Ultrastructural observations of programmed cell death during metanephric development in mouse

Previous studies revealed apoptosis as an only programmed cell death (PCD) during renal morphogenesis before alternative type of PCD, necroptosis were introduced. Evidences of non‐apoptotic PCD during renal development were scarce and needed to be accumulated. The purpose of this study is to investigate whether non‐apoptotic PCD is involved in and observe ultrastructural features of apoptotic cells or non‐apoptotic PCD during metanephros development. For this purpose, light and transmission electron microscopy were used. The most significant finding to come out of this study was that necroptosis was observed during developing metanephros by electron microscopy. The results also provided another fact that apoptosis and necroptosis constituted the PCD during embryonic development of kidney in mouse. Compared to necroptosis, apoptosis was more predominantly evident throughout whole development period and in every compartment of metanephros except for proximal tubule. However, necroptosis was only exhibited in developing nephrons also except for proximal tubule. In addition, outcomes of PCD were related to morphogenetic features of metanephric development. Efferocytosis for apoptotic cell or bodies took place in each type cell and whole period of developing metanephros. Besides efferocytosis blood flow and urine flux were available to remove the corpses of PCD, especially PCD from developing nephrons. Our findings suggested that both apoptosis and necroptosis play important roles during nephrogenesis and observed three ways to clear the PCD cell: efferocytosis, blood flow, and urine flux. Microsc. Res. Tech. 76:467–475, 2013. © 2013 Wiley Periodicals, Inc.     

Oogenesis and programmed cell death of nurse cells in the endoparasitoid,Pteromalus puparum

In this study, we describe the features of oogenesis in the endoparasitoid, Pteromalus puparum, as well as the distinct type of programmed cell death of the nurse cells through conventional light and fluorescent markers for apoptosis and immunofluorescent analysis. Oogenesis in this endoparasitoid is divided into five stages, of which stages 1–2, 3–4, and 5 are corresponding to previtellogenic growth, yolk uptake, and the formation of egg envelopes, respectively. From these studies, we demonstrate two critical events, which are vitellogenin absorption and rapid transfer of nurse cell content, resulting in remarkable increase in the volume of oocytes during oogenesis in this endoparasitoid. Vitellogenin absorption initiates in the oocyte of early stage 3, and bulk transfer of nurse cell content into the oocyte occurs at stage 4 of oogenesis in P. puparum, which is mainly characterized with the programmed cell death in the nurse cell complex. Microsc. Res. Tech., 2010. © 2009 Wiley‐Liss, Inc.     

Having a swell time--mitochondrial morphology and plant cell death programmes

Cell death is a vital process in multi-cellular eukaryotes. Rather than being a contradiction in terms, this statement highlights the importance of limited and localized cell killing to the health and normal development of complex organisms. The main focus of this article is the role of mitochondrial morphological changes during cell death programmes, and the conserved role of mitochondrial permeability transition (increased permeability of either the outer or inner membrane) as an early mechanistic event preceding cell death in both plant and non-plant eukaryotes. A second focus of this article is a review of the terminology and fundamental paradigms underpinning cell death research. Because of the importance of the process of cell death, there has been an enormous quantity of research performed to try to understand the underlying biological mechanisms. One result of such a large and varied research effort, and a result that is perhaps particularly evident to investigators coming into the field anew, is that some of the basic tenets of cell death research appear to have become confused. In this short article, I make an attempt to clarify the subject, focussing on the role of mitochondria, and the difficulties in comprehensibility arising from the sometimes-erroneous, or at least unnecessarily confusing use of specific terminology; there are several key terms in the cell death literature that appear interchangeable when they are not, or are interchanged when they should not be.     

Morphologic and temporal analysis of vascular smooth muscle cell apoptosis induced by c-Myc and E1A

Apoptosis is a physiologic form of cell death present in many disease conditions. When the balance of mitosis versus apoptosis is altered, tumor-like growth or degeneration of tissues may ensue. This appears to occur in several diseases, including those of the cardiovascular system, where apoptosis plays a key role in atherosclerosis and restenosis following angioplasty. Since c-myc is upregulated in the pathogenesis of these diseases, we chose to study the sequential morphologic features of programmed cell death in vascular smooth muscle cells induced by c-myc and by the adenovirus early gene E1A. Morphology and timed events in apoptotic cell cultures were analyzed by scanning electron microscopy, transmission electron microscopy, and time-lapse videomicroscopy. We observed that both c-myc-and E1A-induced apoptosis (in serum-free medium) resulted in numerous, tightly packed clusters of apoptotic blebs, as well as in one or two asymmetrically larger blebs. Transmission electron microscopy analysis revealed the larger blebs contained mostly nuclear chromatin, whereas the many smaller fragments often had little or no chromatin. Time-lapse studies showed that apoptosis was induced at a slower rate in cells stably transfected with c-myc versus those stably transfected with E1A. The early changes of apoptosis, including cell shrinkage and intense blebbing, occurred in under 5 min in both cells. Slight alterations such as cell size and further rounding occurred up to 8 h following the initial changes of apoptosis. Rather than being a part of the apoptotic response, release from the culture floor almost entirely resulted from movement of the culture flask. These studies provide a framework of timed morphologic events for future mechanistic investigation into the key aspects of myc-and E1A-induced apoptosis in vascular smooth muscle.     

Neural stem cell-conditioned medium upregulated the PCMT1 expression and inhibited the phosphorylation of MST1 in SH-SY5Y cells induced by Aβ_25-35

A progressive neurodegenerative disease, Alzheimer’s disease (AD). Studies suggest that highly expressedprotein isoaspartate methyltransferase 1 (PCMT1) in brain tissue. In the current study, we explored the effects ofneural stem cell-conditioned medium (NSC-CDM) on the PCMT1/MST1 pathway to alleviate Aβ_25-35-induceddamage in SH-SY5Y cells. Our data suggested that Aβ25-35 markedly inhibited cell viability. NSC-CDM or Neuralstem cell-complete medium (NSC-CPM) had a suppression effect on toxicity when treatment with Aβ_25-35, with agreater effect observed with NSC-CDM. Aβ_25-35 + NSC-CDM group exhibited an increase in PCMT1 expression.sh-PCMT1 markedly decreased cell proliferation and suppressed the protective role of NSC-CDM through theinduction of apoptosis and improved p-MST1 expression. Overexpression of PCMT1 reversed the Aβ_25-35-induceddecrease in cell proliferation and apoptosis. In summary, our findings suggest that NSC-CDM corrects the Aβ_25-35-induced damage to cells by improving PCMT1 expressions, which in turn reduces phosphorylation of MST1.