<0.05) but absolute fetal and placental weights were not significantly different. The volume fraction of the labyrinthine zone of the placenta, which facilitates maternal-fetal exchange, was reduced in Mct8 knockout placentae (10%, P<0.05). However, there was no effect on mouse placental cell proliferation in vivo. We conclude that MCT8 makes a significant contribution to T3 uptake into human trophoblast cells and has a role in modulating human trophoblast cell invasion and viability. In mice, Mct8 knockout has subtle effects upon fetoplacental growth and does not significantly affect placental cell viability probably due to compensatory mechanisms in vivo.
MeSH term(s)	Analysis of Variance ; Animals ; Apoptosis/physiology ; Cell Movement/physiology ; Cell Proliferation ; Cells, Cultured ; England ; Female ; Humans ; Membrane Transport Proteins/genetics ; Mice ; Mice, Knockout ; Monocarboxylic Acid Transporters/metabolism ; Organ Size ; Placenta/cytology ; Placenta/metabolism ; Placentation ; Pregnancy ; RNA, Small Interfering/genetics ; Symporters ; Thyroid Hormones/metabolism ; Trophoblasts/metabolism
Chemical Substances	Membrane Transport Proteins ; Monocarboxylic Acid Transporters ; RNA, Small Interfering ; SLC16A2 protein, human ; Slc16a2 protein, mouse ; Symporters ; Thyroid Hormones
Language	English
Publishing date	2013-06-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0065402
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