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Article: Periostin and Discoidin Domain Receptor 1: New Biomarkers or Targets for Therapy of Renal Disease.

Prakoura, Niki / Chatziantoniou, Christos

2017 Volume 4, Page(s) 52

Abstract: Chronic kidney disease (CKD) can be a life-threatening condition, which eventually requires renal replacement therapy through dialysis or transplantation. A lot of effort and resources have been invested the last years in the identification of novel ... ...

Abstract	Chronic kidney disease (CKD) can be a life-threatening condition, which eventually requires renal replacement therapy through dialysis or transplantation. A lot of effort and resources have been invested the last years in the identification of novel markers of progression and targets for therapy, in order to achieve a more efficient prognosis, diagnosis, and treatment of renal diseases. Using experimental models of renal disease, we identified and studied two promising candidates: periostin, a matricellular protein with high expression in bone and dental tissues, and discoidin domain receptor 1 (DDR1), a transmembrane collagen receptor of the tyrosine kinase family. Both proteins are inactive in physiological conditions, while they are highly upregulated during development of renal disease and are primarily expressed at the sites of injury. Further studies demonstrated that both periostin and DDR1 are involved in the regulation of inflammation and fibrosis, two major processes implicated in the development of renal disease. Targeting of either protein by genetic deletion or pharmacogenetic inhibition via antisense oligonucleotides highly attenuates renal damage and preserves renal structure and function in several animal models. The scope of this review is to summarize the existing evidence supporting the role of periostin and DDR1 as novel biomarkers and therapeutic targets in CKD.
Language	English
Publishing date	2017-05-09
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2775999-4
ISSN	2296-858X
ISSN	2296-858X
DOI	10.3389/fmed.2017.00052
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Article ; Online: Periostin in kidney diseases.

Prakoura, Niki / Chatziantoniou, Christos

Cellular and molecular life sciences : CMLS

2017 Volume 74, Issue 23, Page(s) 4315–4320

Abstract: Chronic kidney disease is an incurable to date pathology, with renal replacement therapy through dialysis or transplantation being the only available option for end-stage patients. A deeper understanding of the molecular mechanisms governing the ... ...

Abstract	Chronic kidney disease is an incurable to date pathology, with renal replacement therapy through dialysis or transplantation being the only available option for end-stage patients. A deeper understanding of the molecular mechanisms governing the progression of kidney diseases will permit the identification of unknown mediators and potential novel markers or targets of therapy which promise more efficient diagnostic and therapeutic applications. Over the last years, periostin was established by several studies as a novel key player in the progression of renal disease. Periostin is de novo expressed focally by the injured kidney cells during the development of renal disease. In diverse cohorts of renal disease patients, the expression levels of periostin in the kidney and urine were highly correlated with the stage of the pathology and the decline of renal function. Subsequent studies in animal models demonstrated that periostin is centrally involved in mediating renal inflammation and fibrosis, contributing to the deterioration of renal structure and function. Genetic or pharmaco-genetic inhibition of periostin in animal models of renal disease was efficient in arresting the progression of the pathology. This review will summarize the recent advances on periostin in the field of kidney diseases and will discuss its utility of as a novel target of therapy for chronic kidney disease.
MeSH term(s)	Animals ; Antibodies, Monoclonal/therapeutic use ; Cell Adhesion Molecules/antagonists & inhibitors ; Cell Adhesion Molecules/genetics ; Cell Adhesion Molecules/immunology ; Collagen Type I/genetics ; Collagen Type I/immunology ; Cytokines/genetics ; Cytokines/immunology ; Disease Models, Animal ; Disease Progression ; Fibrosis ; Gene Expression Regulation ; Humans ; Kidney/drug effects ; Kidney/immunology ; Kidney/pathology ; Molecular Targeted Therapy/methods ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Renal Insufficiency, Chronic/drug therapy ; Renal Insufficiency, Chronic/genetics ; Renal Insufficiency, Chronic/immunology ; Renal Insufficiency, Chronic/pathology ; Signal Transduction
Chemical Substances	Antibodies, Monoclonal ; Cell Adhesion Molecules ; Collagen Type I ; Cytokines ; POSTN protein, human ; RNA, Small Interfering
Language	English
Publishing date	2017-12
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-017-2650-6
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Article ; Online: Novel Targets for Therapy of Renal Fibrosis.

Prakoura, Niki / Hadchouel, Juliette / Chatziantoniou, Christos

The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society

2019 Volume 67, Issue 9, Page(s) 701–715

Abstract: Renal fibrosis is an important component of chronic kidney disease, an incurable pathology with increasing prevalence worldwide. With a lack of available therapeutic options, end-stage renal disease is currently treated with renal replacement therapy ... ...

Abstract	Renal fibrosis is an important component of chronic kidney disease, an incurable pathology with increasing prevalence worldwide. With a lack of available therapeutic options, end-stage renal disease is currently treated with renal replacement therapy through dialysis or transplantation. In recent years, many efforts have been made to identify novel targets for therapy of renal diseases, with special focus on the characterization of unknown mediators and pathways participating in renal fibrosis development. Using experimental models of renal disease and patient biopsies, we identified four novel mediators of renal fibrosis with potential to constitute future therapeutic targets against kidney disease: discoidin domain receptor 1, periostin, connexin 43, and cannabinoid receptor 1. The four candidates were highly upregulated in different models of renal disease and were localized at the sites of injury. Subsequent studies showed that they are centrally involved in the underlying mechanisms of renal fibrosis progression. Interestingly, inhibition of either of these proteins by different strategies, including gene deletion, antisense administration, or specific blockers, delayed the progression of renal disease and preserved renal structure and function, even when the inhibition started after initiation of the disease. This review will summarize the current findings on these candidates emphasizing on their potential to constitute future targets of therapy.
MeSH term(s)	Animals ; Cell Adhesion Molecules/analysis ; Cell Adhesion Molecules/metabolism ; Connexin 43/analysis ; Connexin 43/metabolism ; Discoidin Domain Receptor 1/analysis ; Discoidin Domain Receptor 1/metabolism ; Drug Discovery/methods ; Extracellular Matrix/drug effects ; Extracellular Matrix/metabolism ; Extracellular Matrix/pathology ; Fibrosis ; Humans ; Kidney/drug effects ; Kidney/metabolism ; Kidney/pathology ; Molecular Targeted Therapy/methods ; Receptor, Cannabinoid, CB1/analysis ; Receptor, Cannabinoid, CB1/metabolism ; Renal Insufficiency, Chronic/drug therapy ; Renal Insufficiency, Chronic/metabolism ; Renal Insufficiency, Chronic/pathology ; Transforming Growth Factor beta/analysis ; Transforming Growth Factor beta/metabolism
Chemical Substances	Cell Adhesion Molecules ; Connexin 43 ; POSTN protein, human ; Receptor, Cannabinoid, CB1 ; Transforming Growth Factor beta ; Discoidin Domain Receptor 1 (EC 2.7.10.1)
Language	English
Publishing date	2019-05-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	218208-7
ISSN	1551-5044 ; 0022-1554
ISSN (online)	1551-5044
ISSN	0022-1554
DOI	10.1369/0022155419849386
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Article: Periostin in kidney diseases

Prakoura, Niki / Christos Chatziantoniou

Cellular and molecular life sciences. 2017 Dec., v. 74, no. 23

2017

Abstract	Chronic kidney disease is an incurable to date pathology, with renal replacement therapy through dialysis or transplantation being the only available option for end-stage patients. A deeper understanding of the molecular mechanisms governing the progression of kidney diseases will permit the identification of unknown mediators and potential novel markers or targets of therapy which promise more efficient diagnostic and therapeutic applications. Over the last years, periostin was established by several studies as a novel key player in the progression of renal disease. Periostin is de novo expressed focally by the injured kidney cells during the development of renal disease. In diverse cohorts of renal disease patients, the expression levels of periostin in the kidney and urine were highly correlated with the stage of the pathology and the decline of renal function. Subsequent studies in animal models demonstrated that periostin is centrally involved in mediating renal inflammation and fibrosis, contributing to the deterioration of renal structure and function. Genetic or pharmaco-genetic inhibition of periostin in animal models of renal disease was efficient in arresting the progression of the pathology. This review will summarize the recent advances on periostin in the field of kidney diseases and will discuss its utility of as a novel target of therapy for chronic kidney disease.
Keywords	animal models ; dialysis ; fibrosis ; inflammation ; kidney cells ; kidney diseases ; kidneys ; patients ; renal function ; therapeutics ; urine
Language	English
Dates of publication	2017-12
Size	p. 4315-4320.
Publishing place	Springer International Publishing
Document type	Article
Note	Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-017-2650-6
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Periostin and Discoidin Domain Receptor 1

Niki Prakoura / Christos Chatziantoniou

Frontiers in Medicine, Vol

New Biomarkers or Targets for Therapy of Renal Disease

2017 Volume 4

Abstract	Chronic kidney disease (CKD) can be a life-threatening condition, which eventually requires renal replacement therapy through dialysis or transplantation. A lot of effort and resources have been invested the last years in the identification of novel markers of progression and targets for therapy, in order to achieve a more efficient prognosis, diagnosis, and treatment of renal diseases. Using experimental models of renal disease, we identified and studied two promising candidates: periostin, a matricellular protein with high expression in bone and dental tissues, and discoidin domain receptor 1 (DDR1), a transmembrane collagen receptor of the tyrosine kinase family. Both proteins are inactive in physiological conditions, while they are highly upregulated during development of renal disease and are primarily expressed at the sites of injury. Further studies demonstrated that both periostin and DDR1 are involved in the regulation of inflammation and fibrosis, two major processes implicated in the development of renal disease. Targeting of either protein by genetic deletion or pharmacogenetic inhibition via antisense oligonucleotides highly attenuates renal damage and preserves renal structure and function in several animal models. The scope of this review is to summarize the existing evidence supporting the role of periostin and DDR1 as novel biomarkers and therapeutic targets in CKD.
Keywords	chronic kidney disease ; biomarkers ; therapeutic targets ; periostin ; discoidin domain receptor 1 ; Medicine (General) ; R5-920
Subject code	616
Language	English
Publishing date	2017-05-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Role of Periostin and Nuclear Factor-κB Interplay in the Development of Diabetic Nephropathy.

Abbad, Lilia / Prakoura, Niki / Michon, Arthur / Chalghoumi, Rym / Reichelt-Wurm, Simone / Banas, Miriam C / Chatziantoniou, Christos

Cells

2022 Volume 11, Issue 14

Abstract: Diabetic nephropathy (DN) remains the most common reason for end-stage renal disease and a leading cause of kidney replacement therapy. Multifactorial pathophysiological mechanisms underlie the development of DN. Among the signalling pathways involved, ... ...

Abstract	Diabetic nephropathy (DN) remains the most common reason for end-stage renal disease and a leading cause of kidney replacement therapy. Multifactorial pathophysiological mechanisms underlie the development of DN. Among the signalling pathways involved, nuclear factor-κB (NF-κB) plays a key role in pathogenesis triggering inflammation, oxidative stress and fibrosis. Recent evidence shows that periostin, a matricellular protein, is involved in the development of renal glomerular diseases through interaction with NF-κB signalling. The aim of the present study is to investigate the contribution of periostin and its interaction with NF-κB in DN development. To this end, we used the BTBR ob/ob mice model of diabetes type 2, and we applied transcriptomic analysis, immunostaining and methods quantifying protein and mRNA expressions. We found that increased periostin expression was correlated with decreased renal function, advanced stage renal damage and fibrosis, and NF-κB activation. Subsequently, we identified novel pathways and genes regulated by the NF-κB-periostin interaction which are involved in the mechanisms of progression of DN. Some of these genes, such as FGF1 and GDF15, have the potential to be new biomarkers and/or targets for the therapy of DN.
MeSH term(s)	Animals ; Cell Adhesion Molecules/metabolism ; Diabetes Mellitus/pathology ; Diabetic Nephropathies/genetics ; Diabetic Nephropathies/metabolism ; Fibrosis ; Kidney/pathology ; Mice ; NF-kappa B/metabolism ; Signal Transduction
Chemical Substances	Cell Adhesion Molecules ; NF-kappa B ; Postn protein, mouse
Language	English
Publishing date	2022-07-15
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11142212
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Article ; Online: Activation of Notch3 in Renal Tubular Cells Leads to Progressive Cystic Kidney Disease.

Djudjaj, Sonja / Kavvadas, Panagiotis / Prakoura, Niki / Bülow, Roman D / Migeon, Tiffany / Placier, Sandrine / Chadjichristos, Christos E / Boor, Peter / Chatziantoniou, Christos

International journal of molecular sciences

2022 Volume 23, Issue 2

Abstract: Background: Polycystic kidney disease (PKD) is a genetic disorder affecting millions of people worldwide that is characterized by fluid-filled cysts and leads to end-stage renal disease (ESRD). The hallmarks of PKD are proliferation and ... ...

Abstract	Background: Polycystic kidney disease (PKD) is a genetic disorder affecting millions of people worldwide that is characterized by fluid-filled cysts and leads to end-stage renal disease (ESRD). The hallmarks of PKD are proliferation and dedifferentiation of tubular epithelial cells, cellular processes known to be regulated by Notch signaling. Methods: We found increased Notch3 expression in human PKD and renal cell carcinoma biopsies. To obtain insight into the underlying mechanisms and the functional consequences of this abnormal expression, we developed a transgenic mouse model with conditional overexpression of the intracellular Notch3 (ICN3) domain specifically in renal tubules. We evaluated the alterations in renal function (creatininemia, BUN) and structure (cysts, fibrosis, inflammation) and measured the expression of several genes involved in Notch signaling and the mechanisms of inflammation, proliferation, dedifferentiation, fibrosis, injury, apoptosis and regeneration. Results: After one month of ICN3 overexpression, kidneys were larger with tubules grossly enlarged in diameter, with cell hypertrophy and hyperplasia, exclusively in the outer stripe of the outer medulla. After three months, mice developed numerous cysts in proximal and distal tubules. The cysts had variable sizes and were lined with a single- or multilayered, flattened, cuboid or columnar epithelium. This resulted in epithelial hyperplasia, which was observed as protrusions into the cystic lumen in some of the renal cysts. The pre-cystic and cystic epithelium showed increased expression of cytoskeletal filaments and markers of epithelial injury and dedifferentiation. Additionally, the epithelium showed increased proliferation with an aberrant orientation of the mitotic spindle. These phenotypic tubular alterations led to progressive interstitial inflammation and fibrosis. Conclusions: In summary, Notch3 signaling promoted tubular cell proliferation, the alignment of cell division, dedifferentiation and hyperplasia, leading to cystic kidney diseases and pre-neoplastic lesions.
MeSH term(s)	Animals ; Biomarkers ; Disease Models, Animal ; Disease Susceptibility ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Fibrosis ; Gene Expression ; Immunohistochemistry ; Kidney Neoplasms/etiology ; Kidney Neoplasms/metabolism ; Kidney Neoplasms/pathology ; Kidney Tubules/metabolism ; Kidney Tubules/pathology ; Mice ; Polycystic Kidney Diseases/etiology ; Polycystic Kidney Diseases/metabolism ; Polycystic Kidney Diseases/pathology ; Receptor, Notch3/genetics ; Receptor, Notch3/metabolism
Chemical Substances	Biomarkers ; Receptor, Notch3
Language	English
Publishing date	2022-01-14
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/ijms23020884
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Article ; Online: Connexin 43: a New Therapeutic Target Against Chronic Kidney Disease.

Prakoura, Niki / Kavvadas, Panagiotis / Chadjichristos, Christos E

Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

2018 Volume 49, Issue 3, Page(s) 985

Abstract: Chronic kidney disease is an incurable to date pathology with a continuously growing incidence that contributes to the increase of the number of deaths worldwide. With currently no efficient prognostic or therapeutic options being available, the only ... ...

Abstract	Chronic kidney disease is an incurable to date pathology with a continuously growing incidence that contributes to the increase of the number of deaths worldwide. With currently no efficient prognostic or therapeutic options being available, the only possibility for treatment of end-stage renal disease is renal replacement therapy through dialysis or transplantation. Understanding the molecular mechanisms participating in the progression of renal diseases and uncovering the pathways implicated will permit the identification of novel and more efficient targets of therapy. Connexin43 was recently identified as a novel player in the development of chronic kidney disease. It was found de novo expressed and/or differentially localized in various renal cell populations during progression of renal disease, indicating an abnormal connexin signaling, both in patients and animal models. Subsequent in vivo studies demonstrated that connexin43 is involved in mediating inflammatory and fibrotic processes contributing to renal damage. Genetic, pharmaco-genetic or peptide-based inhibition of connexin43 in animal models and cell culture systems was successful in preventing the progression of the pathology and preserving the cell phenotypes. This review will summarize the recent advances on connexin43 in the field of kidney diseases and discuss the potential of future connexin43-based therapies against chronic kidney disease.
MeSH term(s)	Connexin 43/antagonists & inhibitors ; Connexin 43/genetics ; Connexin 43/metabolism ; Humans ; Kidney/metabolism ; Mesangial Cells/cytology ; Mesangial Cells/metabolism ; Oligonucleotides, Antisense/therapeutic use ; Peptides/chemistry ; Peptides/metabolism ; Peptides/therapeutic use ; Podocytes/cytology ; Podocytes/metabolism ; Renal Insufficiency, Chronic/drug therapy ; Renal Insufficiency, Chronic/metabolism ; Renal Insufficiency, Chronic/pathology
Chemical Substances	Connexin 43 ; Gap 26 peptide ; Oligonucleotides, Antisense ; Peptides
Language	English
Publishing date	2018-09-07
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	1067572-3
ISSN	1421-9778 ; 1015-8987
ISSN (online)	1421-9778
ISSN	1015-8987
DOI	10.1159/000493230
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Article: Periostin: The Missing Link to Attenuate Kidney Fibrosis

Prakoura, Niki / Chatziantoniou, Christos

American Journal of Nephrology

2017 Volume 46, Issue 6, Page(s) 498–500

Institution	Institut National de la Santé Et de la Recherche Médicale UMRS 1155, Tenon Hospital, Paris, France Sorbonne Université, UPMC Paris 6, Paris, France
Language	English
Publishing date	2017-12-19
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Editorial
ZDB-ID	604540-6
ISSN	1421-9670 ; 0250-8095
ISSN (online)	1421-9670
ISSN	0250-8095
DOI	10.1159/000485324
Database	Karger publisher's database

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Article ; Online: Activation of Notch3 in Renal Tubular Cells Leads to Progressive Cystic Kidney Disease

Sonja Djudjaj / Panagiotis Kavvadas / Niki Prakoura / Roman D. Bülow / Tiffany Migeon / Sandrine Placier / Christos E. Chadjichristos / Peter Boor / Christos Chatziantoniou

International Journal of Molecular Sciences, Vol 23, Iss 884, p

2022 Volume 884

Abstract	Background: Polycystic kidney disease (PKD) is a genetic disorder affecting millions of people worldwide that is characterized by fluid-filled cysts and leads to end-stage renal disease (ESRD). The hallmarks of PKD are proliferation and dedifferentiation of tubular epithelial cells, cellular processes known to be regulated by Notch signaling. Methods: We found increased Notch3 expression in human PKD and renal cell carcinoma biopsies. To obtain insight into the underlying mechanisms and the functional consequences of this abnormal expression, we developed a transgenic mouse model with conditional overexpression of the intracellular Notch3 (ICN3) domain specifically in renal tubules. We evaluated the alterations in renal function (creatininemia, BUN) and structure (cysts, fibrosis, inflammation) and measured the expression of several genes involved in Notch signaling and the mechanisms of inflammation, proliferation, dedifferentiation, fibrosis, injury, apoptosis and regeneration. Results: After one month of ICN3 overexpression, kidneys were larger with tubules grossly enlarged in diameter, with cell hypertrophy and hyperplasia, exclusively in the outer stripe of the outer medulla. After three months, mice developed numerous cysts in proximal and distal tubules. The cysts had variable sizes and were lined with a single- or multilayered, flattened, cuboid or columnar epithelium. This resulted in epithelial hyperplasia, which was observed as protrusions into the cystic lumen in some of the renal cysts. The pre-cystic and cystic epithelium showed increased expression of cytoskeletal filaments and markers of epithelial injury and dedifferentiation. Additionally, the epithelium showed increased proliferation with an aberrant orientation of the mitotic spindle. These phenotypic tubular alterations led to progressive interstitial inflammation and fibrosis. Conclusions: In summary, Notch3 signaling promoted tubular cell proliferation, the alignment of cell division, dedifferentiation and hyperplasia, leading to cystic ...
Keywords	Notch3 ; polycystic kidney disease ; renal cell carcinoma ; renal fibrosis ; chronic kidney disease ; renal inflammation ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	616
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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