scholarly journals Vimentin-Rab7a Pathway Mediates the Migration of MSCs and Lead to Therapeutic Effects on ARDS

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Kai Wang ◽  
Boxiang Du ◽  
Yan Zhang ◽  
Congyou Wu ◽  
Xiuli Wang ◽  
...  
Keyword(s):  
Therapeutic Effect ◽  
Lung Tissue ◽  
Gene Knockout ◽  
Inflammatory Factors ◽  
Mouse Lung ◽  
Therapeutic Effects ◽  
Proliferation And Differentiation ◽  
Differentiation Status ◽  
Mouse Lung Tissue ◽  
Vimentin Gene

Acute respiratory distress syndrome (ARDS) is difficult to treat and has a high mortality rate. Mesenchymal stem cells (MSCs) have an important therapeutic effect in ARDS. While the mechanism of MSC migration to the lungs remains unclear, the role of MSCs is of great clinical significance. To this end, we constructed vimentin knockout mice, extracted bone MSCs from the mice, and used them for the treatment of LPS-induced ARDS. H&E staining and Masson staining of mouse lung tissue allowed us to assess the degree of damage and fibrosis of mouse lung tissue. By measuring serum TNF-α, TGF-β, and INF-γ, we were able to monitor the release of inflammatory factors. Finally, through immunoprecipitation and gene knockout experiments, we identified upstream molecules that regulate vimentin and elucidated the mechanism that mediates MSC migration. As a result, we found that MSCs from wild-type mice can significantly alleviate ARDS and reduce lung inflammation, while vimentin gene knockout reduced the therapeutic effect of MSCs in ARDS. Cytological experiments showed that vimentin gene knockout can significantly inhibit the migration of MSCs and showed that it changes the proliferation and differentiation status of MSCs. Further experiments found that vimentin’s regulation of MSC migration is mainly mediated by Rab7a. Rab7a knockout blocked the migration of MSCs and weakened the therapeutic effect of MSCs in ARDS. In conclusion, we have shown that the Vimentin-Rab7a pathway mediates migration of MSCs and leads to therapeutic effects in ARDS.

scholarly journals Circular RNA profiles in mouse lung tissue induced by radon

2017 ◽  
Vol 22 (1) ◽  
Author(s):  
Weiwei Pei ◽  
Lijing Tao ◽  
Leshuai W. Zhang ◽  
Shuyu Zhang ◽  
Jianping Cao ◽  
...  
Keyword(s):  
Lung Tissue ◽  
Circular Rna ◽  
Mouse Lung ◽  
Mouse Lung Tissue

Normal mouse lung tissue produces a growth-inhibitory factor(s) preferential for mouse monocytic leukemia cells

1989 ◽  
Vol 30 (3) ◽  
pp. 139-144 ◽  
Author(s):  
Togo Ikuta ◽  
Yoshio Honma ◽  
Junko Okabe-Kado ◽  
Takashi Kasukabe ◽  
Motoo Hozumi
Keyword(s):  
Lung Tissue ◽  
Normal Mouse ◽  
Inhibitory Factor ◽  
Leukemia Cells ◽  
Mouse Lung ◽  
Monocytic Leukemia ◽  
Growth Inhibitory Factor ◽  
Growth Inhibitory ◽  
Mouse Lung Tissue

scholarly journals Identification and Functional Analysis of EPOR+ Tumor-Associated Macrophages in Human Osteosarcoma Lung Metastasis

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Yanxing Li ◽  
Ming Li ◽  
Rong Wei ◽  
Junlong Wu
Keyword(s):  
Lung Metastasis ◽  
Lung Tissue ◽  
Disease Free Survival ◽  
Mouse Lung ◽  
Tumor Associated Macrophages ◽  
Free Survival ◽  
Human Osteosarcoma ◽  
Clinicopathologic Factors ◽  
Mouse Lung Tissue ◽  
Disease Free

Background. Tissue-resident macrophages can be educated to tumor-associated macrophages (TAMs) by the tumor microenvironment and many types of macrophages express erythropoietic receptor (EPOR); However, little is known about the expression of EPOR on TAMs and the identity of EPOR+ TAMs in osteosarcoma lung metastasis has thus far remained elusive. Methods. EPOR-eGFPcre mice were used to determine the expression of EPOR on lung tissue-resident macrophages. Flow cytometry, RT-PCR, and Western blot were examined to define the identity of EPOR+ TAMs in 106 osteosarcoma lung metastasis specimens. Moreover, the clinicopathologic factors and prognosis of patients with CD163+EPOR+ macrophages were compared. Results. We found that a subpopulation of mouse lung tissue-resident macrophages express EPOR and EPO enhances the proliferation of EPOR+ macrophages in mouse lung. A subpopulation of CD163+ macrophages expresses EPOR in human osteosarcoma lung metastasis specimens. CD163+EPOR+TAMs increase 2.5 times in human osteosarcoma lung metastasis tissues; CD206, CD163, and PD1, which are known to have a significant role in TAM function had high expression in CD163+EPOR+ TAMs compared with CD163+EPOR- TAMs. Furthermore, CD163+EPOR+ TAMs had higher M2 marker and cytokine expression in osteosarcoma tissues compared with para-osteosarcoma tissues. EPO enhanced the expression of M2 cytokines in primary CD163+EPOR+ TAMs. Importantly, the percentage of CD163+EPOR+ TAMs had a positive linear association with malignant phenotypes as well as poor disease-free survival and overall survival time. Conclusions. We have characterized TAMs expressing EPOR and CD163+EPOR+ macrophages as TAMs in osteosarcoma lung metastasis patients, which are highly associated with tumor aggressiveness.

Mouse Lung Tissue Slice Culture

2019 ◽  
pp. 297-311 ◽  
Author(s):  
Xinhui Wu ◽  
Eline M. van Dijk ◽  
I. Sophie T. Bos ◽  
Loes E. M. Kistemaker ◽  
Reinoud Gosens
Keyword(s):  
Lung Tissue ◽  
Tissue Slice ◽  
Mouse Lung ◽  
Slice Culture ◽  
Mouse Lung Tissue

The effect of benzo[α]pyrene on expression and signaling cross talk of aryl hydrocarbon receptor and NFATc1 in mouse lung tissue

2014 ◽  
Vol 32 (7) ◽  
pp. 1246-1253 ◽  
Author(s):  
Maliheh Parsa ◽  
Seyed Nasser Ostad ◽  
Seyed Mohammad Hossein Noori Moogahi ◽  
Mohammad Bayat ◽  
Mohammad Hossein Ghahremani
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Lung Tissue ◽  
Cross Talk ◽  
Environmental Pollutants ◽  
Lung Damage ◽  
Mouse Lung ◽  
Aryl Hydrocarbon ◽  
Embedded Blocks ◽  
Mouse Lung Tissue ◽  
Imagej Software

Objective: Polycyclic aromatic hydrocarbons (PAHs) are potent environmental pollutants. Benzo[α]pyrene (B[α]P) is the major compound of PAHs that acts by activating aryl hydrocarbon receptor (AhR) in cells. B[α]P is a known carcinogen and an immunotoxicant; however, its role with regard to nuclear factor of activated T cell (NFAT) pathway is unclear. AhR and NFAT signaling pathways have common roles in pathological functions in immunotoxicity and lung cancer. In this study, the effect of AhR activation on expression and signaling cross talk of AhR and NFATc1 pathways in mouse lung tissue has been investigated. Methods: Swiss albino mice were randomly allocated to five groups and administered with cyclosporin A (CsA) and B[α]P for seven constitutive days. Animals were then killed, and lung tissues were obtained after washing the whole blood. Paraffin-embedded blocks were prepared, and 5 µm sections were cut for histopathological and immunohistochemical assessments. The results were scored by observer and digitally analyzed using ImageJ software. Results: Our data showed that CsA administration resulted in a significant reduction of AhR expression. This effect was partly blocked in mice coadministrated with B[α]P and CsA. NFATc1 expression was also reduced in CsA-treated animals. Furthermore, CsA inhibited the pathological effects of B[α]P in mouse lung tissue. Conclusion: AhR expression is dependent on NFATc1 activation, and NFATc1 inhibition remarkably decreases AhR expression. However, it seems that total expression of NFATc1 is not dependent on AhR expression or activation. Moreover, CsA can prevent B[α]P-induced lung tissue damage, and it remarkably decreases NFATc1 expression. The results from this study point toward the molecular interactions of AhR and NFATc1 activation in lung tissue and the benefit of CsA treatment in B[α]P-induced lung damage.

Targeted Therapeutic Effect of Bavachinin Nanospheres on Pathological Site of Chronic Asthmatic Mice Model

2021 ◽  
Vol 21 (2) ◽  
pp. 1085-1090
Author(s):  
Chunxia Zhang ◽  
Qian Qin ◽  
Hongle Li
Keyword(s):  
Therapeutic Effect ◽  
Lung Tissue ◽  
Infrared Imaging ◽  
Oral Drug Delivery ◽  
Inflammatory Cells ◽  
Good Effect ◽  
Oral Drug ◽  
Therapeutic Effects ◽  
Mice Model ◽  
Imaging Results

Steroids are the main drugs currently used to treat asthma. However, the toxic and side effects of these drugs and the tolerance of the drugs due to long-term administration are still problems in the clinical treatment of asthma. Bavachinin has a good effect in the treatment of mouse asthma models, and it can effectively inhibit the expression of a variety of cytokines. However, it is extremely difficult to dissolve in water, has low bioavailability, and is quickly cleared in the blood. These characteristics limit its clinical application potential. In this study, nanotechnology was used to construct an effective oral drug delivery system. Through analysis of serum-related antibodies and cytokines, the system showed significant therapeutic effects on asthma-positive groups. Far-infrared imaging results showed that the system has a good targeted enrichment effect on pathological parts, while showing lower toxicity and higher therapeutic effect. Whether it is the splenocyte flow typing or the analysis of lung tissue, the system has verified the excellent treatment, and through the observation of paraffin sections of lung tissue, it was found that the bronchial morphology returned to normal after drug treatment, and the leakage of inflammatory cells was significantly reduced.

The effect of transplacental administration of ddt on organ cultures of foetal mouse lung tissue

1972 ◽  
Vol 9 (2) ◽  
pp. 365-373 ◽  
Author(s):  
L. M. Shabad ◽  
T. S. Kolesnichenko ◽  
T. V. Nikonova
Keyword(s):  
Lung Tissue ◽  
Mouse Lung ◽  
Organ Cultures ◽  
Mouse Lung Tissue

scholarly journals Transcriptional regulatory mechanisms of fibrosis development in mouse lung tissue exposed to carbon nanotubes

2018 ◽  
Author(s):  
Vadim Zhernovkov ◽  
Tapesh Santra ◽  
Hilary Cassidy ◽  
Oleksii Rukhlenko ◽  
David Matallanas ◽  
...  
Keyword(s):  
Carbon Nanotubes ◽  
Lung Tissue ◽  
Stress Responses ◽  
Expression Profiles ◽  
Cellular Stress ◽  
Interferon Response ◽  
Mouse Lung ◽  
M2 Macrophage ◽  
Cellular Stress Responses ◽  
Mouse Lung Tissue

AbstractBackgroundCarbon nanotubes (CNTs) usage has rapidly increased in the last few decades due to their unique properties, exploited in various industrial and commercial products. Certain types of CNTs cause adverse health effects, including chronic inflammation and fibrosis. Despite the large number of in vitro and in vivo studies evaluating these effects, many important questions remain unanswered due to a lack of mechanistic understanding of how CNTs induce cellular stress responses. In order to predict CNT toxicity, it is important to understand which transcriptional programs are specifically activated in response to CNTs, and what similarities and differences exist in relation to other toxic inducers exerting similar adverse effects.ResultsA systems biology approach was applied to reveal complex interactions at the molecular level in mouse lung tissue in response to different fibrosis inducers: two types of multi-walled CNTs, NM-401 and NRCWE-26, and bleomycin (BLM). Based on mRNA gene expression profiles, we inferred gene regulatory networks (GRNs) to capture functional hierarchical regulatory structures between genes and their regulators. We found that activities of the transcription factors (TFs) Myc, Arid5a and Mxd1 were associated with the regulation of cytokine transcription in response to CNTs, while in response to BLM treatment, Myc was associated with p53 signaling. TF Litaf was identified as the essential regulator for noncanonical signaling of TLR2/4 driven by CNTs. Despite the different nature of the lung injury caused by CNTs and BLM, we identified common stress response modules, that included DNA damage (TFs: E2f8, E2f1, Foxm1), M1/M2 macrophage polarization (TF: Mafb), Interferon response (TFs: Irf7, Stat2 and Irf9) for all agents.ConclusionsThese results suggest that the reconstruction and analysis of TF-centric gene interaction networks can reveal key targets and regulators of cellular stress responses to toxic agents.

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