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1.
BMC Vet Res ; 19(1): 161, 2023 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-37715215

RESUMO

BACKGROUND: Subcutaneous emphysema and pneumomediastinum are rare complications associated with orbital blowout pathological fracture. CASE PRESENTATION: A 7-year old, castrated male Abbysinian cat presented with anorexia, lethargy, nausea, eyelid swelling, nasal discharge, and sneezing. Based on the clinical and diagnostic work-up, the cat was diagnosed with T cell high-grade nasal lymphoma associated with orbital pathological fracture due to the tumour invasion. After chemotherapy, the cat showed massive subcutaneous emphysema from frontal region to abdomen and pneumomediastinum due to orbital blowout pathological fracture. As the nasal mass decreased in volume; the air had moved from the maxillary sinus to the subcutaneous region and the mediastinum through fascial planes in the head and neck region. CONCLUSIONS: This is a first case report of a massive subcutaneous emphysema and pneumomediastinum due to an orbital blowout pathological fracture following chemotherapy in feline nasal lymphoma in veterinary medicine.


Assuntos
Doenças do Gato , Fraturas Espontâneas , Linfoma de Células T Periférico , Linfoma de Células T , Enfisema Mediastínico , Enfisema Subcutâneo , Masculino , Gatos , Animais , Enfisema Mediastínico/etiologia , Enfisema Mediastínico/veterinária , Fraturas Espontâneas/veterinária , Nariz , Enfisema Subcutâneo/etiologia , Enfisema Subcutâneo/veterinária , Linfoma de Células T/veterinária , Linfoma de Células T Periférico/veterinária , Doenças do Gato/etiologia
2.
BMC Vet Res ; 18(1): 261, 2022 Jul 05.
Artigo em Inglês | MEDLINE | ID: mdl-35790968

RESUMO

BACKGROUND: Endothelial cell-specific molecule-1 (ESM-1) has emerged as a potential biomarker for cardiovascular disease in humans. Myxomatous mitral valve disease (MMVD) is the most common heart disease in dogs, and we hypothesized that MMVD causes chronic inflammation that increases susceptibility to endothelial glycocalyx (eGCX) damage. In this study, we measured the concentration of ESM-1 in a group of dogs with MMVD and evaluated factors affecting eGCX damage. RESULTS: Sixty-four dogs (control, n = 6; MMVD, n = 58) were enrolled in this study. There was no significant difference in serum ESM-1 concentrations among the MMVD stages. The serum ESM-1 concentration was significantly higher in the death group than in the alive group in MMVD dogs. (p = 0.006). In five dogs with MMVD, serum ESM-1 concentrations tended to decrease when the cardiac drug (pimobendan, furosemide, and digoxin) dose was increased. CONCLUSIONS: In cases where MMVD progressed to decompensated heart failure with clinical symptoms and resulted in death, the concentration of serum ESM-1 increased significantly. Therefore, ESM-1 could be utilized as a new potential negative prognostic factor in patients with MMVD.


Assuntos
Doenças do Cão , Doenças das Valvas Cardíacas , Animais , Biomarcadores , Cães , Células Endoteliais , Glicocálix , Doenças das Valvas Cardíacas/veterinária , Valva Mitral , Fatores de Transcrição
3.
J Inflamm Res ; 14: 4987-5000, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34616168

RESUMO

INTRODUCTION: Syndecan-2 expression is elevated during chronic inflammation and cancer development, and its shedding is observed in cancer patients. However, it remained unknown whether inflammation triggers syndecan-2 shedding. METHODS: The colitis model was produced in C57BL/6 mice by oral administration of 2-3% dextran sulfate sodium (DSS) in the drinking water. Syndecan-2 and MMP-7 expression levels in tissues and cells were detected by real-time PCR, Western blotting, and immunohistochemistry. Shed syndecan-2 levels were detected by slot blotting. For tissue culture, colon tissues were divided into proximal, transverse, and distal parts, and incubated in culture media. RESULTS: In C57BL/6 mice with DSS-induced colitis, syndecan-2 shedding began to increase after week 12 of chronic inflammation and continued to increase at week 15. The level of shed syndecan-2 correlated with the colocalization of syndecan-2 and MMP-7 in distal colon tissues. The mRNA expression of IL-6 was increased specifically in trans-distal colon tissues from weeks 9 to 15. IL-6 induced syndecan-2 expression and shedding and MMP-7 expression in ex vivo-cultured distal colon tissues and adenoma cell lines derived from the distal colon. IL-6 treatment induced STAT3 phosphorylation and MMP-7 expression in DLD-1 cells. The application of MMP-7 to ex vivo-cultured colon tissues increased the shedding of syndecan-2 to the culture medium. CONCLUSION: Our findings suggest that chronic inflammation induces syndecan-2 shedding via the site-specific colocalization of syndecan-2 with MMP-7 in the distal colon.

4.
FASEB J ; 33(10): 11381-11395, 2019 10.
Artigo em Inglês | MEDLINE | ID: mdl-31311305

RESUMO

We previously reported that syndecan-2 expression is increased on the colonic epithelium during chronic inflammation. Here, we report that syndecan-2 exhibits a different pattern of site-specific colonic expression during acute inflammation. Syndecan-2 expression was up-regulated predominantly in the proximal colon of dextran sulfate sodium-induced colitis mice. The colitis-associated up-regulation of syndecan-2 was barely detected in Rag-1-/- (recombination activating gene 1 knockout) mice under colitis-inducing conditions. Increased syndecan-2 expression correlated with increased levels of infiltrated CD4+ IL-17A+ T cells in the proximal colon. Serum levels of IL-17A were increased during the acute inflammatory response in normal mice but not Rag-1-/- mice. IL-17A directly induced IL-17 receptor (IL-17RA) and syndecan-2 expression in ex vivo-cultured proximal colon tissues and adenoma cell lines from proximal colon. IL-17RA knockdown reduced the IL-17A-mediated syndecan-2 expression in SNU1235 cells. No elevation of syndecan-2 or IL-17RA was observed in colonic tissues from IL-17A-/- mice during colitis induction. Finally, increased expression of syndecan-2 and IL-17RA was observed in the proximal colons of cecal ligation and puncture-induced sepsis mice and infectious pan colitis patients. Together, these data suggest that acute inflammation induces syndecan-2 expression predominantly in the proximal colon via IL-17A-IL-17RA signaling during the early stage of the inflammatory response and that proximal colonic syndecan-2 might be a biomarker for acute inflammation.-Hong, H., Song, H.-K., Hwang, E. S., Lee, A. R., Han, D. S., Kim, S.-E., Oh, E.-S. Up-regulation of syndecan-2 in proximal colon correlates with acute inflammation.


Assuntos
Colo/metabolismo , Inflamação/metabolismo , Sindecana-2/metabolismo , Regulação para Cima/fisiologia , Animais , Linhagem Celular Tumoral , Colite/induzido quimicamente , Colite/metabolismo , Colo/efeitos dos fármacos , Sulfato de Dextrana/farmacologia , Humanos , Inflamação/induzido quimicamente , Interleucina-17/metabolismo , Mucosa Intestinal/efeitos dos fármacos , Mucosa Intestinal/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Receptores de Interleucina-17/metabolismo , Transdução de Sinais/fisiologia , Ativação Transcricional/fisiologia
5.
Cell Signal ; 52: 121-126, 2018 12.
Artigo em Inglês | MEDLINE | ID: mdl-30195038

RESUMO

Cell surface receptors must specifically recognize an extracellular ligand and then trigger an appropriate response within the cell. Their general structure enables this, as it comprises an extracellular domain that can bind an extracellular ligand, a cytoplasmic domain that can transduce a signal inside the cell to produce an appropriate response, and a transmembrane domain that links the two and is responsible for accurately delivering specific information on a binding event from the extracellular domain to the cytoplasmic domain, to trigger the proper response. A vast body of research has focused on elucidating the specific mechanisms responsible for regulating extracellular binding events and the subsequent interactions of the cytoplasmic domain with intracellular signaling. In contrast, far less work has focused on examining how the transmembrane domain links these domains and delivers the necessary information. In this review, we propose the importance of the transmembrane domain as a signal regulator. We highlight the cell adhesion receptor, syndecan, as a special case, and propose that the transmembrane domain-mediated oligomerization of the syndecan cytoplasmic domain is a unique regulatory mechanism in syndecan signaling.


Assuntos
Membrana Celular/metabolismo , Receptores de Superfície Celular/química , Sindecanas/química , Animais , Adesão Celular , Humanos , Domínios Proteicos , Multimerização Proteica , Transdução de Sinais
6.
FASEB J ; 31(4): 1516-1530, 2017 04.
Artigo em Inglês | MEDLINE | ID: mdl-28031321

RESUMO

Chronic inflammation is known to be a key causative factor in tumor progression, but we do not yet fully understand the molecular mechanism through which inflammation leads to cancer. Here, we report that the dextran sulfate sodium (DSS)-induced mouse model of chronic colitis is associated with increases in the serum level of IL-1ß and the colonic epithelial expression of the cell-surface heparan sulfate proteoglycan, syndecan-2. We further show that IL-1ß stimulated the transcription of syndecan-2 via NF-κB-dependent FOXO3a activation in CCD841CoN normal colonic epithelial cells and early-stage HT29 colon cancer cells. Inflammatory hypoxia was observed in the colonic epithelia of mice with chronic colitis, suggesting that hypoxic stress is involved in the regulation of syndecan-2 expression. Consistently, experimental inflammatory hypoxia induced hypoxia inducible factor-1α-dependent FOXO3a expression and the p38 MAPK-mediated nuclear localization of FOXO3a. FOXO3a directly mediated syndecan-2 expression in both cell lines and the colonic epithelia of mice with DSS-induced colitis. Moreover, syndecan-2 expression was detected in azoxymethane/DSS-induced colon tumors. Together, these data demonstrate that inflammatory hypoxia up-regulates syndecan-2 via the IL-1ß-NF-κB-FOXO3a pathway. These findings provide new mechanistic insights into inflammatory hypoxia-mediated syndecan-2 expression to connect chronic inflammation and the development of colon cancer.-Choi, S., Chung, H., Hong, H., Kim, S. Y., Kim, S.-E., Seoh, J.-Y., Moon, C. M., Yang, E. G., Oh, E.-S. Inflammatory hypoxia induces syndecan-2 expression through IL-1ß-mediated FOXO3a activation in colonic epithelia.


Assuntos
Colite Ulcerativa/metabolismo , Colo/metabolismo , Proteína Forkhead Box O3/metabolismo , Interleucina-1beta/metabolismo , Mucosa Intestinal/metabolismo , Oxigênio/metabolismo , Sindecana-2/genética , Animais , Hipóxia Celular , Linhagem Celular , Colo/citologia , Células HT29 , Humanos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , NF-kappa B/metabolismo , Sindecana-2/metabolismo , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
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