RESUMEN
The presence of non-progressive cognitive impairment is recognized as a common feature in a substantial proportion of patients with Duchenne muscular dystrophy (DMD). Concurrently, the amyloid beta peptide (Aß42) protein has been associated with changes in memory and cognitive functions. Also, it has been shown that different subtypes of neural stem/progenitor cells (CD 34, CD 45, nestin) are involved in the innate repair of plasticity mechanisms by the injured brain, in which Nerve Growth Factor (NGF) acts as chemotactic agents to recruit such cells. Accordingly, the present study investigated levels of CD 34, CD 45, nestin and NGF in an attempt to investigate makers of neural regeneration in DMD. Neural damage was assayed in terms of Aß42. Results showed that Aß42 (21.9 ± 6.7 vs. 12.13 ± 4.5) was significantly increased among DMD patients compared to controls. NGF (165.8 ± 72 vs. 89.8 ± 35.9) and mononuclear cells expressing nestin (18.9 ± 6 vs. 9 ± 4), CD 45 (64 ± 5.4 vs. 53.3 ± 5.2) and CD34 (75 ± 6.2 vs. 60 ± 4.8) were significantly increased among DMD patients compared to controls. In conclusion cognitive function decline in DMD patients is associated with increased levels of Aß42, which is suggested to be the cause of brain damage in such patients. The significant increase plasma NFG and in the number of mononuclear cells bearing CD34, CD45 and nestin indicates that regeneration is an ongoing process in these patients. However, this regeneration cannot counterbalance the damage induced by dystrophine mutation and increased Aß42.
Asunto(s)
Antígenos CD34/metabolismo , Trastornos del Conocimiento/metabolismo , Trastornos del Conocimiento/fisiopatología , Antígenos Comunes de Leucocito/metabolismo , Distrofia Muscular de Duchenne/metabolismo , Distrofia Muscular de Duchenne/fisiopatología , Factor de Crecimiento Nervioso/metabolismo , Nestina/metabolismo , Estudios de Casos y Controles , Niño , Ensayo de Inmunoadsorción Enzimática , Humanos , MasculinoRESUMEN
The objective of the study was to investigate the mitogenic and genotoxic effects of He:Ne laser irradiation (632.8 nm) on human peripheral lymphocytes in vitro. We used the cytokinesis-block micronucleus assay, which incorporates cytochalasin B to inhibit cytokinesis while karyokinesis proceeds normally leading to the appearance of proliferating lymphocytes as binucleated cells. Also micronuclei will appear in cases of genotoxicologically-affected cells. Buffy coat leukocytes were exposed to 10 mW He:Ne laser at energy densities of 1, 2, 3 and 5 J/cm(2). Cells were then cultured in media 199 without any supplementation for 24, 48, 72 and 96 h adding cytochalasin B 24 h before harvesting of cells. Our results showed that laser-induced lymphocytes proliferate throughout the four consecutive days post-laser irradiation. The difference in the frequency of micronuclei between pre- and post-laser irradiation indicates that a He:Ne laser at such energy densities 1, 2, 3 and 5 J/cm(2) does not induce micronucleus formation. These results shed some light on the mechanism encountered by lymphocytes in the process of He:Ne laser-induced biostimulation.