Inflammatory cell infiltration and resolution of kidney inflammation is orchestrated by the cold-shock protein Y-box binding protein-1

Anja Bernhardt; Alexander Fehr; Sabine Brandt; Saskia Jerchel; Tobias M Ballhause; Lars Philipsen; Saskia Stolze; Robert Geffers; Honglei Weng; Klaus-Dieter Fischer; Berend Isermann; Monika C Brunner-Weinzierl; Arvind Batra; Britta Siegmund; Cheng Zhu; Jonathan A Lindquist; Peter R Mertens

doi:10.1016/j.kint.2017.03.035

Inflammatory cell infiltration and resolution of kidney inflammation is orchestrated by the cold-shock protein Y-box binding protein-1

Standard

Inflammatory cell infiltration and resolution of kidney inflammation is orchestrated by the cold-shock protein Y-box binding protein-1. / Bernhardt, Anja; Fehr, Alexander; Brandt, Sabine; Jerchel, Saskia; Ballhause, Tobias M; Philipsen, Lars; Stolze, Saskia; Geffers, Robert; Weng, Honglei; Fischer, Klaus-Dieter; Isermann, Berend; Brunner-Weinzierl, Monika C; Batra, Arvind; Siegmund, Britta; Zhu, Cheng; Lindquist, Jonathan A; Mertens, Peter R.

in: KIDNEY INT, Jahrgang 92, Nr. 5, 11.2017, S. 1157-1177.

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

Harvard

Bernhardt, A, Fehr, A, Brandt, S, Jerchel, S, Ballhause, TM, Philipsen, L, Stolze, S, Geffers, R, Weng, H, Fischer, K-D, Isermann, B, Brunner-Weinzierl, MC, Batra, A, Siegmund, B, Zhu, C, Lindquist, JA & Mertens, PR 2017, 'Inflammatory cell infiltration and resolution of kidney inflammation is orchestrated by the cold-shock protein Y-box binding protein-1', KIDNEY INT, Jg. 92, Nr. 5, S. 1157-1177. https://doi.org/10.1016/j.kint.2017.03.035

APA

Bernhardt, A., Fehr, A., Brandt, S., Jerchel, S., Ballhause, T. M., Philipsen, L., Stolze, S., Geffers, R., Weng, H., Fischer, K-D., Isermann, B., Brunner-Weinzierl, M. C., Batra, A., Siegmund, B., Zhu, C., Lindquist, J. A., & Mertens, P. R. (2017). Inflammatory cell infiltration and resolution of kidney inflammation is orchestrated by the cold-shock protein Y-box binding protein-1. KIDNEY INT, 92(5), 1157-1177. https://doi.org/10.1016/j.kint.2017.03.035

Vancouver

Bernhardt A, Fehr A, Brandt S, Jerchel S, Ballhause TM, Philipsen L et al. Inflammatory cell infiltration and resolution of kidney inflammation is orchestrated by the cold-shock protein Y-box binding protein-1. KIDNEY INT. 2017 Nov;92(5):1157-1177. https://doi.org/10.1016/j.kint.2017.03.035

Bibtex

@article{909186f08c6d404f8629b6f31a26f82a,

title = "Inflammatory cell infiltration and resolution of kidney inflammation is orchestrated by the cold-shock protein Y-box binding protein-1",

abstract = "Tubular cells recruit monocytic cells in inflammatory tubulointerstitial kidney diseases. The cell-cell communication that establishes pro- or anti-inflammatory activities is mainly influenced by cytokines, reactive oxygen species, nitric oxide, and phagocytosis. Key proteins orchestrating these processes such as cold-shock proteins linked with chemoattraction and cell maturation have been identified. The prototypic member of the cold-shock protein family, Y-box binding protein (YB)-1, governs specific phenotypic alterations in monocytic cells and was explored in the present study. Following tubulointerstitial injury by unilateral ureteral obstruction, increased inflammatory cell infiltration and tubular cell CCL5 expression was found in conditional Ybx1 knockout animals with specific depletion in monocytes/macrophages (YB-1ΔLysM). Furthermore, YB-1ΔLysM mice exhibit enhanced tissue damage, myofibroblast activation, and fibrosis. To investigate relevant molecular mechanism(s), we utilized bone marrow-derived macrophage cultures and found that YB-1-deficient macrophages display defects in cell polarization and function, including reduced proliferation and nitric oxide production, loss of phagocytic activity, and failure to upregulate IL-10 and CCL5 expression in response to inflammatory stimuli. Co-culture with primary tubular cells confirmed these findings. Thus, monocytic YB-1 has prominent and distinct roles for cellular feed-forward crosstalk and resolution of inflammatory processes by its ability to regulate cell differentiation and cytokine/chemokine synthesis.",

keywords = "Animals, Cell Communication, Cell Differentiation, Chemokine CCL5/metabolism, Coculture Techniques, DNA-Binding Proteins/genetics, Disease Models, Animal, Disease Progression, Female, Fibrosis, Humans, Interleukin-10/metabolism, Kidney Tubules/cytology, Macrophages, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Monocytes/metabolism, Myofibroblasts/metabolism, Nephritis, Interstitial/pathology, Primary Cell Culture",

author = "Anja Bernhardt and Alexander Fehr and Sabine Brandt and Saskia Jerchel and Ballhause, {Tobias M} and Lars Philipsen and Saskia Stolze and Robert Geffers and Honglei Weng and Klaus-Dieter Fischer and Berend Isermann and Brunner-Weinzierl, {Monika C} and Arvind Batra and Britta Siegmund and Cheng Zhu and Lindquist, {Jonathan A} and Mertens, {Peter R}",

year = "2017",

month = nov,

doi = "10.1016/j.kint.2017.03.035",

language = "English",

volume = "92",

pages = "1157--1177",

journal = "KIDNEY INT",

issn = "0085-2538",

publisher = "NATURE PUBLISHING GROUP",

number = "5",

}

RIS

TY - JOUR

T1 - Inflammatory cell infiltration and resolution of kidney inflammation is orchestrated by the cold-shock protein Y-box binding protein-1

AU - Bernhardt, Anja

AU - Fehr, Alexander

AU - Brandt, Sabine

AU - Jerchel, Saskia

AU - Ballhause, Tobias M

AU - Philipsen, Lars

AU - Stolze, Saskia

AU - Geffers, Robert

AU - Weng, Honglei

AU - Fischer, Klaus-Dieter

AU - Isermann, Berend

AU - Brunner-Weinzierl, Monika C

AU - Batra, Arvind

AU - Siegmund, Britta

AU - Zhu, Cheng

AU - Lindquist, Jonathan A

AU - Mertens, Peter R

PY - 2017/11

Y1 - 2017/11

N2 - Tubular cells recruit monocytic cells in inflammatory tubulointerstitial kidney diseases. The cell-cell communication that establishes pro- or anti-inflammatory activities is mainly influenced by cytokines, reactive oxygen species, nitric oxide, and phagocytosis. Key proteins orchestrating these processes such as cold-shock proteins linked with chemoattraction and cell maturation have been identified. The prototypic member of the cold-shock protein family, Y-box binding protein (YB)-1, governs specific phenotypic alterations in monocytic cells and was explored in the present study. Following tubulointerstitial injury by unilateral ureteral obstruction, increased inflammatory cell infiltration and tubular cell CCL5 expression was found in conditional Ybx1 knockout animals with specific depletion in monocytes/macrophages (YB-1ΔLysM). Furthermore, YB-1ΔLysM mice exhibit enhanced tissue damage, myofibroblast activation, and fibrosis. To investigate relevant molecular mechanism(s), we utilized bone marrow-derived macrophage cultures and found that YB-1-deficient macrophages display defects in cell polarization and function, including reduced proliferation and nitric oxide production, loss of phagocytic activity, and failure to upregulate IL-10 and CCL5 expression in response to inflammatory stimuli. Co-culture with primary tubular cells confirmed these findings. Thus, monocytic YB-1 has prominent and distinct roles for cellular feed-forward crosstalk and resolution of inflammatory processes by its ability to regulate cell differentiation and cytokine/chemokine synthesis.

AB - Tubular cells recruit monocytic cells in inflammatory tubulointerstitial kidney diseases. The cell-cell communication that establishes pro- or anti-inflammatory activities is mainly influenced by cytokines, reactive oxygen species, nitric oxide, and phagocytosis. Key proteins orchestrating these processes such as cold-shock proteins linked with chemoattraction and cell maturation have been identified. The prototypic member of the cold-shock protein family, Y-box binding protein (YB)-1, governs specific phenotypic alterations in monocytic cells and was explored in the present study. Following tubulointerstitial injury by unilateral ureteral obstruction, increased inflammatory cell infiltration and tubular cell CCL5 expression was found in conditional Ybx1 knockout animals with specific depletion in monocytes/macrophages (YB-1ΔLysM). Furthermore, YB-1ΔLysM mice exhibit enhanced tissue damage, myofibroblast activation, and fibrosis. To investigate relevant molecular mechanism(s), we utilized bone marrow-derived macrophage cultures and found that YB-1-deficient macrophages display defects in cell polarization and function, including reduced proliferation and nitric oxide production, loss of phagocytic activity, and failure to upregulate IL-10 and CCL5 expression in response to inflammatory stimuli. Co-culture with primary tubular cells confirmed these findings. Thus, monocytic YB-1 has prominent and distinct roles for cellular feed-forward crosstalk and resolution of inflammatory processes by its ability to regulate cell differentiation and cytokine/chemokine synthesis.

KW - Animals

KW - Cell Communication

KW - Cell Differentiation

KW - Chemokine CCL5/metabolism

KW - Coculture Techniques

KW - DNA-Binding Proteins/genetics

KW - Disease Models, Animal

KW - Disease Progression

KW - Female

KW - Fibrosis

KW - Humans

KW - Interleukin-10/metabolism

KW - Kidney Tubules/cytology

KW - Macrophages

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Monocytes/metabolism

KW - Myofibroblasts/metabolism

KW - Nephritis, Interstitial/pathology

KW - Primary Cell Culture

U2 - 10.1016/j.kint.2017.03.035

DO - 10.1016/j.kint.2017.03.035

M3 - SCORING: Journal article

C2 - 28610763

VL - 92

SP - 1157

EP - 1177

JO - KIDNEY INT

JF - KIDNEY INT

SN - 0085-2538

IS - 5

ER -