Diagnostic validity of hepatocyte growth factor as marker for rejection in the follow-up of patients after heart transplantation

Żwirska-Korczala, K; Zakliczyńśki, Michał; Berdowska, Agnieszka; Zembala, Marian; Jochem, Jerzy; Gajewska, Katarzyna

doi:10.1016/j.healun.2004.02.007

Cited by 10 publications

(6 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…[11][12][13][14][15][16][17][18] In the current study, we found a decrease in plasma HGF levels from those with angiography silent to angiography-evident CAV. The inverse correlation between HGF and CAV severity was further confirmed by the lineal regression between plasma levels and IVUS measurements, including volume index and maximum area stenosis.…”

Section: Discussionsupporting

confidence: 61%

“…10 Hepatocyte growth factor (HGF), a disulfide-linked heterodimeric growth factor, has pleiotropic effects on endothelial integrity and allograft rejection. [11][12][13][14][15][16][17][18] The proinflammatory effects of HGF were supported by the findings that serum HGF concentrations correlated with carotid or peripheral atherosclerosis, 11,12 with cardiovascular events after coronary revascularization, 13 or with cellular rejection after heart transplantation. 18 However, HGF may attenuate apoptosis of endothelial cells, enhance endothelial cell proliferation, and augment collateral vessel development in the ischemic limb or in myocardium.…”

mentioning

confidence: 89%

See 1 more Smart Citation

Intravascular Ultrasound Evidence of Angiographically Silent Allograft Vasculopathy Inversely Correlates With Circulating Level of Hepatocyte Growth Factor

Lee

Chou

et al. 2006

The Journal of Heart and Lung Transplantation

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 61%

mentioning

confidence: 89%

Intravascular Ultrasound Evidence of Angiographically Silent Allograft Vasculopathy Inversely Correlates With Circulating Level of Hepatocyte Growth Factor

Lee

Chou

et al. 2006

The Journal of Heart and Lung Transplantation

View full text Add to dashboard Cite

“…Isosorbide dinitrate reduced calcification in the present study, possibly from improved wound healing, angiogenesis, and vascular perfusion during dystrophy. The potent effect of NO to release HGF from damaged fibers (3,81,82) and endothelial cells (64) will secondarily promote HGF-mediated angiogenesis and antiapoptosis (64,98) while stimulating SC activation, and thus coordinate the early regenerative process. NO is also reported to decrease vascular calcification by directly inhibiting TGF-␤ signaling (44); similar pathways may prevent differentiation to an osteoblastic lineage in skeletal muscle and thereby reduce calcification.…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide donors improve prednisone effects on muscular dystrophy in the mdx mouse diaphragm

Mizunoya¹,

Upadhaya²,

Burczynski

et al. 2011

American Journal of Physiology-Cell Physiology

View full text Add to dashboard Cite

Mizunoya W, Upadhaya R, Burczynski FJ, Wang G, Anderson JE. Nitric oxide donors improve prednisone effects on muscular dystrophy in the mdx mouse diaphragm. Am J Physiol Cell Physiol 300: C1065-C1077, 2011. First published January 26, 2011 doi:10.1152/ajpcell.00482.2010.-In Duchenne muscular dystrophy (DMD), palliative glucocorticoid therapy can produce myopathy or calcification. Since increased nitric oxide synthase activity in dystrophic mice promotes regeneration, the outcome of two nitric oxide (NO) donor drugs, MyoNovin (M) and isosorbide dinitrate (I), on the effectiveness of the anti-inflammatory drug prednisone (P) in alleviating progression of dystrophy was tested. Dystrophic mdx mice were treated (18 days) as controls or with an NO donor Ϯ P. Fiber permeability and DNA synthesis were labeled by Evans blue dye (EBD) and bromodeoxyuridine uptake, respectively. P decreased body weight gain, M increased quadriceps mass, and I increased heart mass. P increased fiber permeability (%EBDϩ fibers) and calcification in diaphragm. Treatment with NO donors ϩ P (MϩP, IϩP) reduced %EBDϩ fibers and calcification vs. P alone. %EBDϩ fibers in MϩP diaphragm did not differ from control. NO donor treatment reduced proliferation and the population of c-metϩ cells and accelerated fiber regeneration. Concurrent with P, NO donor treatment suppressed two important detrimental effects of P in mice, possibly by accelerating regeneration, rebalancing satellite cell quiescence and activation in dystrophy, and/or increasing perfusion. Results suggest that NO donors could improve current therapy for DMD.Duchenne muscular dystrophy; skeletal muscle; satellite cells; glucocorticoid MUSCULAR DYSTROPHIES are lethal genetic muscle diseases, and the most common form, Duchenne muscular dystrophy (DMD), is caused by mutation in the dystrophin gene (37). Absence of dystrophin from the cytoskeleton in DMD fibers leads to disruption of the sarcolemma by mechanical stress or exercise and progressive muscle weakness and wasting (20,27,56,69). Investigations of possible therapeutic interventions using the mdx mouse model of DMD have examined gene therapy by viral delivery of full-length dystrophin (28) or microdystrophin (97), stem (satellite) cell transplantation (40), and read-through (91) or exon-skipping approaches (2, 55, 93) to restore dystrophin expression. As these investigations are ongoing, pharmacological treatment with glucocorticoids remains the current "gold standard" therapy in DMD.Treatment with prednisone promotes a palliative reduction in inflammation and delays disease progression (57, 58) in DMD. In DMD patients and mdx mice, prednisone and deflazacort reduce the secondary inflammation that extends muscle fiber necrosis outside the region of primary damage that is caused by exercise-induced membrane breaks or eccentric contraction (25, 63). In addition, deflazacort also upregulates the calcineurin/nuclear factor of activated T cells (NFAT) pathway activity, which counteracts the muscle-specific activation of JNK1 that damages...

show abstract

“…The study of Mahmoud et al provided evidence that HGF (together with soluble CD30) might be predictive for the development of acute renal allograft rejection (20). Another group evaluated HGF as marker for cellular rejection in heart transplant patients (21). Nevertheless, to our best knowledge, no data supporting or contradicting these reports have been published up till now.…”

Section: Introductionmentioning

confidence: 99%

Hepatocyte growth factor and antibodies to HLA and MICA antigens in heart transplant recipients

et al. 2010

View full text Add to dashboard Cite

Recent unconfirmed literature data suggest that elevated concentrations of the multifunctional cytokine hepatocyte growth factor (HGF) might be a marker of increased incidence of acute rejection after organ transplantation. The aim of this study was to test the hypothesis that HGF levels may correlate with the rejection and/or with the production of HLA and MHC Class I chain-related antigens A (MICA) specific antibodies. Sixty-three heart transplant recipients were included into the study. Hundred and eighty-five endomyocardial biopsies (EMB) obtained up to 6 months after transplantation were retrospectively analyzed for signs of cellular (CR) and antibody-mediated rejection (AMR). Pre- and post-transplant sera were tested for HGF concentrations and antibodies to HLA class I, class II and MICA antigens by xMap technology (Luminex). Pre-transplant HGF did not correlate with the incidence of CR or AMR. However, higher HGF concentrations correlated significantly with HLA antibody production before and after transplantation (P = 0.006 and P < 0.0001 respectively). Patients with both HLA class I and class II antibodies before transplantation had significantly lower AMR-free survival. Furthermore, recipients with pre-transplant donor-specific antibodies (DSA) had significantly lower AMR-free survival (50%) than recipients without pre-transplant HLA antibodies (90%) and patients with antibodies not specific to donor antigens (92%) (P = 0.005). Post-transplant MICA antibodies tended to be more frequent in patients with AMR (P = 0.063). In conclusion, elevated HGF concentrations in our study were not associated with the incidence of CR and/or AMR but with the presence of HLA-specific antibodies. Testing for DSA before heart transplantation by Luminex may be helpful for the identification of patients with increased risk of AMR.

show abstract

Diagnostic validity of hepatocyte growth factor as marker for rejection in the follow-up of patients after heart transplantation

Cited by 10 publications

References 17 publications

Intravascular Ultrasound Evidence of Angiographically Silent Allograft Vasculopathy Inversely Correlates With Circulating Level of Hepatocyte Growth Factor

Intravascular Ultrasound Evidence of Angiographically Silent Allograft Vasculopathy Inversely Correlates With Circulating Level of Hepatocyte Growth Factor

Nitric oxide donors improve prednisone effects on muscular dystrophy in the mdx mouse diaphragm

Hepatocyte growth factor and antibodies to HLA and MICA antigens in heart transplant recipients

Contact Info

Product

Resources

About