ELISEO JOJI SEKIYA
Projetos de Pesquisa
Unidades Organizacionais
LIM/31 - Laboratório de Genética e Hematologia Molecular, Hospital das Clínicas, Faculdade de Medicina
3 resultados
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bookPart Fundamentos da terapia celular(2013) JANZ, Felipe de Lara; DEBES, Adriana de Aguiar; SEKIYA, Elíseo Joji; ALVES, Adelson; BYDLOWSKI, Sérgio PauloconferenceObject MESENCHYMAL STEM CELLS FROM ADIPOSE TISSUE IN THE TREATMENT OF AMYOTROPHIC LATERAL SCLEROSIS - A CASE REPORT(2013) SEKIYA, E. J.; JORDY, S. S.; KUHN, T. I.; FORTE, A.; BRUNIERA, G.; ALVES, A.; BYDLOWSKI, S. P.Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease that selectively affects motor neurons in the brain and spinal cord leading to bulbar and respiratory muscle weakness. Currently there is no treatment proven effective and the disease is considered incurable. Mesenchymal Stem Cells (MSCs) derived from adipose tissue have immunomodulatory properties, inducing suppression and differentiation into neural cell types in vitro. Here we describe a compassionate intervention in a 66 years old male patient with Amyotrophic Lateral Sclerosis. The patient is suffering from Amyotrophic Lateral Sclerosis diagnosed 4 years ago, unsuccessfully treated with Riluzole. It was observed atrophy of the shoulder girdle, upper limbs and thenar and hypothenar regions, fasciculations, tetra-pyramidal release (Hoffmann and Babinsky bilateral and global hyperre flexia) and inexhaustible clonus in the lower limbs. ALSFRS (ALS Functional Rating Scale) and its revised version ALSFRS-R were ALSFRS18 and ALSFRS-R26, respectively. After approval by the Ethics Committee, adipose tissue was collected from abdominal region by liposuction. Adipose tissue-derived MSCs were expanded under GMP conditions and administered intrathecaly. Five days after the first infusion of 1 10 7 cells, patient showed improvement of overall muscle strength and speech, exhaustible clonus in limbs, absence of Babinsky in lower left limb, and ALSFRS25 and ALSFRS-R33. One month later clinical condition worsened, with ALSFRS18 and ALSFRS-R26. The patient received other two higher dose infusions (5 10 7 and 10 10 7 cells) during the next 6 months and clinical data improved (ALSFRS25 and ALSFRS-R33) for a longer period. Moreover, no adverse effects were observed by MSC administration. In conclusion, although the study was performed in a single patient, intra-thecal administration of autologous adipose tissue-derived MSC is potentially safe. It is tempting to speculate that administration of these cells could be beneficial for ALS patients, mainly using higher doses.conferenceObject CONDITIONED MEDIUM FROM HUMAN MESENCHYMAL STEM CELLS (MSC) FROM DIFFERENT SOURCES INDUCE PROLIFERATION OR CELL DEATH IN HEPG-2 AND JURKAT CANCER CELLS DEPENDING ON ITS ORIGIN(2013) RUIZ, Jorge Luis; LEVY, Debora; CARVALHO, Ana Carolina; SEKIYA, Eliseo; BYDLOWSKI, SergioThe use of MSCs after cancer treatment present some thoughtful concerns, as their interaction with tumors can enhance tumor cell growth or inhibit its proliferation, depending on the tumor type. To further explore this issue, we analyzed the effect of conditioned media (CM) obtained from cultured MSCs from 3 different sources (adipose tissue (AT), amniotic liquid (AL) and Wharton’s jelly (WJ)) on two cancer cell lines, HepG-2 (hepatocellular carcinoma) and Jurkat (T-cell leukemia) cells. The CMs were collected after 24hs of incubation of sub-confluent MSCs with a - MEM containing 20% of FBS. CMs were centrifuged, and passed through 0,22 m m filters and stored at -20 C. CMs from HepG-2, Jurkat cells and MRC-5 normal fibroblast were used as control. Effects of CMs on tumour cell proliferation were tested by MTT assay, in several concentrations after 24 h incubation. Cell cycle of HepG-2 and Jurkat cells treated with 25%, 50% or 75% CM was analysed by cytometry (IP staining) using Modfit LT software. Gene expression of bcl-2, bcl-6, ccnd1, ccnd2 and foxp-1 was assayed by q-PCR of Jurkat. We found that CM from AT enhances HepG-2 and Jurkat cell proliferation. CM from AL led to Jurkat cell proliferation with no effect in HepG2 cells. CM from WJ induced cell dead in Jurkat cells, while increased HepG-2 cell proliferation. MRC-5 CM has no effect on proliferation rate or death of HepG-2 and Jurkat cells. CM from WJ induced increase of ccnd2 and fox-p1 expression in Jurkat cells but not of bcl-2, bcl-6 and ccnd1 expression. CM from AT and AL had no effect. It seems that younger cells, as MSCs from Wharton‘s jelly, can secrete factors that act on differential pathways of death in Jurkat cells. In conclusions, CMs from hMSC led to proliferation or cell death in Jurkat and HepG-2 cell lines depending on the origin of the stem cells.