Periostin is induced in glomerular injury and expressed de novo in interstitial renal fibrosis

Kontheari Sen; Maja T Lindenmeyer; Ariana Gaspert; Felix Eichinger; Matthias A Neusser; Matthias Kretzler; Stephan Segerer; Clemens D Cohen

doi:10.1016/j.ajpath.2011.06.002

Periostin is induced in glomerular injury and expressed de novo in interstitial renal fibrosis

Standard

Periostin is induced in glomerular injury and expressed de novo in interstitial renal fibrosis. / Sen, Kontheari; Lindenmeyer, Maja T; Gaspert, Ariana; Eichinger, Felix; Neusser, Matthias A; Kretzler, Matthias; Segerer, Stephan; Cohen, Clemens D.

in: AM J PATHOL, Jahrgang 179, Nr. 4, 10.2011, S. 1756-67.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Sen, K, Lindenmeyer, MT, Gaspert, A, Eichinger, F, Neusser, MA, Kretzler, M, Segerer, S & Cohen, CD 2011, 'Periostin is induced in glomerular injury and expressed de novo in interstitial renal fibrosis', AM J PATHOL, Jg. 179, Nr. 4, S. 1756-67. https://doi.org/10.1016/j.ajpath.2011.06.002

APA

Sen, K., Lindenmeyer, M. T., Gaspert, A., Eichinger, F., Neusser, M. A., Kretzler, M., Segerer, S., & Cohen, C. D. (2011). Periostin is induced in glomerular injury and expressed de novo in interstitial renal fibrosis. AM J PATHOL, 179(4), 1756-67. https://doi.org/10.1016/j.ajpath.2011.06.002

Vancouver

Sen K, Lindenmeyer MT, Gaspert A, Eichinger F, Neusser MA, Kretzler M et al. Periostin is induced in glomerular injury and expressed de novo in interstitial renal fibrosis. AM J PATHOL. 2011 Okt;179(4):1756-67. https://doi.org/10.1016/j.ajpath.2011.06.002

Bibtex

@article{4433efd2b33c4964acdcf2f6c3a3631f,

title = "Periostin is induced in glomerular injury and expressed de novo in interstitial renal fibrosis",

abstract = "Matricellular proteins participate in the pathogenesis of chronic kidney diseases. We analyzed glomerular gene expression profiles from patients with proteinuric diseases to identify matricellular proteins contributing to the progression of human nephropathies. Several genes encoding matricellular proteins, such as SPARC, THBS1, and CTGF, were induced in progressive nephropathies, but not in nonprogressive minimal-change disease. Periostin showed the highest induction, and its transcript levels correlated negatively with glomerular filtration rate in both glomerular and tubulointerstitial specimen. In well-preserved renal tissue, periostin localized to the glomerular tuft, the vascular pole, and along Bowman's capsule; no signal was detected in the tubulointerstitial compartment. Biopsies from patients with glomerulopathies and renal dysfunction showed enhanced periostin expression in the mesangium, tubular interstitium, and sites of fibrosis. Periostin staining correlated negatively with renal function. α-smooth muscle actin-positive mesangial and interstitial cells localized close to periostin-positive sites, as indicated by co-immunofluorescence. In vitro stimulation of mesangial cells by external addition of TGF-β1 resulted in robust induction of periostin. Addition of periostin to mesangial cells induced cell proliferation and decreased the number of cells expressing activated caspase-3, a marker of apoptosis. These human data indicate for the first time a role of periostin in glomerular and interstitial injury in acquired nephropathies.",

keywords = "Adolescent, Adult, Aged, Aged, 80 and over, Apoptosis, Biopsy, Cell Adhesion Molecules, Cell Proliferation, Female, Fibrosis, Humans, Immunohistochemistry, Kidney Failure, Chronic, Kidney Glomerulus, Male, Mesangial Cells, Middle Aged, Oligonucleotide Array Sequence Analysis, Protein Transport, Proteinuria, Reverse Transcriptase Polymerase Chain Reaction, Tissue Preservation, Transcription, Genetic, Young Adult, Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't",

author = "Kontheari Sen and Lindenmeyer, {Maja T} and Ariana Gaspert and Felix Eichinger and Neusser, {Matthias A} and Matthias Kretzler and Stephan Segerer and Cohen, {Clemens D}",

year = "2011",

month = oct,

doi = "10.1016/j.ajpath.2011.06.002",

language = "English",

volume = "179",

pages = "1756--67",

journal = "AM J PATHOL",

issn = "0002-9440",

publisher = "Elsevier Inc.",

number = "4",

}

RIS

TY - JOUR

T1 - Periostin is induced in glomerular injury and expressed de novo in interstitial renal fibrosis

AU - Sen, Kontheari

AU - Lindenmeyer, Maja T

AU - Gaspert, Ariana

AU - Eichinger, Felix

AU - Neusser, Matthias A

AU - Kretzler, Matthias

AU - Segerer, Stephan

AU - Cohen, Clemens D

PY - 2011/10

Y1 - 2011/10

N2 - Matricellular proteins participate in the pathogenesis of chronic kidney diseases. We analyzed glomerular gene expression profiles from patients with proteinuric diseases to identify matricellular proteins contributing to the progression of human nephropathies. Several genes encoding matricellular proteins, such as SPARC, THBS1, and CTGF, were induced in progressive nephropathies, but not in nonprogressive minimal-change disease. Periostin showed the highest induction, and its transcript levels correlated negatively with glomerular filtration rate in both glomerular and tubulointerstitial specimen. In well-preserved renal tissue, periostin localized to the glomerular tuft, the vascular pole, and along Bowman's capsule; no signal was detected in the tubulointerstitial compartment. Biopsies from patients with glomerulopathies and renal dysfunction showed enhanced periostin expression in the mesangium, tubular interstitium, and sites of fibrosis. Periostin staining correlated negatively with renal function. α-smooth muscle actin-positive mesangial and interstitial cells localized close to periostin-positive sites, as indicated by co-immunofluorescence. In vitro stimulation of mesangial cells by external addition of TGF-β1 resulted in robust induction of periostin. Addition of periostin to mesangial cells induced cell proliferation and decreased the number of cells expressing activated caspase-3, a marker of apoptosis. These human data indicate for the first time a role of periostin in glomerular and interstitial injury in acquired nephropathies.

AB - Matricellular proteins participate in the pathogenesis of chronic kidney diseases. We analyzed glomerular gene expression profiles from patients with proteinuric diseases to identify matricellular proteins contributing to the progression of human nephropathies. Several genes encoding matricellular proteins, such as SPARC, THBS1, and CTGF, were induced in progressive nephropathies, but not in nonprogressive minimal-change disease. Periostin showed the highest induction, and its transcript levels correlated negatively with glomerular filtration rate in both glomerular and tubulointerstitial specimen. In well-preserved renal tissue, periostin localized to the glomerular tuft, the vascular pole, and along Bowman's capsule; no signal was detected in the tubulointerstitial compartment. Biopsies from patients with glomerulopathies and renal dysfunction showed enhanced periostin expression in the mesangium, tubular interstitium, and sites of fibrosis. Periostin staining correlated negatively with renal function. α-smooth muscle actin-positive mesangial and interstitial cells localized close to periostin-positive sites, as indicated by co-immunofluorescence. In vitro stimulation of mesangial cells by external addition of TGF-β1 resulted in robust induction of periostin. Addition of periostin to mesangial cells induced cell proliferation and decreased the number of cells expressing activated caspase-3, a marker of apoptosis. These human data indicate for the first time a role of periostin in glomerular and interstitial injury in acquired nephropathies.

KW - Adolescent

KW - Adult

KW - Aged

KW - Aged, 80 and over

KW - Apoptosis

KW - Biopsy

KW - Cell Adhesion Molecules

KW - Cell Proliferation

KW - Female

KW - Fibrosis

KW - Humans

KW - Immunohistochemistry

KW - Kidney Failure, Chronic

KW - Kidney Glomerulus

KW - Male

KW - Mesangial Cells

KW - Middle Aged

KW - Oligonucleotide Array Sequence Analysis

KW - Protein Transport

KW - Proteinuria

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Tissue Preservation

KW - Transcription, Genetic

KW - Young Adult

KW - Journal Article

KW - Research Support, N.I.H., Extramural

KW - Research Support, Non-U.S. Gov't

U2 - 10.1016/j.ajpath.2011.06.002

DO - 10.1016/j.ajpath.2011.06.002

M3 - SCORING: Journal article

C2 - 21854746

VL - 179

SP - 1756

EP - 1767

JO - AM J PATHOL

JF - AM J PATHOL

SN - 0002-9440

IS - 4

ER -