Lamins of ocular lens epithelial cells

Abstract

Experiments were performed to characterize a prominent nuclear matrix (NM) protein isolated from tissue cultured mouse lens epithelial cells. This NM protein was separated by SDS-PAGE and the stained gel band was analyzed by mass spectroscopy. Blast analysis of the amino acid sequence derived by mass spectroscopy revealed the presence of Lamin C in the NM of the mouse lens epithelial cells. We also examined nuclear proteins of adult and fetal human lenses. Data collected from these experiments showed the presence of Lamin C in both adult and fetal lens cells. However fetal lens cells only show Lamin C dimers, whereas adult human lens contained dimers, monomers and degraded Lamin C. Early and late passaged tissue cultured mouse lens epithelial cells also contained Lamin C in the nucleus with a preponderance of the dimer in the early passaged cells. The biological significance of the presence of dimers in human fetal lens cells and early passaged mouse lens cells is not known. However, it could suggest an enhanced docking capability of Lamin C dimers for other physiologically important nuclear proteins.

Effect of thermal stress on early and late passaged mouse lens epithelial cells

“…Heydari et al [1993] reported that the age related decline in HSP‐70 expression was caused at the transcriptional level, by decreased binding of HSF‐1 to the heat shock element of HSP‐70. The down regulation of hsp synthesis could also be modulated by alterations in the nuclear matrix organization initiated by changes in the aging Lamin‐C structure [Stein, 1993; Bagchi et al, 2007]. The lens epithelial cells (αTN‐4) used in these experiments were immortalized with introduction of α‐crystallin promoter fused with T‐antigen, thus these cells do not display proliferative senescence and an age related decrease of HSF‐1 activities.…”

<p>Chronic Wasting Disease In Cervids: Prevalence, Impact And Management Strategies</p>

“…In 1997, Prusiner and collaborators won the Nobel Prize for the discovery of “Prions – a new biological principle of infection” and for their contribution on prion research development. While the consensus is that prion proteins (denoted PrP SC from Scrapie) are the causative agents of prion diseases, and further evidence support that PRNP —a host gene that regulates the expression of the prion protein PrP C —plays a crucial role in the development of TSEs,16 some researchers proposed bacterias17,18 and viruses19 as causative agents of TSEs. However, these theories were soon dismissed 20–22…”