The effect of transforming growth factor β1 on the crosstalk between autophagy and apoptosis in the annulus fibrosus cells under serum deprivation

Ni, Binbin; Li, Bo; Yang, Yueping; Chen, Jiangwei; Chen, Ke; Jiang, Sheng‐Dan; Jiang, Lei‐Sheng

doi:10.1016/j.cyto.2014.07.249

Cited by 52 publications

(41 citation statements)

References 70 publications

(85 reference statements)

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“…BAF, an inhibitor of the proton pump, inhibited the combination of autophagosome and lysosome. 49 In the study, we found that inhibition of the late stage of autophagy by BAF had no evident effect on Mn-induced activation of the NLRP3 inflammasome and release of proinflammatory cytokines, indicating that disorder of the fusion of autophagosome and lysosome and degradation was not involved in Mn-induced activation of the NLRP3 inflammasome.…”

Section: Discussionmentioning

confidence: 78%

The role of NLRP3-CASP1 in inflammasome-mediated neuroinflammation and autophagy dysfunction in manganese-induced, hippocampal-dependent impairment of learning and memory ability

et al. 2017

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Central nervous system (CNS) inflammation and autophagy dysfunction are known to be involved in the pathology of neurodegenerative diseases. Manganese (Mn), a neurotoxic metal, has the potential to induce microglia-mediated neuroinflammation as well as autophagy dysfunction. NLRP3 (NLR family, pyrin domain containing 3)-CASP1 (caspase 1) inflammasome-mediated neuroinflammation in microglia has specific relevance to neurological diseases. However, the mechanism driving these phenomena remains poorly understood. We demonstrate that Mn activates the NLRP3-CASP1 inflammasome pathway in the hippocampus of mice and BV2 cells by triggering autophagy-lysosomal dysfunction. The autophagylysosomal dysfunction is induced by lysosomal damage caused by excessive Mn accumulation, damaging the structure and normal function of these organelles. Additionally, we show that the release of lysosomal CTSB (cathepsin B) plays an important role in Mn-induced NLRP3-CASP1 inflammasome activation, and that the increased autophagosomes in the cytoplasm are not the main cause of NLRP3-CASP1 inflammasome activation. The accumulation of proinflammatory cytokines, such as IL1B (interleukin 1 b) and IL18 (interleukin 18), as well as the dysfunctional autophagy pathway may damage hippocampal neuronal cells, thus leading to hippocampal-dependent impairment in learning and memory, which is associated with the pathogenesis of Alzheimer disease (AD).

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Section: Discussionmentioning

confidence: 78%

The role of NLRP3-CASP1 in inflammasome-mediated neuroinflammation and autophagy dysfunction in manganese-induced, hippocampal-dependent impairment of learning and memory ability

et al. 2017

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“…As mentioned above, SIRT1 protects against apoptosis of human NP cells via induction of autophagy in the presence of nutrition deprivation [103]. In contrast to this work, Ni et al showed that exposure of rat AF cells to TGF-β1 significantly attenuates apoptosis under starvation through prevention of excessive autophagy due to activation of the PI3K/AKT/mTOR and extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathways [139], suggesting that autophagy may play a detrimental role in the protective effects of TGF-β1 on disc degeneration. Additionally, oxidative stress has been defined as a disturbance in the prooxidant-antioxidant balance in favor of the former, thus leading to potential damage.…”

Section: Accepted Manuscriptmentioning

confidence: 79%

Autophagy: A double-edged sword in intervertebral disk degeneration

Zhang

Yang

Wang

et al. 2016

Clinica Chimica Acta

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“…f Nuclear localization of phospho-Smad (red) and DNA (blue) in midgut ECs is high in −16 h RFP, with reduced levels in −8 h RPF and low-nuclear levels in −4 h RPF. Scale bar represents 10 μm regulating excessive autophagy [19]. Thus the physiological relationship between TGF-β signaling and autophagydependent cell death remains poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Dpp regulates autophagy-dependent midgut removal and signals to block ecdysone production

Denton

Dayan

et al. 2018

Cell Death Differ

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Animal development and homeostasis require the programmed removal of cells. Autophagy-dependent cell deletion is a unique form of cell death often involved in bulk degradation of tissues. In Drosophila the steroid hormone ecdysone controls developmental transitions and triggers the autophagy-dependent removal of the obsolete larval midgut. The production of ecdysone is exquisitely coordinated with signals from numerous organ systems to mediate the correct timing of such developmental programs. Here we report an unexpected role for the Drosophila bone morphogenetic protein/transforming growth factor β ligand, Decapentaplegic (Dpp), in the regulation of ecdysone-mediated midgut degradation. We show that blocking Dpp signaling induces premature autophagy, rapid cell death, and midgut degradation, whereas sustained Dpp signaling inhibits autophagy induction. Furthermore, Dpp signaling in the midgut prevents the expression of ecdysone responsive genes and impairs ecdysone production in the prothoracic gland. We propose that Dpp has dual roles: one within the midgut to prevent improper tissue degradation, and one in interorgan communication to coordinate ecdysone biosynthesis and developmental timing.

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The effect of transforming growth factor β1 on the crosstalk between autophagy and apoptosis in the annulus fibrosus cells under serum deprivation

Cited by 52 publications

References 70 publications

The role of NLRP3-CASP1 in inflammasome-mediated neuroinflammation and autophagy dysfunction in manganese-induced, hippocampal-dependent impairment of learning and memory ability

The role of NLRP3-CASP1 in inflammasome-mediated neuroinflammation and autophagy dysfunction in manganese-induced, hippocampal-dependent impairment of learning and memory ability

Autophagy: A double-edged sword in intervertebral disk degeneration

Dpp regulates autophagy-dependent midgut removal and signals to block ecdysone production

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