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1.
World J Clin Cases ; 12(17): 3144-3150, 2024 Jun 16.
Article in English | MEDLINE | ID: mdl-38898861

ABSTRACT

BACKGROUND: Myositis ossificans (MO) is a rare disease involving the formation of bone outside the musculoskeletal system. While surgical intervention is the main treatment approach, preventing recurrence and standardized rehabilitation are also crucial. Here, we present a surgical strategy to prevent the recurrence of MO. CASE SUMMARY: A 28-year-old female patient was admitted for the first time for a comminuted fracture of the left olecranon. However, incorrect postoperative rehabilitation resulted in the development of elbow joint stiffness with ectopic ossification, causing a loss of normal range of motion. The patient was diagnosed with MO based on physical examination, X-ray findings, and clinical presentation. We devised a surgical strategy to remove MO, followed by fixation with an Ilizarov frame, and implemented a scientifically reasonable rehabilitation plan. The surgery lasted for 3 h with an estimated blood loss of 45 mL. A drainage tube was placed after surgery, and fluid was aspirated through ultrasound-guided puncture. The patient experienced a significant reduction in joint stiffness after surgery. In the final follow-up at 9 mouths, there was evident improvement in the range of motion of the elbow joint, and no other symptoms were reported. CONCLUSION: The Ilizarov frame is an advantageous surgical technique for facilitating rehabilitation after MO removal. It offers benefits such as passive recovery, individualized treatment, and prompt recovery.

2.
Front Immunol ; 13: 1110774, 2022.
Article in English | MEDLINE | ID: mdl-36685535

ABSTRACT

Macrophages play an essential role in maintaining the normal function of the innate and adaptive immune responses during host defence. Macrophages acquire diverse functional phenotypes in response to various microenvironmental stimuli, and are mainly classified into classically activated macrophages (M1) and alternatively activated macrophages (M2). Macrophage polarization participates in the inflammatory, fibrotic, and oncogenic processes of diverse respiratory diseases by changing phenotype and function. In recent decades, with the advent of broad-range profiling methods such as microarrays and next-generation sequencing, the discovery of RNA transcripts that do not encode proteins termed "noncoding RNAs (ncRNAs)" has become more easily accessible. As one major member of the regulatory ncRNA family, long noncoding RNAs (lncRNAs, transcripts >200 nucleotides) participate in multiple pathophysiological processes, including cell proliferation, differentiation, and apoptosis, and vary with different stimulants and cell types. Emerging evidence suggests that lncRNAs account for the regulation of macrophage polarization and subsequent effects on respiratory diseases. In this review, we summarize the current published literature from the PubMed database concerning lncRNAs relevant to macrophage polarization and the underlying molecular mechanisms during the occurrence and development of respiratory diseases. These differentially expressed lncRNAs are expected to be biomarkers and targets for the therapeutic regulation of macrophage polarization during disease development.


Subject(s)
RNA, Long Noncoding , Respiration Disorders , Respiratory Tract Diseases , Humans , RNA, Long Noncoding/genetics , RNA, Long Noncoding/metabolism , Macrophages , Biomarkers/metabolism , Cell Differentiation/genetics , Respiratory Tract Diseases/genetics , Respiratory Tract Diseases/metabolism
3.
Int J Biol Sci ; 12(1): 120-32, 2016.
Article in English | MEDLINE | ID: mdl-26722223

ABSTRACT

Photodynamic therapy (PDT), a regulatory approved cancer treatment, is reported to be capable of causing immunogenic apoptosis. The current data reveal PDT can cause the dysregulation of "eat me" and "don't eat me" signal by generating reactive oxygen species (ROS) -mediated endoplasmic reticulum (ER) stress. This dysregulation probably contribute to the increased uptake of PDT-killed Lewis lung carcinoma (LLC) cells by homologous dendritic cells (DCs), accompanied by phenotypic maturation (CD80(high), CD86(high), and CD40(high)) and functional stimulation (NO(high), IL-10(absent)) of dendritic cells as well as subsequent T-cell responses. Morevover, C57BL/6 mice vaccinated with dendritic cells (DCs) pulsed with PDT-treated LLCs (PDT-DCs) or PDT-treated LLCs alone (PDT-LLCs) exhibited potent immunity against LLC tumors. In the current study, the PDT-induced immune response was characterized as a process related with the dysregulation of "eat me" signal and "don't eat me" signal, revealing the possibility for developing PDT into an antitumor vaccination strategy for personalized cancer immunotherapy.


Subject(s)
Cancer Vaccines/immunology , Dendritic Cells/immunology , Photochemotherapy/methods , Animals , Apoptosis/drug effects , Blotting, Western , Cancer Vaccines/therapeutic use , Carcinoma, Lewis Lung/immunology , Carcinoma, Lewis Lung/therapy , Cell Line, Tumor , Male , Mice , Mice, Inbred C57BL , Photosensitizing Agents
4.
Int Immunopharmacol ; 23(1): 192-204, 2014 Nov.
Article in English | MEDLINE | ID: mdl-25138378

ABSTRACT

The indoleamine 2,3-dioxygenase-(IDO-) mediated microenvironment plays an important role in tumor immune escape. It is known that ganoderic acid Me can enhance IFN-γ expression and IDO is preferentially induced by IFN-γ. However, whether GA-Me can induce IDO expression has not been clarified yet. We established stable clones of IDO-overexpressing 2 LL cells (2LL-EGFP-IDO). After co-culturing with IDO expressing or control vector-transfected 2LL-EGFP cells, T cell apoptosis was determined and the proportion of the regulatory T cells (Tregs) and CD8+ T cell subset was measured. The total cellular protein samples of 2 LL-EGFP-IDO cells were isolated for detecting JAK-STAT1 signalling pathway. Co-culture supernatants were used to detect amino acids and cytokines. IDO transfected 2 LL cells yielded high level of IDO enzymatic activity, resulting in complete depletion of tryptophan from the culture medium. We found that apoptosis occurred in T cells after cocultured with IDO+2LL cells and the proportion of CD4+CD25+ cells and FoxP3+ cells increased while CD8+ cells decreased. The specific inhibitor of IDO, 1-D-MT and GA-Me efficiently enhanced T cell apoptosis, increased Tregs, and reduced CD8+ T cells in vitro. Increased expression of IDO, p-JAK1 and p-STAT1 were confirmed by Western blot analysis. The levels of IFN-γ, IL-10, LDH and kynurenine in co-culture supernatant correspondingly increased, while tryptophan reduced. These results suggest that GA-Me contributing to IDO helps to create a tolerogenic milieu in lung tumors by directly inducing T cell apoptosis, restraining CD8+ T cell activation, and enhancing Treg-mediated immunosuppression.


Subject(s)
CD8-Positive T-Lymphocytes/drug effects , Carcinoma, Lewis Lung/drug therapy , Indoleamine-Pyrrole 2,3,-Dioxygenase/metabolism , Phytotherapy/methods , T-Lymphocytes, Regulatory/drug effects , Triterpenes/pharmacology , Animals , Apoptosis/drug effects , CD8-Positive T-Lymphocytes/immunology , Carcinoma, Lewis Lung/immunology , Clone Cells , Coculture Techniques , Humans , Indoleamine-Pyrrole 2,3,-Dioxygenase/genetics , Interferon-gamma/metabolism , Interleukin-1/metabolism , Janus Kinases/metabolism , Mice , Mice, Inbred C57BL , Reishi/immunology , STAT1 Transcription Factor/metabolism , Signal Transduction/drug effects , T-Lymphocytes, Regulatory/immunology , Tumor Escape
5.
J Cancer Res Clin Oncol ; 140(11): 1883-90, 2014 Nov.
Article in English | MEDLINE | ID: mdl-24980548

ABSTRACT

PURPOSE: Tumor cells have developed multiple mechanisms to escape immune recognition mediated by T cells. Indoleamine 2,3-dioxygenase (IDO), a tryptophan-catabolizing enzyme inducing immune tolerance, is involved in tumor escape from host immune systems in mice. Astragaloside IV (AS-IV), an extract from a commonly used Chinese medicinal plant Astragalus membranaceus, has been shown to be capable of restoring the impaired T-cell functions in cancer patients. The purpose of this study was to investigate the mechanisms underlying the anticancer properties of AS-IV. METHODS: Here, we used IDO-overexpressed murine Lewis lung carcinoma cells to establish an orthotopic lung cancer model in C57BL/6 mice. Next, tumor growth was evaluated in several different treatment groups: control (saline), AS-IV, paclitaxel, and 1-methyl tryptophan (an inhibitor of IDO). We then analyzed the percentages of various immune cell subsets among the splenic lymphocytes of lung cancer mice by flow cytometry. The level of IDO was measured by real-time PCR and Western blot. RESULTS: We showed that the growth of tumor was suppressed by AS-IV treatment in vivo. AS-IV also could down-regulate regulatory T cells (Tregs) and up-regulate cytotoxic T lymphocytes (CTLs) in vivo and in vitro. Consistent with its ability to interfere with T-cell immunity, AS-IV blocked IDO induction both in vitro and in vivo. CONCLUSIONS: The results of these studies indicate that AS-IV has in vivo anticancer activity and can enhance the immune response by inhibiting the Tregs frequency and induce the activity of CTLs, which might be related to the inhibition of IDO expression.


Subject(s)
Antineoplastic Agents/pharmacology , Carcinoma, Lewis Lung/immunology , Indoleamine-Pyrrole 2,3,-Dioxygenase/metabolism , Saponins/pharmacology , T-Lymphocytes, Cytotoxic/drug effects , T-Lymphocytes, Regulatory/drug effects , Triterpenes/pharmacology , Animals , Antineoplastic Agents/therapeutic use , Carcinoma, Lewis Lung/drug therapy , Carcinoma, Lewis Lung/enzymology , Carcinoma, Lewis Lung/pathology , Cell Line, Tumor , Coculture Techniques , Disease Progression , Drug Screening Assays, Antitumor , Female , Indoleamine-Pyrrole 2,3,-Dioxygenase/antagonists & inhibitors , Mice, Inbred C57BL , Neoplasm Transplantation , Paclitaxel/pharmacology , Paclitaxel/therapeutic use , Saponins/therapeutic use , T-Lymphocytes, Cytotoxic/immunology , T-Lymphocytes, Regulatory/immunology , Triterpenes/therapeutic use , Tryptophan/analogs & derivatives , Tryptophan/pharmacology , Tryptophan/therapeutic use , Tumor Burden/drug effects , Tumor Escape/drug effects
6.
Cell Stress Chaperones ; 19(6): 927-37, 2014 Nov.
Article in English | MEDLINE | ID: mdl-24984699

ABSTRACT

Photodynamic therapy (PDT) is a recently developed antitumor modality utilizing the generation of reactive oxygen species (ROS), through light irradiation of photosensitizers (PSs) localized in tumor. Interference with proper functioning of endoplasmic reticulum (ER) by ER-targeting PDT is a newly proposed strategy to achieve tumor cell death. The aim of this study is to establish a multifunctional model to screen and assess ER-targeting PSs based on luciferase reporters system. Upregulation of GRP78 is a biomarker for the onset of ER stress. CHOP is a key initiating player in ER stress-induced cell death. Here, the most sensitive fragments of GRP78 and CHOP promoters responding to ER-targeting PDT were mapped and cloned into pGL3-basic vector, forming -702/GRP78-Luc and -443/CHOP-Luc construct, respectively. We demonstrated that -702/GRP78-Luc expression can be used to indicate the ER-targeting of PSs, meanwhile estimate the ROS level induced by low-dose ER-targeting PDT. Moreover, the luciferase signaling of -443/CHOP-Luc showed highly consistence with apoptosis rate caused by ER-targeting PDT, suggesting that -443/CHOP-Luc can evaluate the antitumor properties of PSs. Hypericin, Foscan® and methylene blue were applied to verify the sensitivity and reliability of our model. These results proved that GRP78-CHOP model may be suitable to screen ER-targeting photosensitive compounds with lower cost and higher sensitivity than traditional ways.


Subject(s)
Endoplasmic Reticulum/drug effects , Heat-Shock Proteins/genetics , High-Throughput Screening Assays/methods , Luciferases/biosynthesis , Photochemotherapy , Photosensitizing Agents/pharmacology , Promoter Regions, Genetic/drug effects , Transcription Factor CHOP/genetics , Anthracenes , Apoptosis/drug effects , Dose-Response Relationship, Drug , Endoplasmic Reticulum/metabolism , Endoplasmic Reticulum/pathology , Endoplasmic Reticulum Chaperone BiP , Genes, Reporter , Humans , Luciferases/genetics , MCF-7 Cells , Mesoporphyrins/pharmacology , Methylene Blue/pharmacology , Oxidative Stress/drug effects , Perylene/analogs & derivatives , Perylene/pharmacology , Reactive Oxygen Species/metabolism , Transfection
7.
Biochem Pharmacol ; 2014 Feb 06.
Article in English | MEDLINE | ID: mdl-24508834

ABSTRACT

In our study, we find that photodynamic therapy (PDT), which generates reactive oxygen species (ROS) -mediated endoplasmic reticulum (ER) stress to inflict trauma in the targeted lesion, can break the balance between membrane damage-associated molecular patterns (DAMPs) and integrin-associated protein (CD47). The imbalance undermines the ability of lewis lung carcinoma (LLC) cells to escape immune attack by increasing the uptake of hypericin-mediated PDT(hyp-PDT) killed lewis lung carcinoma (LLC) cells by homologous dendritic cells (DCs), accompanied by phenotypic maturation (CD80high, CD86high, and CD40high) and functional stimulation (NOhigh, IL-10absent) of dendritic cells as well as subsequent T-cell response. Besides, C57BL/6 mice vaccinated with dendritic cells (DCs) pulsed with PDT-treated LLCs (PDT-DCs) or PDT-treated LLCs alone (PDT-LLCs) show potent immunity against LLC tumor. These data identify hypericin-induced PDT as a strong inducer of immunogenic apoptosis, providing an antitumor vaccination strategy for personalized cancer Immunotherapy.

8.
J Clin Immunol ; 33(3): 567-76, 2013 Apr.
Article in English | MEDLINE | ID: mdl-23196978

ABSTRACT

Myasthenia gravis (MG) are T-cell dependent antibody-mediated autoimmune disorders, microRNAs are important regulators of human autoimmune disease pathogenesis. Here, we investigated the miRNAs expression profiles in MG for the first time and found that miR-320a was significantly downregulated in MG patients compared to normal healthy people. Meanwhile, pro-inflammatory cytokins in MG patients were overexpressed. Furthermore, we identified MAPK1 as a direct target of miR-320a. Downregulation of miR-320a induced the overexpression of pro-inflammatory cytokins through promoting COX-2 expression. This process was modulated by ERK/ NF-κB pathways. Taken together, our findings suggested that miR-320a could play a role in modulation of inflammatory cytokins production.


Subject(s)
Cytokines/genetics , Inflammation Mediators , MicroRNAs/genetics , Mitogen-Activated Protein Kinase 1/genetics , Myasthenia Gravis/genetics , Adult , Aged , Base Sequence , Case-Control Studies , Cell Line, Tumor , Cluster Analysis , Cytokines/metabolism , Female , Gene Expression Profiling , Gene Expression Regulation , Humans , Male , MicroRNAs/chemistry , Middle Aged , Mitogen-Activated Protein Kinase 1/metabolism , Myasthenia Gravis/metabolism , NF-kappa B/metabolism , RNA Processing, Post-Transcriptional , Signal Transduction
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