The role of alternative autophagy in cell viability and response to paclitaxel treatment in v-Ha-ras-transformed NIH 3T3 cells.

In confluent v-Ha-ras-transformed NIH 3T3 fibroblasts (Ras-NIH 3T3), LC3 downregulation may precede a decrease in canonical autophagy, thus contributing to cell survival. Herein, we aimed to investigate the role of alternative autophagy in the viability of long-term cultures of Ras-NIH 3T3 cells and their parental NIH 3T3 cells. As cell confluence increased with the culture period, the level of alternative autophagy, as assessed through Lamp2-Rab9 co-localization, gradually decreased in both cell lines.

Atg5 knockout induces alternative autophagy via the downregulation of Akt expression.

Unlabelled: Autophagy play contradictory roles in cellular transformation. We previously found that the knockout (KO) of autophagy-related 5 (Atg5), which is essential for autophagy, leads to the malignant transformation of NIH 3T3 cells. In this study, we explored the mechanism by which autophagy contributes to this malignant transformation using two transformed cell lines, Atg5 KO and Ras-NIH 3T3.

Transformed cells maintain survival by downregulating autophagy at a high cell confluency.

Autophagy plays a dual role in tumorigenesis by functioning as both a tumor suppressor and promoter, depending on the stage of tumorigenesis. However, it is still unclear at what stage the role of autophagy changes during tumorigenesis. Herein, we investigated the differences in the basal levels and roles of autophagy in five cell lines at different stages of cell transformation.

Periodontal Regeneration with Amnion-Chorion Membrane on Root Surface: A Retrospective Case Series.

This retrospective case series investigated the clinical and radiographic outcomes in 19 intrabony defects treated with periodontal regenerative therapy utilizing a combined approach. Placing an amnion-chorion membrane (ACM) as a biologic modifier on the root surface of the periodontally diseased tooth, combined with bone substitutes and an additional ACM as a barrier membrane, the treated sites were examined 8 to 24 months after the therapy. The preoperative (baseline) mean probing pocket depth (PPD) was 7.

Contributory Role of BLT2 in the Production of Proinflammatory Cytokines in Cecal Ligation and Puncture-Induced Sepsis.

BLT2 is a low-affinity receptor for leukotriene B, a potent lipid mediator of inflammation generated from arachidonic acid via the 5-lipoxygenase pathway. The aim of this study was to investigate whether BLT2 plays any role in sepsis, a systemic inflammatory response syndrome caused by infection. A murine model of cecal ligation and puncture (CLP)-induced sepsis was used to evaluate the role of BLT2 in septic inflammation.