Endothelin-1 release from cultured endothelial cells induced by sera from patients with systemic lupus erythematosus.

Yoshio, Taku; Masuyama, Jun-Ichi; Matsubara, Akio; Takeda, Akinori; Minota, Seiji; Kano, Shogo

doi:10.1136/ard.54.5.361

Cited by 77 publications

(49 citation statements)

References 18 publications

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“…36 This finding is in line with recent reports indicating that aECs from patients with autoimmune disorders are related to endothelin levels 37 and that aECs induce endothelin release in cultured human endothelial cells. 38 Furthermore, endothelin levels in the BHT men studied here were also enhanced, as reported earlier. 30 However, endothelin in sera has been suggested to be a marker of endothelial damage in individuals with autoimmune disorders, 37 and it is possible that the statistical association noted here is also related to endothelial damage.…”

Section: Discussionsupporting

confidence: 87%

Antibodies to Endothelial Cells in Borderline Hypertension

Frostegård

Gillis-Hægerstrand

et al. 1998

Circulation

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Background-Antibodies to endothelial cells (aECs) and to cardiolipin (aCLs) are implicated in autoimmune diseases like systemic lupus erythematosus vasculitis. ␤ 2 -Glycoprotein 1 (␤2GP1) is a cofactor for aCLs. The present study investigated the possible role of aECs, aCLs, and a␤2GP1 in borderline hypertension. Methods and Results-Seventy-three men with borderline hypertension (BHT) and 73 age-matched normotensive (NT) men (diastolic blood pressure, 85 to 94 and Ͻ80 mm Hg, respectively) were recruited from a population screening program. Antibody levels were determined by ELISA. Presence of carotid atherosclerosis was determined by B-mode ultrasonography, and 29 individuals had atherosclerotic plaques. BHT men had significantly higher aEC and a␤2GP1 levels of IgG class than NT control subjects (Pϭ0.029 and Pϭ0.0001, respectively). aEC levels of IgM class were higher in BHT (Pϭ0.012), but not a␤2GP1 levels. There was no correlation between aCL levels and BHT. Individuals with atherosclerotic plaques had significantly higher aEC levels of both IgG (Pϭ0.042) and IgM subclasses (Pϭ0.018) than those without plaques, but no difference was found in aCL and a␤2GP1 levels. Endothelin and aECs of IgM class were significantly associated. Conclusions-We demonstrate the first evidence of a significant elevation of aEC and a␤2GP1 levels in borderline hypertension. These findings provide a new link between hypertension and atherosclerosis and indicate that humoral immune reactions to the endothelium may play an important role in both conditions.

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Section: Discussionsupporting

confidence: 87%

Antibodies to Endothelial Cells in Borderline Hypertension

Frostegård

Gillis-Hægerstrand

et al. 1998

Circulation

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“…One mechanism by which treatment with rosiglitazone might protect the kidneys and reduce inflammation during SLE is through its effects to lower renal endothelin (ET-1). A potential pathogenic role for ET-1 has been proposed in the development of vascular injury (28) and lupus nephritis in humans, and plasma ET-1 concentrations directly correlate with SLE activity (62). In addition, previous studies using the NZBWF1 model of SLE show that renal ET-1 expression is increased and that treatment with an ET-1 receptor antagonist (ETA) reduces renal injury, proteinuria, and blood pressure (37).…”

Section: Discussionmentioning

confidence: 99%

Rosiglitazone decreases blood pressure and renal injury in a female mouse model of systemic lupus erythematosus

Venegas-Pont

Sartori‐Valinotti

Maric

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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-Women with systemic lupus erythematosus (SLE) exhibit a high prevalence of hypertension and renal injury. Rosiglitazone (Rosi), a peroxisome proliferator activator receptor gamma (PPAR␥) agonist, has renal protective and antihypertensive effects. We tested whether Rosi ameliorates hypertension and renal injury in a female mouse model of SLE (NZBWF1). Thirty-week-old SLE and control (NZW/LacJ) mice (n Ն 6/group) were fed Rosi (5 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 in standard chow) or standard chow for 4 wk. SLE mice had increased blood pressure (BP in mmHg) compared with controls (139 Ϯ 4 vs. 111 Ϯ 4, P Ͻ 0.05). Rosi treatment lowered BP in SLE mice (127 Ϯ 4, P Ͻ 0.05) but not in controls (111 Ϯ 4). Urinary albumin (g/mg creatinine) was increased in SLE mice compared with controls (12,396 Ϯ 6,525 vs. 50 Ϯ 6) and reduced with Rosi treatment (148 Ϯ 117). Glomerulosclerosis (% of glomeruli with sclerosis) was reduced in Rosi-treated SLE mice (4.2 Ϯ 1.6 vs. 0.4 Ϯ 0.3, P Ͻ 0.05). Renal monocyte/ macrophage numbers (cell number/1,320 points counted) were reduced in SLE mice treated with Rosi (32.6 Ϯ 11.0 vs. 10.6 Ϯ 3.6, P Ͻ 0.05) but unchanged in controls (3.7 Ϯ 1.6 vs. 3.7 Ϯ 2.0). Renal osteopontin expression, a cytokine-regulating macrophage recruitment, was reduced in Rosi-treated SLE mice. Urinary endothelin (in pg/mg creatinine) was increased in SLE mice compared with controls (1.9 Ϯ 0.59 vs. 0.6 Ϯ 0.04, P Ͻ 0.05) and reduced in SLE mice treated with Rosi (0.8 Ϯ 0.11, P Ͻ 0.05). PPAR␥ protein expression in the renal cortex was significantly lower in SLE mice compared with controls and was unaffected by Rosi. These data suggest that Rosi may be an important therapeutic option for the treatment of SLE hypertension and renal injury. lupus; inflammation; endothelin; glomerulosclerosis; proliferator activated receptor gamma SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) is a chronic autoimmune inflammatory disorder that has a strong predilection for women during their reproductive years. The hallmark of the disease is the production of autoantibodies such as antinuclear antibodies, and more specifically anti-double-stranded DNA (antidsDNA) antibodies. Accumulating evidence indicates that the major cause of death among patients with SLE is cardiovascular disease (17,22,23,26). Indeed, studies have reported that women with SLE are at a 50-fold greater risk for developing cardiovascular disease independent of traditional Framingham Heart Study risk factors (35). One of the major factors contributing to the progression of cardiovascular disease is increased arterial pressure. Importantly, SLE is associated with a high incidence of hypertension (1, 41, 56).The kidneys are prominently affected during SLE in the form of immune complex glomerulonephritis. This occurs in greater than 50% of patients with SLE (18) and is caused, in part, by circulating anti-dsDNA antibody-mediated formation of immune complexes (51). Few advances have been made toward the treatment of SLE and the associated nephritis and hypertension in the past 40 years. Patients with SL...

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“…The sample size was calculated by using the results of previous studies that investigated the levels of ADMA (10)(11)(12), and ET-1 (13)(14)(15) Results were presented as mean±SD, and † median±IQR. p values <0.05 accepted as statistically significant.…”

Section: Patients and Controlsmentioning

confidence: 99%

“…(27). Elevated ET-1 levels have been reported in inflammatory rheumatic diseases particularly in scleroderma (28), SLE (14), Behcet's disease (15) and RA (13) …”

Section: Patients and Controlsmentioning

confidence: 99%

Increased Levels of Asymmetric Dimethylarginine (ADMA) in Patients with Ankylosing Spondylitis

et al. 2009

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Objective Endothelial dysfunction is present in ankylosing spondylitis (AS). 05). Serum ADMA concentrations were also significantly higher in AS than in controls. Plasma levels of ET-1 did not differ between the groups (p>0.05). Comparison of three groups (conventional and anti-TNF treatment groups and controls) revealed that ADMA was significantly higher in the conventional treated AS than in controls. The levels of ADMA were not different between anti-TNF group and healthy subjects. Plasma ET-1 concentrations were similar between groups (p>0.05). Correlation analysis yielded significant correlations between ADMA, hsCRP, LDL cholesterol, HDL cholesterol and triglycerides (p<0.05

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Endothelin-1 release from cultured endothelial cells induced by sera from patients with systemic lupus erythematosus.

Cited by 77 publications

References 18 publications

Antibodies to Endothelial Cells in Borderline Hypertension

Antibodies to Endothelial Cells in Borderline Hypertension

Rosiglitazone decreases blood pressure and renal injury in a female mouse model of systemic lupus erythematosus

Increased Levels of Asymmetric Dimethylarginine (ADMA) in Patients with Ankylosing Spondylitis

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