7 research outputs found
Reactive oxygen species and male reproductive hormones
Reports of the increasing incidence of male infertility paired with decreasing semen quality have triggered studies
on the effects of lifestyle and environmental factors on the male reproductive potential. There are numerous exogenous
and endogenous factors that are able to induce excessive production of reactive oxygen species (ROS) beyond that of
cellular antioxidant capacity, thus causing oxidative stress. In turn, oxidative stress negatively affects male reproductive
functions and may induce infertility either directly or indirectly by affecting the hypothalamus-pituitary-gonadal (HPG)
axis and/or disrupting its crosstalk with other hormonal axes. This review discusses the important exogenous and
endogenous factors leading to the generation of ROS in different parts of the male reproductive tract. It also highlights
the negative impact of oxidative stress on the regulation and cross-talk between the reproductive hormones. It further
describes the mechanism of ROS-induced derangement of male reproductive hormonal profiles that could ultimately
lead to male infertility. An understanding of the disruptive effects of ROS on male reproductive hormones would
encourage further investigations directed towards the prevention of ROS-mediated hormonal imbalances, which in turn
could help in the management of male infertility
Memo1-mediated tiling of radial glial cells facilitates cerebral cortical development
Polarized, non-overlapping, regularly spaced, tiled organization of radial glial cells (RGCs) serves as a framework to generate and organize cortical neuronal columns, layers, and circuitry. Here, we show that mediator of cell motility 1 (Memo1) is a critical determinant of radial glial tiling during neocortical development. Memo1 deletion or knockdown leads to hyperbranching of RGC basal processes and disrupted RGC tiling, resulting in aberrant radial unit assembly and neuronal layering. Memo1 regulates microtubule (MT) stability necessary for RGC tiling. Memo1 deficiency leads to disrupted MT minus-end CAMSAP2 distribution, initiation of aberrant MT branching, and altered polarized trafficking of key basal domain proteins such as GPR56, and thus aberrant RGC tiling. These findings identify Memo1 as a mediator of RGC scaffold tiling, necessary to generate and organize neurons into functional ensembles in the developing cerebral cortex
Memo1-mediated tiling of radial glial cells facilitates cerebral cortical development
Polarized, non-overlapping, regularly spaced, tiled organization of radial glial cells (RGCs) serves as a framework to generate and organize cortical neuronal columns, layers, and circuitry. Here, we show that mediator of cell motility 1 (Memo1) is a critical determinant of radial glial tiling during neocortical development. Memo1 deletion or knockdown leads to hyperbranching of RGC basal processes and disrupted RGC tiling, resulting in aberrant radial unit assembly and neuronal layering. Memo1 regulates microtubule (MT) stability necessary for RGC tiling. Memo1 deficiency leads to disrupted MT minus-end CAMSAP2 distribution, initiation of aberrant MT branching, and altered polarized trafficking of key basal domain proteins such as GPR56, and thus aberrant RGC tiling. These findings identify Memo1 as a mediator of RGC scaffold tiling, necessary to generate and organize neurons into functional ensembles in the developing cerebral cortex