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Andreas Bergmann - One of the best experts on this subject based on the ideXlab platform.

  • killers creating new life caspases drive apoptosis Induced Proliferation in tissue repair and disease
    Cell Death & Differentiation, 2017
    Co-Authors: Caitlin E Fogarty, Andreas Bergmann
    Abstract:

    Killers creating new life: caspases drive apoptosis-Induced Proliferation in tissue repair and disease

  • extracellular reactive oxygen species drive apoptosis Induced Proliferation via drosophila macrophages
    Current Biology, 2016
    Co-Authors: Caitlin E Fogarty, Neha Diwanji, Jillian L Lindblad, Meghana Tare, Alla Amcheslavsky, Kalpana Makhijani, Katja Bruckner, Yun Fan, Andreas Bergmann
    Abstract:

    Summary Apoptosis-Induced Proliferation (AiP) is a compensatory mechanism to maintain tissue size and morphology following unexpected cell loss during normal development, and may also be a contributing factor to cancer and drug resistance. In apoptotic cells, caspase-initiated signaling cascades lead to the downstream production of mitogenic factors and the Proliferation of neighboring surviving cells. In epithelial cells of Drosophila imaginal discs, the Caspase-9 ortholog Dronc drives AiP via activation of Jun N-terminal kinase (JNK); however, the specific mechanisms of JNK activation remain unknown. Here we show that caspase-Induced activation of JNK during AiP depends on an inflammatory response. This is mediated by extracellular reactive oxygen species (ROSs) generated by the NADPH oxidase Duox in epithelial disc cells. Extracellular ROSs activate Drosophila macrophages (hemocytes), which in turn trigger JNK activity in epithelial cells by signaling through the tumor necrosis factor (TNF) ortholog Eiger. We propose that in an immortalized ("undead") model of AiP, signaling back and forth between epithelial disc cells and hemocytes by extracellular ROSs and TNF/Eiger drives overgrowth of the disc epithelium. These data illustrate a bidirectional cell-cell communication pathway with implication for tissue repair, regeneration, and cancer.

  • The role of apoptosis-Induced Proliferation for regeneration and cancer.
    Cold Spring Harbor perspectives in biology, 2012
    Co-Authors: Hyung Don Ryoo, Andreas Bergmann
    Abstract:

    Genes dedicated to killing cells must have evolved because of their positive effects on organismal survival. Positive functions of apoptotic genes have been well established in a large number of biological contexts, including their role in eliminating damaged and potentially cancerous cells. More recently, evidence has suggested that proapoptotic proteins-mostly caspases-can induce Proliferation of neighboring surviving cells to replace dying cells. This process, that we will refer to as "apoptosis-Induced Proliferation," may be critical for stem cell activity and tissue regeneration. Depending on the caspases involved, at least two distinct types of apoptosis-Induced Proliferation can be distinguished. One of these types have been studied using a model in which cells have initiated cell death, but are prevented from executing it because of effector caspase inhibition, thereby generating "undead" cells that emit persistent mitogen signaling and overgrowth. Such conditions are likely to contribute to certain forms of cancer. In this review, we summarize the current knowledge of apoptosis-Induced Proliferation and discuss its relevance for tissue regeneration and cancer.

Qihai Gong - One of the best experts on this subject based on the ideXlab platform.

  • rutaecarpine inhibits angiotensin ii Induced Proliferation in rat vascular smooth muscle cells
    Chinese Journal of Integrative Medicine, 2014
    Co-Authors: Yanju Li, Qihai Gong, Qin Wu, Feng Zhang, Limei Yu
    Abstract:

    Objective To evaluate the effects and possible mechanisms of rutaecarpine on angiotensin II (Ang II)-Induced Proliferation in cultured rat vascular smooth muscle cells (VSMCs).

  • effects of isorhynchophylline on angiotensin ii Induced Proliferation in rat vascular smooth muscle cells
    Journal of Pharmacy and Pharmacology, 2008
    Co-Authors: Feng Zhang, Ansheng Sun, Qihai Gong
    Abstract:

    Proliferation of vascular smooth muscle cells (VSMCs) is a crucial event in cardiovascular diseases. Isorhynchophylline, an alkaloid from a traditional Chinese medicine Gambirplant, has been used to treat cardiovascular diseases. The aim of this study was to investigate the effects of isorhynchophylline on angiotensin II (Ang II)-Induced Proliferation of rat VSMCs. VSMCs were isolated from rat artery and cultured for 14 days before experimentation. The effect of isorhynchophylline on Ang II-Induced Proliferation was evaluated by cell number, MTT assay and flow cytometry, and nitric oxide (NO) content and activity of NO synthase (NOS) were measured. The expression of proto-oncogene c-fos, osteopontin (OPN) and proliferating cell nuclear antigen (PCNA) mRNAs was measured by real-time RT-PCR. VSMC cultures were verified by morphology and immunostaining with alpha-smooth muscle actin. Isorhynchophylline (0.1-10.0 microM) was not toxic to VSMCs, but markedly decreased Ang II (1.0 microM)-enhanced cell number and MTT intensity, and blocked cell transition from G(0)/G(1) to S phase. Furthermore, isorhynchophylline increased the NO content and NOS activity, and suppressed Ang II-Induced over-expression of c-fos, OPN and PCNA. Thus, isorhynchophylline was effective against Ang-II Induced cell Proliferation, an effect that appears to be due, at least in part, to increased NO production, regulation of the cell cycle, and depressed expression of c-fos, OPN and PCNA related to VMSC Proliferation.

Massimo Trucco - One of the best experts on this subject based on the ideXlab platform.

  • human proinsulin c peptide reduces high glucose Induced Proliferation and nf κb activation in vascular smooth muscle cells
    Atherosclerosis, 2008
    Co-Authors: Vincenza Cifarelli, Patrizia Luppi, Hubert M Tse, Jon D Piganelli, Massimo Trucco
    Abstract:

    Excessive Proliferation of vascular smooth muscle cells (VSMCs) is one of the primary lesions in atherosclerosis development during diabetes. High glucose triggers VSMC Proliferation and initiates activation of the transcription factor nuclear factor (NF)-kappaB. Recently, clinical studies have demonstrated that replacement therapy with C-peptide, a cleavage product of insulin, to type 1 diabetic (T1D) patients is beneficial on a variety of diabetes-associated vascular complications. However, the mechanisms underlying the beneficial activity of C-peptide on the vasculature in conditions of hyperglycemia are largely unknown. The effects of C-peptide on the Proliferation of human umbilical artery smooth muscle cell (UASMC) and aortic smooth muscle cell (AoSMC) lines cultured under high glucose for 48 h were tested. To gain insights on potential intracellular signaling pathways affected by C-peptide, we analyzed NF-kappaB activation in VSMCs since this pathway represents a key mechanism for the accelerated vascular disease observed in diabetes. High glucose conditions (25 mmol/L) stimulated NF-kappaB-dependent VSMC Proliferation since the addition of two NF-kappaB-specific inhibitors, BAY11-7082 and PDTC, prevented Proliferation. C-peptide at the physiological concentrations of 0.5 and 1 nmol/L decreased high glucose-Induced Proliferation of VSMCs that was accompanied by decreased phosphorylation of IkappaB and reduced NF-kappaB nuclear translocation. These results suggest that in conditions of hyperglycemia C-peptide reduces Proliferation of VSMCs and NF-kappaB nuclear translocation. In patients with T1D, physiological C-peptide levels may exert beneficial effects on the vasculature that, under high glucose conditions, is subject to progressive dysfunction.

Feng Zhang - One of the best experts on this subject based on the ideXlab platform.

  • rutaecarpine inhibits angiotensin ii Induced Proliferation in rat vascular smooth muscle cells
    Chinese Journal of Integrative Medicine, 2014
    Co-Authors: Yanju Li, Qihai Gong, Qin Wu, Feng Zhang, Limei Yu
    Abstract:

    Objective To evaluate the effects and possible mechanisms of rutaecarpine on angiotensin II (Ang II)-Induced Proliferation in cultured rat vascular smooth muscle cells (VSMCs).

  • effects of isorhynchophylline on angiotensin ii Induced Proliferation in rat vascular smooth muscle cells
    Journal of Pharmacy and Pharmacology, 2008
    Co-Authors: Feng Zhang, Ansheng Sun, Qihai Gong
    Abstract:

    Proliferation of vascular smooth muscle cells (VSMCs) is a crucial event in cardiovascular diseases. Isorhynchophylline, an alkaloid from a traditional Chinese medicine Gambirplant, has been used to treat cardiovascular diseases. The aim of this study was to investigate the effects of isorhynchophylline on angiotensin II (Ang II)-Induced Proliferation of rat VSMCs. VSMCs were isolated from rat artery and cultured for 14 days before experimentation. The effect of isorhynchophylline on Ang II-Induced Proliferation was evaluated by cell number, MTT assay and flow cytometry, and nitric oxide (NO) content and activity of NO synthase (NOS) were measured. The expression of proto-oncogene c-fos, osteopontin (OPN) and proliferating cell nuclear antigen (PCNA) mRNAs was measured by real-time RT-PCR. VSMC cultures were verified by morphology and immunostaining with alpha-smooth muscle actin. Isorhynchophylline (0.1-10.0 microM) was not toxic to VSMCs, but markedly decreased Ang II (1.0 microM)-enhanced cell number and MTT intensity, and blocked cell transition from G(0)/G(1) to S phase. Furthermore, isorhynchophylline increased the NO content and NOS activity, and suppressed Ang II-Induced over-expression of c-fos, OPN and PCNA. Thus, isorhynchophylline was effective against Ang-II Induced cell Proliferation, an effect that appears to be due, at least in part, to increased NO production, regulation of the cell cycle, and depressed expression of c-fos, OPN and PCNA related to VMSC Proliferation.

Patricia A Damore - One of the best experts on this subject based on the ideXlab platform.