Proteomic analysis in monocytes of antiphospholipid syndrome patients: Deregulation of proteins related to the development of thrombosis

Hospital Universitario Reina Sofía, Córdoba, Spain.
Arthritis & Rheumatology (Impact Factor: 7.76). 09/2008; 58(9):2835-44. DOI: 10.1002/art.23756
Source: PubMed


Antiphospholipid antibodies (aPL) are closely related to the development of thrombosis, but the exact mechanism(s) leading to thrombotic events remains unknown. In this study, using proteomic techniques, we evaluated changes in protein expression of monocytes from patients with antiphospholipid syndrome (APS) related to the pathophysiology of the syndrome.
Fifty-one APS patients were included. They were divided into 2 groups: patients with previous thrombosis, and patients with recurrent spontaneous abortion. As controls, we studied patients with thrombosis but without aPL, and age- and sex-matched healthy subjects.
The proteins that were more significantly altered among monocytes from APS patients with thrombosis (annexin I, annexin II, protein disulfide isomerase, Nedd8, RhoA proteins, and Hsp60) were functionally related to the induction of a procoagulant state as well as to autoimmune-related responses. Proteins reported to be connected to recurrent spontaneous abortion (e.g., fibrinogen and hemoglobin) were also determined to be significantly deregulated in APS patients without thrombosis. In vitro treatment with IgG fractions purified from the plasma of APS patients with thrombosis changed the pattern of protein expression of normal monocytes in the same way that was observed in vivo for monocytes from APS patients with thrombosis.
For the first time, proteomic analysis has identified novel proteins that may be involved in the pathogenic mechanisms of APS, thus providing potential new targets for pathogenesis-based therapies for the disease.

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Available from: Nuria Barbarroja, Apr 02, 2014
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    • "Cancer PDI P Endometrial cancer (with NS-398 treatment) [243] ERp57 P Prostate cancer (metastatic cell lines) [244] PDI, ERp57 P Leukemia (with ascorbate or photodynamic therapy) [245] [246] ERp57 P Esophageal cancer (cell lines) [247] ERp57, PDI P, I, G Gastric cancer (cancer/metastases vs control tissues; in serum, after vs before operation; in chemotherapy-resistant vs nonresistant cells) [248] [249] [250] PDI P, G Human bladder transitional carcinoma (cells) [251] PDIp I Pancreatic cancer (cell lines) [252] ERp57 P, I Glioblastoma multiforme (in astrocytomas) [253] ERp57 P, I Malignant follicular thyroid carcinoma [254] ERp57 P Lung metastatic cancer (cell lines) [255] Neurologic PDI, ERp44 I Neurodegenerative diseases (in ts1-infected astrocytes) [256] PDI P, I Neurologic dysfunction (in immunodeficiency mouse model) [257] PDI G Traumatic brain injury (in rat model) [258] Inflammation PDI P, I Edematous pancreatitis (in acinar cells) [259] ERp57 P Acute colitis (in colonic mucosa) [260] Others PDI P, I Osteoporosis (in osteoblasts or in circulating monocytes) [261] [262] ERp57 G Toxin exposure (diethylhexyl phthalate, in liver) [263] PDI P Exposure to arsenic and ionizing radiation (in keratinocytes) [264] ERp57 P Chronic vestibular compensation (after unilateral labyrinthectomy) [265] PDI P, I, G Antiphospholipid syndrome (in monocytes) [266] ERp57, ERp46, ERp29 P, I Insulin resistance and dyslipidemia (in hepatocytes) [229] ERp72, ERp57 P Caloric restriction (in liver) [201] ERp57 P Idiopathic pulmonary fibrosis (in bronchoalveolar fluid) [267] PDI P Obstructive sleep apnea syndrome (in kidney) [242] ERp57 P Preeclamptic trophoblasts [217] "
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