Interferon-γ and Interleukin-10 Reciprocally Regulate Endothelial Junction Integrity and Barrier Function

Oshima, Tadayuki; Laroux, F. Stephen; Coe, Laura; Morise, Zenichi; Kawa, Shigeyuki; Bauer, Philippe R.; Grisham, Matthew B.; Specian, Robert D.; Carter, Patsy; Jennings, Stephen R.; Granger, D. Neil; Joh, Takashi; Alexander, J. Steven

doi:10.1006/mvre.2000.2288

Cited by 161 publications

(66 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The role of IL-10 in reducing microvascular leakage has been shown in many previous studies. Thus it has been shown [23,24] that IL-10 is a powerful inhibitor of the secretion of vascular permeability factor (VPF) of peripheral blood mononuclear cells, and that this occurs in a dose-dependent fashion [25]. Moreover, in rats with acute lung injury the treatment with endothelial progenitor cells resulted in a dramatical increase of IL-10 levels and the reduction of pulmonary edema [26].…”

Section: Methodsmentioning

confidence: 99%

Cytokine response to diabetic ketoacidosis (DKA) in children with type 1 diabetes (T1DM)

et al. 2011

View full text Add to dashboard Cite

Section: Methodsmentioning

confidence: 99%

Cytokine response to diabetic ketoacidosis (DKA) in children with type 1 diabetes (T1DM)

et al. 2011

View full text Add to dashboard Cite

“…Permeability was determined by measuring the transepithelial passage of FITC-bovine serum albumin (BSA) from apical to basolateral compartment of transwell bicameral chambers (0.4-m pore; Corning Costar Corporation, Cambridge, MA) as described previously 30 with slight modifications. Confluent differentiated podocytes were exposed to test medium or Ang II 10 Ϫ7 mol/L for 1 hour.…”

Section: Permeability Studiesmentioning

confidence: 99%

Permselective Dysfunction of Podocyte-Podocyte Contact upon Angiotensin II Unravels the Molecular Target for Renoprotective Intervention

Macconi

Abbate

Morigi

et al. 2006

The American Journal of Pathology

View full text Add to dashboard Cite

Ameliorating the function of the glomerular barrier to circulating proteins by blocking angiotensin II (Ang II) translates into less risk of progression toward endstage renal failure in diabetic and nondiabetic nephropathies. However, the mechanisms underlying this barrier protection are not clear. Specialized contacts between adjacent podocytes are major candidate targets, and the actin cytoskeleton is emerging as a regulatory element. Here, we present data demonstrating that Ang II induced reorganization of F-actin fibers and redistribution of zonula occludens-1 (ZO-1) that is physically associated with actin in murine podocytes. These effects were paralleled by increased albumin permeability across podocyte monolayers. The F-actin stabilizer jasplakinolide prevented both ZO-1 redistribution and albumin leakage, suggesting that actin cytoskeleton rearrangement is instrumental to podocyte permselective dysfunction induced by Ang II. Changes in both F-actin and ZO-1 patterns were confirmed in glomeruli of rat isolated perfused kidneys on short infusion of Ang II, leading to increased protein excretion. Podocyte dysfunction was mediated by Ang II type 1 receptor and was partly dependent on Src kinase-phospholipase C activation. These data demonstrate that strategies aimed at stabilizing podocyte-podocyte contacts and targeting the relevant intracellular signal transduction are crucial to renoprotection.

show abstract

“…Inserts were air dried overnight, incubated at 60°C for 2 h and then conditioned with MCDB 131/10 mmol/l L-glutamine/EC-derived growth factor (TCS Biologicals)/20% FCS for 2-4 h. Endothelium was then seeded at 2 ϫ 10 5 cells per transwell insert in the same medium and allowed to grow to confluence for 7-10 days, with replenishment of the media every 2-3 days. Endothelial integrity was assessed by measurement of the resistance across the upper and lower transwell chamber using an EVOM (electrical voltage ohm meter) (21). Resistance measurements ranged between 115-120⍀ after seeding and were maintained at his level as ECs grew to confluence.…”

Section: Type 1 Diabetes Is Characterized By T-cell Infiltration Of Tmentioning

confidence: 99%

Processing and Presentation of the Islet Autoantigen GAD by Vascular Endothelial Cells Promotes Transmigration of Autoreactive T-Cells

et al. 2003

View full text Add to dashboard Cite

Type 1 diabetes is characterized by T-cell infiltration of the islets of Langerhans and abundant HLA class II molecule expression on islet endothelial cells (ECs).The specificity of infiltrating T-cells for islet autoantigens has been amply demonstrated in animal models, and is implicit in human diabetes, but the processes regulating endothelial transmigration of islet autoantigen-specific T-cells into islets are not known. We examined the ability of ECs expressing HLA class II molecules to process and present the islet autoantigen GAD65 and examined the effects of presentation on transmigration of GAD65-specific T-cells. Primary cultures of human vascular ECs expressing the DRB1*0401 (VEC1) and DRB1*0301 (VEC2) genotypes were established and de novo expression of HLA class II molecules induced with interferon-␥. Under these conditions, VEC1 efficiently processed and presented whole GAD65 to the HLA-DR4 -restricted murine T-cell hybridoma T33.1 that recognizes the 274-286 epitope of GAD65. Using a transwell system, we examined the effect of GAD65 presentation on migration of GAD65-specific T-cells across EC monolayers. Migration of T33.1 hybridoma cells and of the human T-cell clone, PM1#11 (recognizes GAD65 epitope 339-352 presented by HLA-DR3) across VEC1 and VEC2, respectively, were greatly enhanced in the presence of GAD65, commencing more rapidly and achieving a higher peak migration at 3 h. Migrated PM1#11 cells retained full proliferative capacity. These results support the hypothesis that presentation of autoantigens by islet endothelium in vivo could promote transmigration of circulating islet autoantigen-specific T-cells primed in regional lymph nodes against islet autoantigens. Diabetes 52:717-725, 2003

show abstract

Interferon-γ and Interleukin-10 Reciprocally Regulate Endothelial Junction Integrity and Barrier Function

Cited by 161 publications

References 36 publications

Cytokine response to diabetic ketoacidosis (DKA) in children with type 1 diabetes (T1DM)

Cytokine response to diabetic ketoacidosis (DKA) in children with type 1 diabetes (T1DM)

Permselective Dysfunction of Podocyte-Podocyte Contact upon Angiotensin II Unravels the Molecular Target for Renoprotective Intervention

Processing and Presentation of the Islet Autoantigen GAD by Vascular Endothelial Cells Promotes Transmigration of Autoreactive T-Cells

Contact Info

Product

Resources

About