The cellular kinetics of lung alveolar epithelial cells and its relationship with lung tissue repair after acute lung injury

Yang, Xuechao; Li, Haisheng; Li, Yong; Yang, Chen; Gu, Wei; Zhou, Yin-han; Du, Juan; Wang, Haiyan; Sun, Jianhui; Wen, Dalin; Jiang, Jianxin

doi:10.1186/s12931-016-0480-y

Cited by 22 publications

(15 citation statements)

References 25 publications

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“…On the seventh day after ALI, the number of YAP1+ cells began to decline (Figure B). The expression time irregularity of YAP in lung tissue after ALI was consistent with that of AEC2s proliferation (Zeng et al, ); therefore, we supposed that AEC2s could be the main cells expressing YAP1 after ALI.…”

Section: Resultssupporting

confidence: 84%

“…The expression began to decline on the seventh day after injury ( Figure 1B). The changes in Hippo-YAP expression were consistent with the regular pattern of AEC2 proliferation after ALI (Zeng et al, 2016). The expression of Mer in Hippo pathway increased on the first and fifth day post ALI, while the expression of Ajuba in Hippo pathway increased on the third day post ALI.…”

Section: Expression Of the Hippo-yap Pathway At Various Time Points Asupporting

confidence: 79%

“…The hemorrhagic shock and LPS‐induced lung injury mouse model was established as previously described, with 4.5 mg/kg LPS instilled intratracheally (Zeng et al, ). The average survival rate of mice exposed to 4.5 mg/kg LPS was ~80% and ~30% of the lung showed evidence of pulmonary hemorrhaging.…”

Section: Resultsmentioning

confidence: 99%

“…Alveolar epithelial cells were isolated as previously described (Zeng et al, ). In brief, we used rat immunoglobulin G panning to deplete immunocytes expressing FcR.…”

Section: Methodsmentioning

confidence: 99%

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The Hippo–YAP pathway regulates the proliferation of alveolar epithelial progenitors after acute lung injury

Sun

et al. 2019

Cell Biology International

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Regeneration of pulmonary epithelial cells plays an important role in the recovery of acute lung injury (ALI), which is defined by pulmonary epithelial cell death. However, the mechanism of the regenerative capacity of alveolar epithelial cells is unknown. Using a lung injury mouse model induced by hemorrhagic shock and lipopolysaccharide, a protein mass spectrometry‐based high‐throughput screening and linage tracing technology to mark alveolar epithelial type 2 cells (AEC2s), we analyzed the mechanism of alveolar epithelial cells proliferation. We demonstrated that the expression of Hippo‐yes‐associated protein 1 (YAP1) key proteins were highly consistent with the regularity of the proliferation of alveolar epithelial type 2 cells after ALI. Furthermore, the results showed that YAP1+ cells in lung tissue after ALI were mainly Sftpc lineage‐labeled AEC2s. An in vitro proliferation assay of AEC2s demonstrated that AEC2 proliferation was significantly inhibited by both YAP1 small interfering RNA and Hippo inhibitor. These findings revealed that YAP functioned as a key regulator to promote AEC2s proliferation, with the Hippo signaling pathway playing a pivotal role in this process.

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Section: Resultssupporting

confidence: 84%

Section: Expression Of the Hippo-yap Pathway At Various Time Points Asupporting

confidence: 79%

Section: Resultsmentioning

confidence: 99%

“…Alveolar epithelial cells were isolated as previously described (Zeng et al, ). In brief, we used rat immunoglobulin G panning to deplete immunocytes expressing FcR.…”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

The Hippo–YAP pathway regulates the proliferation of alveolar epithelial progenitors after acute lung injury

Sun

et al. 2019

Cell Biology International

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“…In this study, both in vivo and in vitro data showed that PSN inhibited pro-inflammatory cytokine expression and protected against LPS-induced ALI and inflammatory responses. During the early stage of lung injury, inflammatory cells, especially neutrophils and macrophages, are recruited into lungs and contribute to LPS-induced inflammatory responses [46][47][48] , including the production of nitric oxide (NO) and inflammatory cytokines (eg, TNF-α, IL-1β, and IL-6) [2,3] . The expression of iNOS and NO are hallmarks of classically activated macrophages.…”

Section: Discussionmentioning

confidence: 99%

Protostemonine effectively attenuates lipopolysaccharide-induced acute lung injury in mice

Nie

et al. 2017

Acta Pharmacol Sin

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Protostemonine (PSN) is the main anti-inflammatory alkaloid extracted from the roots of Stemona sessilifolia (known as "Baibu" in traditional Chinese medicine). Here, we reported the inhibitory effects of PSN on lipopolysaccharide (LPS)-induced macrophage activation in vitro and LPS-induced acute lung injury in mice. Macrophage cell line RAW264.7 cells and mouse bone marrow-derived macrophages (BMDMs) were treated with PSN (1, 3, 10, 30 and 100 μmol/L) for 0.5 h and then challenged with LPS (0.1 μg/mL) for 24 h. Pretreatment with PSN significantly inhibited LPS-induced phosphorylation of MAPKs and AKT, iNOS expression and NO production in the macrophages. C57BL/6 mice were intratracheally injected with LPS (5 mg/kg) to induce acute lung injury (ALI). The mice were subsequently treated with PSN (10 mg/kg, ip) at 4 and 24 h after LPS challenge. PSN administration significantly attenuated LPS-induced inflammatory cell infiltration, reduced pro-inflammatory cytokine (TNF-α, IL-1β and IL-6) production and eliminated LPS-mediated lung edema. Furthermore, PSN administration significantly inhibited LPS-induced pulmonary MPO activity. Meanwhile, LPS-induced phosphorylation of p38 MAPK, iNOS expression and NO production in the lungs were also suppressed. The results demonstrate that PSN effectively attenuates LPS-induced inflammatory responses in vitro and in vivo; the beneficial effects are associated with the decreased phosphorylation of MAPK and AKT and the reduced expression of pro-inflammatory mediators, such as iNOS, NO and cytokines. These data suggest that PSN may be a potential therapeutic agent in the treatment of ALI.

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In Vitro Models for Studying Transport Across Epithelial Tissue Barriers

et al. 2018

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Epithelial barriers are the body's natural defense system to regulating passage from one domain to another. In our efforts to understand what can and cannot cross these barriers, models have emerged as a reductionist approach to rigorously study and investigate this question. In particular, in vitro tissue models have become prominent as there is an increased exploration of understanding biological molecular transport. Herein, we introduce the pertinent physiology, then discuss recent studies and approaches for building models of five epithelial tissues: skin, the gastrointestinal tract, the lungs, the blood-brain barrier, and the placenta. In particular, we evaluated literature from the past 5 years utilizing a tissue model to evaluate molecular transport. We then compare physiology of these tissues and discuss similarities in approaches, across tissues, to validate these models. We conclude with a summary of the approaches of growing interest across multiple tissues and an outlook on future steps to improve these models.

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The cellular kinetics of lung alveolar epithelial cells and its relationship with lung tissue repair after acute lung injury

Cited by 22 publications

References 25 publications

The Hippo–YAP pathway regulates the proliferation of alveolar epithelial progenitors after acute lung injury

The Hippo–YAP pathway regulates the proliferation of alveolar epithelial progenitors after acute lung injury

Protostemonine effectively attenuates lipopolysaccharide-induced acute lung injury in mice

In Vitro Models for Studying Transport Across Epithelial Tissue Barriers

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