Renal tubular fluid shear stress facilitates monocyte activation toward inflammatory macrophages

Autor: Mathieu Miravete, Muriel Mercier-Bonin, Bénédicte Buffin-Meyer, Jean-Loup Bascands, Bernard Pipy, Christiane Pecher, Julie Klein, Julien Gonzalez, Cécile Caubet, Joost P. Schanstra, Romain Dissard
Přispěvatelé: Simon, Marie Francoise, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Infections Parasitaires : Transmission, Physiopathologie et Thérapeutiques (IP-TPT), Institut de Recherche pour le Développement (IRD)-Aix Marseille Université (AMU)-Assistance Publique - Hôpitaux de Marseille (APHM)-Service de Santé des Armées, Laboratoire d'Ingénierie des Systèmes Biologiques et des Procédés (LISBP), Institut National de la Recherche Agronomique (INRA)-Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Institut National des Sciences Appliquées (INSA)-Université Fédérale Toulouse Midi-Pyrénées-Institut National des Sciences Appliquées (INSA)-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS), The work was funded, in part, by the 111 des Arts (France) and Bonus Qualite Recherche of Paul-Sabatier University (Toulouse, France). M. Miravete and R. Dissard were supported by a grant from the Ministere de l'Education Nationale de la Recherche et de la Technologie (France), J. Klein was supported by the FP7 eLICO European Project, J. Gonzalez was supported by a grant of the Societe de Nephrologie (France), and C. Caubet was financed by the Agence Nationale pour la Recherche (Grant ANR-07-PHYSIO-004-01) program (France). J. L. Bascands and J. P. Schanstra were supported by INSERM and the Direction de la Recherche Medicale et Innovation (CHU de Toulouse, France) under the Contrat Hospitalier de Recherche Translationnelle program, Service de Santé des Armées-Assistance Publique - Hôpitaux de Marseille (APHM)-Aix Marseille Université (AMU)-Institut de Recherche pour le Développement (IRD), Centre National de la Recherche Scientifique (CNRS)-Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Institut National de la Recherche Agronomique (INRA), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Centre National de la Recherche Scientifique (CNRS), Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Centre National de la Recherche Scientifique (CNRS)
Jazyk: angličtina
Rok vydání: 2012
Předmět:
MESH: Inflammation
Pathology
Physiology
[SDV]Life Sciences [q-bio]
Tubular fluid
MESH: Membrane Glycoproteins
030232 urology & nephrology
Lipocalin
Urine
infiltration
MESH: Monocytes
Monocytes
MESH: Urine
0302 clinical medicine
[SDV.IDA]Life Sciences [q-bio]/Food engineering
MESH: Animals
Hepatitis A Virus Cellular Receptor 1
Receptor
0303 health sciences
Kidney
MESH: Cytokines
Membrane Glycoproteins
MESH: Stress
Mechanical
MESH: Culture Media
Conditioned
MESH: Macrophage Activation
[SDV.IDA] Life Sciences [q-bio]/Food engineering
Lipocalins
3. Good health
[SDV] Life Sciences [q-bio]
medicine.anatomical_structure
Kidney Tubules
MESH: Kidney Tubules
Cytokines
Receptors
Virus
MESH: Lipocalins
MESH: Acute-Phase Proteins
medicine.medical_specialty
[SPI.GPROC] Engineering Sciences [physics]/Chemical and Process Engineering
Urinary system
macrophage
Biology
In Vitro Techniques
Cell Line
03 medical and health sciences
Lipocalin-2
Proto-Oncogene Proteins
medicine
Shear stress
Animals
Humans
[SPI.GPROC]Engineering Sciences [physics]/Chemical and Process Engineering
RNA
Messenger
MESH: Urodynamics
030304 developmental biology
MESH: RNA
Messenger
Inflammation
mechanical insult
MESH: Humans
Tumor Necrosis Factor-alpha
Monocyte
Fluid shear stress
Macrophage Activation
hydrodynamic forces
MESH: Receptors
Virus
MESH: Cell Line
MESH: Proto-Oncogene Proteins
Urodynamics
Culture Media
Conditioned
MESH: Tumor Necrosis Factor-alpha
Immunology
Stress
Mechanical
renal tubular damage
Acute-Phase Proteins
Zdroj: AJP Renal Physiology
AJP Renal Physiology, 2012, 302 (11), pp.F1409-17. ⟨10.1152/ajprenal.00409.2011⟩
AJP Renal Physiology, American Physiological Society, 2012, 302 (11), pp.F1409-17. ⟨10.1152/ajprenal.00409.2011⟩
ISSN: 0363-6127
1522-1466
DOI: 10.1152/ajprenal.00409.2011
Popis: International audience; Modified urinary fluid shear stress (FSS) induced by variations of urinary fluid flow and composition is observed in early phases of most kidney diseases. Recently, we reported that renal tubular FSS promotes endothelial cell activation and subsequent adhesion of human monocytes, thereby suggesting that changes in urinary FSS can induce the development of inflammation (Miravète M, Klein J, Besse-Patin A, Gonzalez J, Pecher C, Bascands JL, Mercier-Bonin M, Schanstra JP, Buffin-Meyer B, BBRC 407: 813-817, 2011). Here, we evaluated the influence of tubular FSS on monocytes as they play an important role in the progression of inflammation in nephropathies. Human renal tubular cells (HK-2) were exposed to FSS 0.01 Pa for 30 min or 5 h. Treatment of human THP-1 monocytes with the resulting conditioned medium (FSS-CM) modified the expression of macrophage differentiation markers, suggesting differentiation toward the inflammatory M1-type macrophage. The effect was confirmed in freshly isolated human monocytes. In contrast to endothelial cells, the activation of monocytes by FSS-CM did not require TNF-α. Cytokine array analysis of FSS-CM showed that FSS modified secretion of cytokines by HK-2 cells, particularly by increasing secretion of TGF-β and by decreasing secretion of C-C chemokine ligand 2 (CCL2). Neutralization of TGF-β or CCL2 supplementation attenuated the effect of FSS-CM on macrophage differentiation. Finally, FSS-injured HK-2 cells expressed and secreted early biomarkers of tubular damage such as kidney injury molecule 1 and neutrophil gelatinase-associated lipocalin. In conclusion, changes in urinary FSS should now also be considered as potential insults for tubular cells that initiate/perpetuate interstitial inflammation.
Databáze: OpenAIRE
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