10 research outputs found
LIM-homeobox gene Lhx5 is required for normal development of Cajal-Retzius cells
Cajal-Retzius (C-R) cells play important roles in the lamination of the mammalian cortex via reelin secretion. The genetic mechanisms underlying the development of these neurons have just begun to be unraveled. Here, we show that two closely related LIM-homeobox genes Lhx1 and Lhx5 are expressed in reelin+ cells in various regions in the mouse telencephalon at or adjacent to sites where the C-R cells are generated, including the cortical hem, the mantle region of the septal/retrobulbar area, and the ventral pallium. Whereas Lhx5 is expressed in all of these reelin-expressing domains, Lhx1 is preferentially expressed in the septal area and in a continuous domain spanning from lateral olfactory region to caudomedial territories. Genetic ablation of Lhx5 results in decreased reelin+ and p73+ cells in the neocortical anlage, in the cortical hem, and in the septal, olfactory, and caudomedial telencephalic regions. The overall reduction in number of C-R cells in Lhx5 mutants is accompanied by formation of ectopic reelin+ cell clusters at the caudal telencephalon. Based on differential expression of molecular markers and by fluorescent cell tracing in cultured embryos, we located the origin of reelin+ ectopic cell clusters at the caudomedial telencephalic region. We also confirmed the existence of a normal migration stream of reelin+ cells from the caudomedial area to telencephalic olfactory territories in wild-type embryos. These results reveal a complex role for Lhx5 in regulating the development and normal distribution of C-R cells in the developing forebrain. Copyright © 2010 the authors.Peer Reviewe
LIM-homeobox gene Lhx5 is required for normal development of Cajal-Retzius cells.
Cajal-Retzius (C-R) cells play important roles in the lamination of the mammalian cortex via reelin secretion. The genetic mechanisms underlying the development of these neurons have just begun to be unraveled. Here, we show that two closely related LIM-homeobox genes Lhx1 and Lhx5 are expressed in reelin+ cells in various regions in the mouse telencephalon at or adjacent to sites where the C-R cells are generated, including the cortical hem, the mantle region of the septal/retrobulbar area, and the ventral pallium. Whereas Lhx5 is expressed in all of these reelin-expressing domains, Lhx1 is preferentially expressed in the septal area and in a continuous domain spanning from lateral olfactory region to caudomedial territories. Genetic ablation of Lhx5 results in decreased reelin+ and p73+ cells in the neocortical anlage, in the cortical hem, and in the septal, olfactory, and caudomedial telencephalic regions. The overall reduction in number of C-R cells in Lhx5 mutants is accompanied by formation of ectopic reelin+ cell clusters at the caudal telencephalon. Based on differential expression of molecular markers and by fluorescent cell tracing in cultured embryos, we located the origin of reelin+ ectopic cell clusters at the caudomedial telencephalic region. We also confirmed the existence of a normal migration stream of reelin+ cells from the caudomedial area to telencephalic olfactory territories in wild-type embryos. These results reveal a complex role for Lhx5 in regulating the development and normal distribution of C-R cells in the developing forebrain
Chronic administration of thiamine pyrophosphate decreases age-related histological atrophic testicular changes and improves sexual behavior in male Wistar rats
Aging is a multifactorial universal process
and constitutes the most important risk factor for
chronic-degenerative diseases. Although it is a natural
process, pathological aging arises when these changes
occur quickly and the body is not able to adapt. This is
often associated with the generation of reactive oxygen
species (ROS), inflammation, and a decrease in the
endogenous antioxidant systems, constituting a
physiopathological state commonly found in chronicdegenerative
diseases. At the testicular level, aging is
associated with tissue atrophy, decreased steroidogenesis
and spermatogenesis, and sexual behavior disorders.
This situation, in addition to the elevated generation of
ROS in the testicular steroidogenesis, provides a critical
cellular environment causing oxidative damage at
diverse cellular levels. To assess the effects of a
reduction in the levels of ROS, thiamine pyrophosphate
(TPP) was chronically administered in senile Wistar rats.
TPP causes an activation of intermediate metabolism
routes, enhancing cellular respiration and decreasing the
generation of ROS. Our results show an overall decrease
of atrophic histological changes linked to aging, with
higher levels of serum testosterone, sexual activity, and
an increase in the levels of endogenous antioxidant
enzymes in TPP-treated animals. These results suggest
that TPP chronic administration decreases the
progression of age-related atrophic changes by
improving the intermediate metabolism, and by
increasing the levels of antioxidant enzymes